CINXE.COM

<!DOCTYPE html> <html lang="en" dir="ltr"> <head>  <script async src="https://www.googletagmanager.com/gtag/js?id=G-P63WKM1TM1"></script> <script> window.dataLayer = window.dataLayer || []; function gtag(){dataLayer.push(arguments);} gtag('js', new Date()); gtag('config', 'G-P63WKM1TM1'); </script>  <script type="text/javascript" > (function(m,e,t,r,i,k,a){m[i]=m[i]||function(){(m[i].a=m[i].a||[]).push(arguments)}; m[i].l=1*new Date(); for (var j = 0; j < document.scripts.length; j++) {if (document.scripts[j].src === r) { return; }} k=e.createElement(t),a=e.getElementsByTagName(t)[0],k.async=1,k.src=r,a.parentNode.insertBefore(k,a)}) (window, document, "script", "https://mc.yandex.ru/metrika/tag.js", "ym"); ym(55165297, "init", { clickmap:false, trackLinks:true, accurateTrackBounce:true, webvisor:false }); </script> <noscript><div><img src="https://mc.yandex.ru/watch/55165297" style="position:absolute; left:-9999px;" alt="" /></div></noscript>    <title>Search results for: Nrf2 oxidative stress</title> <meta name="description" content="Search results for: Nrf2 oxidative stress"> <meta name="keywords" content="Nrf2 oxidative stress"> <meta name="viewport" content="width=device-width, initial-scale=1, minimum-scale=1, maximum-scale=1, user-scalable=no"> <meta charset="utf-8"> <link href="https://cdn.waset.org/favicon.ico" type="image/x-icon" rel="shortcut icon"> <link href="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/css/bootstrap.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/plugins/fontawesome/css/all.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/css/site.css?v=150220211555" rel="stylesheet"> </head> <body> <header> <div class="container"> <nav class="navbar navbar-expand-lg navbar-light"> <a class="navbar-brand" href="https://waset.org"> <img src="https://cdn.waset.org/static/images/wasetc.png" alt="Open Science Research Excellence" title="Open Science Research Excellence" /> </a> <button class="d-block d-lg-none navbar-toggler ml-auto" type="button" data-toggle="collapse" data-target="#navbarMenu" aria-controls="navbarMenu" aria-expanded="false" aria-label="Toggle navigation"> <span class="navbar-toggler-icon"></span> </button> <div class="w-100"> <div class="d-none d-lg-flex flex-row-reverse"> <form method="get" action="https://waset.org/search" class="form-inline my-2 my-lg-0"> <input class="form-control mr-sm-2" type="search" placeholder="Search Conferences" value="Nrf2 oxidative stress" name="q" aria-label="Search"> <button class="btn btn-light my-2 my-sm-0" type="submit"><i class="fas fa-search"></i></button> </form> </div> <div class="collapse navbar-collapse mt-1" id="navbarMenu"> <ul class="navbar-nav ml-auto align-items-center" id="mainNavMenu"> <li class="nav-item"> <a class="nav-link" href="https://waset.org/conferences" title="Conferences in 2024/2025/2026">Conferences</a> </li> <li class="nav-item"> <a class="nav-link" href="https://waset.org/disciplines" title="Disciplines">Disciplines</a> </li> <li class="nav-item"> <a class="nav-link" href="https://waset.org/committees" rel="nofollow">Committees</a> </li> <li class="nav-item dropdown"> <a class="nav-link dropdown-toggle" href="#" id="navbarDropdownPublications" role="button" data-toggle="dropdown" aria-haspopup="true" aria-expanded="false"> Publications </a> <div class="dropdown-menu" aria-labelledby="navbarDropdownPublications"> <a class="dropdown-item" href="https://publications.waset.org/abstracts">Abstracts</a> <a class="dropdown-item" href="https://publications.waset.org">Periodicals</a> <a class="dropdown-item" href="https://publications.waset.org/archive">Archive</a> </div> </li> <li class="nav-item"> <a class="nav-link" href="https://waset.org/page/support" title="Support">Support</a> </li> </ul> </div> </div> </nav> </div> </header> <main> <div class="container mt-4"> <div class="row"> <div class="col-md-9 mx-auto"> <form method="get" action="https://publications.waset.org/abstracts/search"> <div id="custom-search-input"> <div class="input-group"> <i class="fas fa-search"></i> <input type="text" class="search-query" name="q" placeholder="Author, Title, Abstract, Keywords" value="Nrf2 oxidative stress"> <input type="submit" class="btn_search" value="Search"> </div> </div> </form> </div> </div> <div class="row mt-3"> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Commenced</strong> in January 2007</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Frequency:</strong> Monthly</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Edition:</strong> International</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Paper Count:</strong> 4134</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: Nrf2 oxidative stress</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4134</span> Role of Sulforaphane on Alleviating Duchenne Muscular Dystrophy(DMD) through Activation of Nrf2</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Sulforaphane (SFN) possesses powerful chemo-preventive effects and plays a crucial role on oxidative stress and inflammatory. In our recent study, SFN treatment could relieve muscular dystrophy in mdx mice by activating Nrf2 (NF-E2 related factor 2). Moreover, our findings indicated that SFN-activated Nrf2 alleviated muscle inflammation in dystrophin-deficient mdx mice through suppressing NF-κB signaling pathway. Collectively, SFN-induced Nrf2 molecular pathway might be a promising approach for treatment of the patients with Duchenne muscular dystrophy. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=sulforaphane" title="sulforaphane">sulforaphane</a>, <a href="https://publications.waset.org/abstracts/search?q=Duchenne%20muscular%20dystrophy" title=" Duchenne muscular dystrophy"> Duchenne muscular dystrophy</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title=" fibrosis"> fibrosis</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a> </p> <a href="https://publications.waset.org/abstracts/41533/role-of-sulforaphane-on-alleviating-duchenne-muscular-dystrophydmd-through-activation-of-nrf2" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/41533.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">214</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4133</span> Ramification of Pemphigus Vulgaris Sera and the Monoclonal Antibody Against Desmoglein-3 on Nrf2 Expression in Keratinocyte Cultures</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Faris%20Mohsin%20Alabeedi">Faris Mohsin Alabeedi</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Pemphigus Vulgaris (PV) is a life-threatening autoimmune blistering disease characterized by the presence of autoantibodies directed against the epidermis's surface proteins. There are two forms of PV, mucocutaneous and mucosal-dominant PV. Disruption of the cell junctions is a hallmark of PV due to the autoantibodies targeting the desmosomal cadherins, desmoglein-3 (Dsg3) and desmoglein-1, leading to acantholysis in the skin and mucous membrane. Although the pathogenesis of PV is known, the detailed molecular events remain not fully understood. Our recent study has shown that both the PV sera and pathogenic anti-Dsg3 antibody AK23 can induce ROS and cause oxidative stress in cultured keratinocytes. In line with our finding, other independent studies also demonstrate oxidative stress in PV. Since Nrf2 plays a crucial role in cellular anti-oxidative stress response, we hypothesize that the expression of Nrf2 may alter in PV. Thus, treatment of cells with PV sera or AK23 may cause changes in Nrf2 expression and distribution. The purpose of this study was to examine the effect of AK23 and PV sera on Nrf2 in a normal human keratinocyte cell line, such as NTERT cells. Both a time-course and dose-dependent experiments with AK23, alongside the matched isotype control IgG, were performed in keratinocyte cultures and analysed by immunofluorescence for Nrf2 and Dsg3. Additionally, the same approach was conducted with the sera from PV patients and healthy individuals that served as a control in this study. All the fluorescent images were analysed using ImageJ software. Each experiment was repeated twice. In general, variations were observed throughout this study. In the dose-response experiments, although enhanced Dsg3 expression was consistently detected in AK23 treated cells, the expression of Nrf2 showed no consistent findings between the experiments, although changes in its expression were noticeable in cells treated with AK23. In the time-course study, a trend with induction of Nrf2 over time was shown in control cells treated with mouse isotype IgG. Treatment with AK23 showed a reduction of Nrf2 in a time-dependent manner, especially at the 24-hour time point. However, the earlier time points, such as 2 hours and 6 hours with AK23 treatments, detected somewhat variations. Finally, PV sera caused a decrease of Dsg3, but on the other hand, variations were observed in Nrf2 expression in PV sera treated cells. In general, PV sera seemed to cause a reduction of Nrf2 in the majority of PV sera treated samples. In addition, more pronounced cytoplasmic expression of Nrf2 has been observed in PV sera treated cells than those treated with AK23, suggesting that polyclonal and monoclonal IgG might induce a different effect on Nrf2 expression and distribution. Further experimental studies are crucial to obtain a more coincide global view of Nrf2-mediated gene regulation. In particular, Pemphigus Voulgaris studies assessing how the Nrf2-dependent network changes from a physiological to a pathological condition can provide insight into disease mechanisms and perhaps initiate further treatment approaches. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=pemphigus%20vulgaris" title="pemphigus vulgaris">pemphigus vulgaris</a>, <a href="https://publications.waset.org/abstracts/search?q=monoclonal%20antibody%20against%20desmoglein-3" title=" monoclonal antibody against desmoglein-3"> monoclonal antibody against desmoglein-3</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2%20oxidative%20stress" title=" Nrf2 oxidative stress"> Nrf2 oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=keratinocyte%20cultures" title=" keratinocyte cultures"> keratinocyte cultures</a> </p> <a href="https://publications.waset.org/abstracts/156971/ramification-of-pemphigus-vulgaris-sera-and-the-monoclonal-antibody-against-desmoglein-3-on-nrf2-expression-in-keratinocyte-cultures" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/156971.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">75</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4132</span> Sulforaphane Attenuates Muscle Inflammation in Dystrophin-Deficient Mdx Mice via Nrf2/HO-1 Signaling Pathway</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Ruilin%20Xue"> Ruilin Xue</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Backgrounds: Inflammation is widely distributed in patients with Duchenne muscular dystrophy (DMD), and ultimately leads to progressive deterioration of muscle function with the co-effects of chronic muscle damage, oxidative stress, and reduced oxidative capacity. NF-E2-related factor 2 (Nrf2) plays a critical role in defending against inflammation in different tissues via activation of phase II enzymes, heme oxygenase-1 (HO-1). However, whether Nrf2/HO-1 pathway can attenuate muscle inflammation on DMD remains unknown. The purpose of this study was to determine the anti-inflammatory effects of Sulforaphane (SFN) on DMD. Methods: 4-week-old male mdx mice were treated with SFN by gavage (2 mg/kg body weight per day) for 4 weeks. Gastrocnemius, tibial anterior and triceps brachii muscles were collected for related analysis. Immune cell infiltration in skeletal muscles was analyzed by H&E staining and immuno-histochemistry. Moreover, the expressions of inflammatory cytokines,pro-inflammatory cytokines and Nrf2/HO-1 pathway were detected by western blot, qRT-PCR, immunohistochemistry and immunofluorescence assays. Results: Our results demonstrated that SFN treatment increased the expression of muscle phase II enzymes HO-1 in Nrf2 dependent manner. Inflammation in mdx skeletal muscles was reduced by SFN treatment as indicated by decreased immune cell infiltration and lower expressions of the inflammatory cytokines CD45, pro-inflammatory cytokines tumour necrosis factor-α and interleukin-6 in the skeletal muscles of mdx mice. Conclusions: Collectively, these results show that SFN can ameliorate muscle inflammation in mdx mice by Nrf2/HO-1 pathway, which indicates Nrf2/HO-1 pathway may represent a new therapeutic target for DMD. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=sulforaphane" title="sulforaphane">sulforaphane</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a>, <a href="https://publications.waset.org/abstracts/search?q=HO-1" title=" HO-1"> HO-1</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a> </p> <a href="https://publications.waset.org/abstracts/19664/sulforaphane-attenuates-muscle-inflammation-in-dystrophin-deficient-mdx-mice-via-nrf2ho-1-signaling-pathway" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/19664.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">334</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4131</span> Involvement of Nrf2 in Kolaviron-Mediated Attenuation of Behavioural Incompetence and Neurodegeneration in a Murine Model of Parkinson's Disease</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Yusuf%20E.%20Mustapha">Yusuf E. Mustapha</a>, <a href="https://publications.waset.org/abstracts/search?q=Inioluwa%20A%20Akindoyeni"> Inioluwa A Akindoyeni</a>, <a href="https://publications.waset.org/abstracts/search?q=Oluwatoyin%20G.%20Ezekiel"> Oluwatoyin G. Ezekiel</a>, <a href="https://publications.waset.org/abstracts/search?q=Ifeoluwa%20O.%20Awogbindin"> Ifeoluwa O. Awogbindin</a>, <a href="https://publications.waset.org/abstracts/search?q=Ebenezer%20O.%20Farombi"> Ebenezer O. Farombi</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Parkinson's disease (PD) is the most prevalent motor disorder. Available therapies are palliative with no effect on disease progression. Kolaviron (KV), a natural anti-inflammatory and antioxidant agent, has been reported to possess neuroprotective effects in Parkinsonian flies and rats. Objective: The present study investigates the neuroprotective effect of KV, focusing on the DJ1/Nrf2 signaling pathway. Methodology: All-trans retinoic acid (ATRA, 10 mg/kg, i.p.) was used to inhibit Nrf2. Murine model of PD was established with four doses of MPTP (20 mg/kg i.p.) at 2 hours interval. MPTP mice were pre-treated with either KV (200 mg/kg/day p.o), ATRA, or both conditions for seven days before PD induction. Motor behaviour was evaluated, and markers of oxidative stress/damage and its regulators were assessed with immunofluorescence and ELISA techniques. Results: MPTP-treated mice covered less distance with reduced numbers of anticlockwise rotations, heightened freezing, and prolonged immobility when compared to control. However, KV significantly attenuated these deficits. Pretreatment of MPTP mice with KV upregulated Nrf2 expression beyond MPTP level with a remarkable reduction in Keap1 expression and marked elevation of DJ-1 level, whereas co-administration with ATRA abrogated these effects. KV treatment restored MPTP-mediated depletion of endogenous antioxidant, striatal oxidative stress, oxidative damage, and inhibition of acetylcholinesterase activity. However, ATRA treatment potentiated acetylcholinesterase inhibition and attenuated the protective effect of KV on the level of nitric oxide and activities of catalase and superoxide dismutase. Conclusion: Kolaviron protects Parkinsonian mice by stabilizing and activating the Nrf2 signaling pathway. Thus, kolaviron can be explored as a pharmacological lead in PD management. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Garcinia%20kola" title="Garcinia kola">Garcinia kola</a>, <a href="https://publications.waset.org/abstracts/search?q=Kolaviron" title=" Kolaviron"> Kolaviron</a>, <a href="https://publications.waset.org/abstracts/search?q=Parkinson%20Disease" title=" Parkinson Disease"> Parkinson Disease</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a>, <a href="https://publications.waset.org/abstracts/search?q=behavioral%20incompetence" title=" behavioral incompetence"> behavioral incompetence</a>, <a href="https://publications.waset.org/abstracts/search?q=neurodegeneration" title=" neurodegeneration"> neurodegeneration</a> </p> <a href="https://publications.waset.org/abstracts/129217/involvement-of-nrf2-in-kolaviron-mediated-attenuation-of-behavioural-incompetence-and-neurodegeneration-in-a-murine-model-of-parkinsons-disease" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/129217.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">101</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4130</span> Effect of Auraptene on the Enzymatic Glutathione Redox-System in Nrf2 Knockout Mice</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ludmila%20A.%20Gavriliuc">Ludmila A. Gavriliuc</a>, <a href="https://publications.waset.org/abstracts/search?q=Jerry%20McLarty"> Jerry McLarty</a>, <a href="https://publications.waset.org/abstracts/search?q=Heather%20E.%20Kleiner"> Heather E. Kleiner</a>, <a href="https://publications.waset.org/abstracts/search?q=J.%20Michael%20Mathis"> J. Michael Mathis</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Abstract -- Background: The citrus coumarine Auraptene (Aur) is an effective chemopreventive agent, as manifested in many models of diseases and cancer. Nuclear factor erythroid 2-related factor (Nrf2) is an important regulator of genes induced by oxidative stress, such as glutathione S-transferases, heme oxygenase-1, and peroxiredoxin 1, by activating the antioxidant response element (ARE). Genetic and biochemical evidence has demonstrated that glutathione (GSH) and glutathione-dependent enzymes, glutathione reductase (GR), glutathione peroxidases (GPs), glutathione S-transferases (GSTs) are responsible for the control of intracellular reduction-oxidation status and participate in cellular adaptation to oxidative stress. The effect of Aur on the activity of GR, GPs (Se-GP and Se-iGP), and content of GSH in the liver, kidney, and spleen is insufficiently explored. Aim: Our goal was the examination of the Aur influence on the redox-system of GSH in Nrf2 wild type and Nrf2 knockout mice via activation of Nrf2 and ARE. Methods: Twenty female mice, 10 Nrf2 wild-type (WT) and 10 Nrf2 (-/-) knockout (KO), were bred and genotyped for our study. The activity of GR, Se-GP, Se-iGP, GST, G6PD, CytP450 reductase, catalase (Cat), and content of GSH were analyzed in the liver, kidney, and spleen using Spectrophotometry methods. The results of the specific activity of enzymes and the amount of GSH were analyzed with ANOVA and Spearman statistical methods. Results: Aur (200 mg/kg) treatment induced hepatic GST, GR, Se-GP activity and inhibited their activity in the spleen of mice, most likely via activation of the ARE through Nrf2. Activation in kidney Se-GP and G6PD by Aur is also controlled, apparently through Nrf2. Results of the non-parametric Spearman correlation analysis indicated the strong positive correlation between GR and G6PD only in the liver in WT control mice (r=+0.972; p < 0.005) and in the kidney KO control mice (r=+0.958; p < 0.005). The observed low content of GSH in the liver of KO mice indicated an increase in its participation in the neutralization of toxic substances with the absence of induction of GSH-dependent enzymes, such as GST, GR, Se-GP, and Se-iGP. Activation of CytP450 in kidney and spleen and Cat in the liver in KO mice probably revealed another regulatory mechanism for these enzymes. Conclusion: Thereby, obtained results testify that Aur can modulate the activity of genes and antioxidant enzymatic redox-system of GSH, responsible for the control of intracellular reduction-oxidation status. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=auraptene" title="auraptene">auraptene</a>, <a href="https://publications.waset.org/abstracts/search?q=glutathione" title=" glutathione"> glutathione</a>, <a href="https://publications.waset.org/abstracts/search?q=GST" title=" GST"> GST</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a> </p> <a href="https://publications.waset.org/abstracts/133552/effect-of-auraptene-on-the-enzymatic-glutathione-redox-system-in-nrf2-knockout-mice" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/133552.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">149</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4129</span> Anethum graveolens Prevents Liver and Kidney Injury, Oxidative Stress and Inflammation in Mice Exposed to Nicotine Perinatally</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Saleh%20N.%20Maodaa">Saleh N. Maodaa</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Perinatal exposure to nicotine imbalances the redox status in newborns. This study investigated the effect of Anethum graveolens (dill) extract on oxidative stress and tissue injury in the liver and kidney of mice newborns exposed to nicotine perinatally. Pregnant mice received nicotine (0.25 mg/kg) on gestational day 12 to day 5 after birth and/or A. graveolens extract on a gestational day 1 to day 15 after birth. Newborn mice exposed to nicotine showed multiple histopathological alterations in the kidney and liver, including inflammatory cell infiltration and degenerative changes. Nicotine exposure increased hepatic and renal reactive oxygen species (ROS), lipid peroxidation, tumor necrosis factor (TNF-_), interleukin-6 (IL-6), and inducible nitric oxide synthase (iNOS) (p < 0.001), and decreased antioxidant defenses (p < 0.001). A. graveolens supplementation significantly prevented liver and kidney injury, suppressed ROS generation (p < 0.001), lipid peroxidation (p < 0.001), and inflammatory response (p < 0.001), and enhanced antioxidant defenses. In addition, A. graveolens upregulated hepatic and renal Nrf2 and HO-1 mRNA and increased HO-1 activity in normal and nicotine-exposed mice. In conclusion, A. graveolens protects against perinatal nicotine-induced oxidative stress, inflammation, and tissue injury in the liver and kidney of newborn mice. A. graveolens upregulated hepatic and renal Nrf2/HO-1 signaling and enhanced antioxidant defenses in mice. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=dill" title="dill">dill</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=cytokines" title=" cytokines"> cytokines</a>, <a href="https://publications.waset.org/abstracts/search?q=nicotine" title=" nicotine"> nicotine</a> </p> <a href="https://publications.waset.org/abstracts/159904/anethum-graveolens-prevents-liver-and-kidney-injury-oxidative-stress-and-inflammation-in-mice-exposed-to-nicotine-perinatally" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/159904.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">80</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4128</span> Silica Nanoparticles Induced Oxidative Stress and Inflammation in MRC-5 Human Lung Fibroblasts </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Anca%20Dinischiotu">Anca Dinischiotu</a>, <a href="https://publications.waset.org/abstracts/search?q=Sorina%20Nicoleta%20Voicu"> Sorina Nicoleta Voicu</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Silica nanoparticles (SiO2-NPs) are widely used in consumer products such as paints, plastics, insulation materials, tires, concrete production, as well as in gene delivery systems and imaging procedures. Environmental human exposure to them occurs during utilization of these products, in a time-dependent manner, the uptake being by topic and inhalation route especially. SiO2-NPs enter cells and induce membrane damage, oxidative stress and inflammatory reactions in a concentration-dependent manner. In this study, MRC-5 cells (human fetal lung fibroblasts) were exposed to amorphous SiO2-NPs at a dose of 62.5 μg/ml for 24, 48 and 72 hours. The size distribution of NPs was a lognormal function, in the range 3-14 nm. A time-dependent decrease of total reduced glutathione concentration by 36%, 50%, and 78% and an increase of NO level by 62%, 32%, respectively 24% compared to control were noticed. An up-regulation of NF-kB expression by 20%, 50% respectively 10% and of Nrf-2 by 139%, 58%, and 16% compared to control after 24, 48 and 72 hours was noticed also. The expression of IL-1β, IL-6, IL-8, and COX-2 was up-regulated in a time-dependent manner. Also, the expression of MMP-2 and MMP-9 were down-regulated after 48 and 72 hours, whereas their activities raised in a time-dependent manner. Exposure of cells to NPs up-regulated the expression of inducible NO synthase, as previously was shown, and probably this is the reason for the increased level of NO, that can react with the thiol groups of reduced glutathione molecules, diminishing its concentration Nrf2 is a transcription factor translocated in nucleus, under oxidative stress, where downstream gene expression activates in order to modulate the adaptive intracellular response against oxidative stress. The cross-talk between Nrf2 and NF-kB activities regulates the inflammatory processes. The activation of NF-kB could activate up-regulation of IL-1β, IL-6, and IL-8. The increase of COX-2 expression could be correlated with IL-1β one. Also, probably in response to the pro-inflammatory cytokines, MMP-2 and MMP-9 were induced and activated. In conclusion, the exposure of MRC-5 cells to SiO2-NPs generated inflammation in a time-dependent manner. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=inflammation" title="inflammation">inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=MRC-5%20cells" title=" MRC-5 cells"> MRC-5 cells</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=silica%20nanoparticles" title=" silica nanoparticles"> silica nanoparticles</a> </p> <a href="https://publications.waset.org/abstracts/94598/silica-nanoparticles-induced-oxidative-stress-and-inflammation-in-mrc-5-human-lung-fibroblasts" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/94598.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">146</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4127</span> Neuroprotective Effect of Tangeretin against Potassium Dichromate-Induced Acute Brain Injury via Modulating AKT/Nrf2 Signaling Pathway in Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ahmed%20A.%20Sedik">Ahmed A. Sedik</a>, <a href="https://publications.waset.org/abstracts/search?q=Doaa%20Mahmoud%20Shuaib"> Doaa Mahmoud Shuaib</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Brain injury is a cause of disability and death worldwide. Potassium dichromate (PD) is an environmental contaminant widely recognized as teratogenic, carcinogenic, and mutagenic towards animals and humans. The aim of the present study was to investigate the possible neuroprotective effects of tangeretin (TNG) on PD-induced brain injury in rats. Forty male adult Wistar rats were randomly and blindly allocated into four groups (8 rats /group). The first group received saline intranasally (i.n.). The second group received a single dose of PD (2 mg/kg, i.n.). The third group received TNG (50 mg/kg; orally) for 14 days, followed by i.n. of PD on the last day of the experiment. Four groups received TNG (100 mg/kg; orally) for 14 days, followed by i.n. of PD on the last day of the experiment. 18- hours after the final treatment, behavioral parameters, neuro-biochemical indices, FTIR analysis, and histopathological studies were evaluated. Results of the present study revealed that rats intoxicated with PD promoted oxidative stress and inflammation via an increase in MDA and a decrease in Nrf2 signaling pathway and GSH levels with an increase in brain contents of TNF-α, IL-10, and NF-kβ and reduced AKT levels in brain homogenates. Treatment with TNG (100 mg/kg; orally) ameliorated behavioral, cholinergic activities and oxidative stress, decreased the elevated levels of pro-inflammatory mediators; TNF-α, IL-10, and NF-κβ elevated AKT pathway with corrected FTIR spectra with a decrease in brain content of chromium residues detected by atomic absorption spectrometry. Also, TNG administration restored the morphological changes as degenerated neurons and necrosis associated with PD intoxication. Additionally, TNG decreased Caspase-3 expression in the brain of PD rats. TNG plays a crucial role in AKT/Nrf2 pathway that is responsible for their antioxidant, anti-inflammatory effects, and apoptotic pathway against PD-induced brain injury in rats. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=tangeretin" title="tangeretin">tangeretin</a>, <a href="https://publications.waset.org/abstracts/search?q=potassium%20dichromate" title=" potassium dichromate"> potassium dichromate</a>, <a href="https://publications.waset.org/abstracts/search?q=brain%20injury" title=" brain injury"> brain injury</a>, <a href="https://publications.waset.org/abstracts/search?q=AKT%2FNrf2%20signaling%20pathway" title=" AKT/Nrf2 signaling pathway"> AKT/Nrf2 signaling pathway</a>, <a href="https://publications.waset.org/abstracts/search?q=FTIR" title=" FTIR"> FTIR</a>, <a href="https://publications.waset.org/abstracts/search?q=atomic%20absorption%20spectrometry" title=" atomic absorption spectrometry"> atomic absorption spectrometry</a> </p> <a href="https://publications.waset.org/abstracts/155926/neuroprotective-effect-of-tangeretin-against-potassium-dichromate-induced-acute-brain-injury-via-modulating-aktnrf2-signaling-pathway-in-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/155926.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">103</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4126</span> Sulforaphane Alleviates Muscular Dystrophy in Mdx Mice by Activation of Nrf2</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Ruilin%20Xue"> Ruilin Xue</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Backgrounds: Sulforaphane, one of the most important isothiocyanates in the human diet, is known to have chemopreventive and antioxidant activities in different tissues via activation of NF-E2-related factor 2 (Nrf2)-mediated induction of antioxidant/phase II enzymes, such as heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1). However, its effects on muscular dystrophy remain unknown. This work was undertaken to evaluate the effects of Sulforaphane on Duchenne muscular dystrophy (DMD). Methods: 4-week-old mdx mice were treated with SFN by gavage (2 mg/kg body weight per day) for 8 weeks. Blood was collected from eye socket every week, and tibial anterior, extensor digitorum longus, gastrocnemius, soleus, triceps brachii muscles and heart samples were collected after 8-week gavage. Force measurements and mice exercise capacity assays were detected. GSH/GSSG ratio, TBARS, CK and LDH levels were analyzed by spectrophotometric methods. H&E staining was used to analyze histological and morphometric of skeletal muscles of mdx mice, and Evas blue dye staining was made to detect sarcolemmal integrity of mdx mice. Further, the role of Sulforaphane on Nrf2/ARE signaling pathway was analyzed by ELISA, western blot and qRT-PCR. Results: Our results demonstrated that SFN treatment increased the expression and activity of muscle phase II enzymes NQO1 and HO-1 with Nrf2 dependent manner. SFN significantly increased skeletal muscle mass, muscle force (~30%), running distance (~20%) and GSH/GSSG ratio (~3.2 folds) of mdx mice, and decreased the activities of plasma creatine phosphokinase (CK) (~45%) and lactate dehydrogenase (LDH) (~40%), gastrocnemius hypertrophy (~25%), myocardial hypertrophy (~20%) and MDA levels (~60%). Further, SFN treatment also reduced the central nucleation (~40%), fiber size variability, inflammation and improved the sarcolemmal integrity of mdx mice. Conclusions: Collectively, these results show that SFN can improve muscle function, pathology and protect dystrophic muscle from oxidative damage in mdx mice through Nrf2 signaling pathway, which indicate Nrf2 may have clinical implications for the treatment of patients with muscular dystrophy. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=sulforaphane" title="sulforaphane">sulforaphane</a>, <a href="https://publications.waset.org/abstracts/search?q=duchenne%20muscular%20dystrophy" title=" duchenne muscular dystrophy"> duchenne muscular dystrophy</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a> </p> <a href="https://publications.waset.org/abstracts/19659/sulforaphane-alleviates-muscular-dystrophy-in-mdx-mice-by-activation-of-nrf2" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/19659.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">322</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4125</span> Mechanism of Action of Troxerutin in Reducing Oxidative Stress</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Nasrin%20Hosseinzad">Nasrin Hosseinzad</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Troxerutin, a trihydroxyethylated derived of rutin, is a flavonoid existing in tea, coffee, cereal grains, various fruits and vegetables have been conveyed to display radioprotective, antithrombotic, nephron-protective and hepato-protective possessions. Troxerutin, has been well-proved to utilize hepatoprotective assets. Troxerutin could upturn the resistance of hippocampal neurons alongside apoptosis by lessening the action of AChE and oxidative stress. Consequently, troxerutin may have advantageous properties in the administration of Alzheimer's disease and cancer. Troxerutin has been testified to have several welfares and medicinal stuffs. It could shelter the mouse kidney against d-gal-induced damage by refining renal utility, decreasing histopathologic changes, dropping ROS construction, reintroducing the activities of antioxidant enzymes and reducing DNA oxidative destruction. The DNA cleavage study clarifies that troxerutin showed DNA protection against hydroxyl radical persuaded DNA mutilation. Troxerutin uses anti-cancer effect in HuH-7 hepatocarcinoma cells conceivably through synchronized regulation of the molecular signalling pathways, Nrf2 and NF-κB. DNA binding at slight channel by troxerutin may have donated to feature breaks leading to improved radiation brought cell death. Furthermore, the mechanism principal the observed variance in the antioxidant activities of troxerutin and its esters was qualified to equally their free radical scavenging capabilities and dissemination on the cell membrane outward. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=troxerutin" title="troxerutin">troxerutin</a>, <a href="https://publications.waset.org/abstracts/search?q=DNA" title=" DNA"> DNA</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=antioxidant" title=" antioxidant"> antioxidant</a>, <a href="https://publications.waset.org/abstracts/search?q=free%20radical" title=" free radical"> free radical</a> </p> <a href="https://publications.waset.org/abstracts/143250/mechanism-of-action-of-troxerutin-in-reducing-oxidative-stress" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/143250.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">160</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4124</span> Epigallocatechin Gallate Protects against Oxidative Stress-Mediated Neurotoxicity and Hippocampus Dysfunction Induced by Fluoride in Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=S.%20Thangapandiyan">S. Thangapandiyan</a>, <a href="https://publications.waset.org/abstracts/search?q=S.%20Miltonprabu"> S. Miltonprabu</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Fl (Fl) exposure engenders neurodegeneration and induces oxidative stress in the brain. The Neuroprotective role of EGCG on oxidative stress-mediated neurotoxicity in Fl intoxicated rat hippocampus has not yet been explored so far. Hence, the present study is focused on witnessing whether EGCG (40mg/kg) supplementation prevents Fl induced oxidative stress in the brain of rats with special emphasis on the hippocampus. Fl (25mg/kg) intoxication for four weeks in rats showed an increase in Fl concentration along with the decrease the AChE, NP, DA, and 5-HT activity in the brain. The oxidative stress markers (ROS, TBARS, NO, and PC) were significantly increased with decreased enzymatic (SOD, CAT, GPx, GR, GST, and G6PD) and non-enzymatic antioxidants (GSH, TSH, and Vit.C) in Fl intoxicated rat hippocampus. Moreover, Fl intoxicated rats exhibited an intrinsic and extrinsic pathway mediated apoptosis in the hippocampus of rats. Fl intoxication significantly increased the DNA damage as evidenced by increased DNA fragmentation. Furthermore, the toxic impact of Fl on hippocampus was also proved by the immunohistochemical, histological, and ultrastructural studies. Pre-administration of EGCG has significantly protected the Fl induced oxidative stress, biochemical changes, cellular apoptotic, and histological alternations in the hippocampus of rats. In conclusion, EGCG supplementation significantly attenuated the Fl induced oxidative stress mediated neurotoxicity via its free radical scavenging and antioxidant activity. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=brain" title="brain">brain</a>, <a href="https://publications.waset.org/abstracts/search?q=hippocampal" title=" hippocampal"> hippocampal</a>, <a href="https://publications.waset.org/abstracts/search?q=NaF" title=" NaF"> NaF</a>, <a href="https://publications.waset.org/abstracts/search?q=ROS" title=" ROS"> ROS</a>, <a href="https://publications.waset.org/abstracts/search?q=EGCG" title=" EGCG"> EGCG</a> </p> <a href="https://publications.waset.org/abstracts/17597/epigallocatechin-gallate-protects-against-oxidative-stress-mediated-neurotoxicity-and-hippocampus-dysfunction-induced-by-fluoride-in-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/17597.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">392</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4123</span> Protective Role of Peroxiredoxin V against Ischemia/Reperfusion-Induced Acute Kidney Injury in Mice</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Eun%20Gyeong%20Lee">Eun Gyeong Lee</a>, <a href="https://publications.waset.org/abstracts/search?q=Ji%20Young%20Park"> Ji Young Park</a>, <a href="https://publications.waset.org/abstracts/search?q=Hyun%20Ae%20Woo"> Hyun Ae Woo</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Reactive oxygen species (ROS) production is involved in ischemia/reperfusion (I/R) injury in kidney of mice. Oxidative stress develops from an imbalance between ROS production and reduced antioxidant defenses. Many enzymatic and nonenzymatic antioxidant systems including peroxiredoxins (Prxs) are present in kidney to maintain an appropriate level of ROS and prevent oxidative damage. Prxs are a family of peroxidases that reduce peroxides, with a conserved cysteine residue serving as the site of oxidation by peroxides. In this study, we examined the protective role of Prx V against I/R-induced acute kidney injury (AKI) using Prx V wild type (WT) and knockout (KO) mice. We compared the response of Prx V WT and KO mice in mice model of I/R injury. Renal structure, functions, oxidative stress markers, protein levels of oxidative damage marker were worse in Prx V KO mice. Ablation of Prx V enhanced susceptibility to I/R-induced oxidative stress. Prx V KO mice were seen to have more severe renal damage than Prx V WT mice in mice model of I/R injury. Our results demonstrate that Prx V is protective against I/R-induced AKI. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=peroxiredoxin" title="peroxiredoxin">peroxiredoxin</a>, <a href="https://publications.waset.org/abstracts/search?q=ischemia%2Freperfusion" title=" ischemia/reperfusion"> ischemia/reperfusion</a>, <a href="https://publications.waset.org/abstracts/search?q=kidney" title=" kidney"> kidney</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a> </p> <a href="https://publications.waset.org/abstracts/47859/protective-role-of-peroxiredoxin-v-against-ischemiareperfusion-induced-acute-kidney-injury-in-mice" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/47859.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">386</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4122</span> The Antioxidant Effect of Vitamin C against Oxidative Stress Generate by Dietary Zn-Deficiency in Diabetic Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Zine%20Kechrid">Zine Kechrid</a> </p> <p class="card-text"><strong>Abstract:</strong></p> This study was carried out to investigate the antioxidant effect of vitamin C on oxidative stress induced by dietary Zn-deficiency in albino diabetic rats. Thirty two males alloxan-diabetic rats divided into two groups of 16 individuals each; the first group was fed a zinc adequate diet (54 mg zinc/kg). The second group had given low zinc diet (1 mg zinc/kg). Then, half of each group was treated with vitamin C (1 g/l) in drinking water. After four weeks, animals were sacrificed and different parameters were determined. The findings showed that dietary deficiency zinc intake significantly increased serum glucose. Zn-deficiency was also led to an increase in oxidative stress, which was indicated by an increase of MDA level and glutathione-S-transferase activity. Meanwhile it was result in a decrease of reduced glutathione (GSH) content, glutathione peroxidase GSH-Px and catalase activities in liver. However, the administration of vitamin C restored all the previous parameters approximately to their normal values. In conclusion, vitamin C probably played a key role strong as antioxidant factor against oxidative stress provoked by dietary zinc inadequate. Therefore, it might be contributed in reduction diabetes complications. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=vitamin%20C" title="vitamin C">vitamin C</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=zinc" title=" zinc"> zinc</a>, <a href="https://publications.waset.org/abstracts/search?q=experimental%20diabetes" title=" experimental diabetes"> experimental diabetes</a>, <a href="https://publications.waset.org/abstracts/search?q=rats" title=" rats "> rats </a> </p> <a href="https://publications.waset.org/abstracts/7136/the-antioxidant-effect-of-vitamin-c-against-oxidative-stress-generate-by-dietary-zn-deficiency-in-diabetic-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/7136.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">415</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4121</span> Appraisal of Oxidative Stress in Pregnant and Non-Pregnant Non Descript Goat from Arid Tracts in India</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sudha%20Summarwar">Sudha Summarwar</a>, <a href="https://publications.waset.org/abstracts/search?q=Sudesh%20Agarwal"> Sudesh Agarwal</a>, <a href="https://publications.waset.org/abstracts/search?q=Deepali%20%20Lall"> Deepali Lall</a>, <a href="https://publications.waset.org/abstracts/search?q=Nalini%20Kataria"> Nalini Kataria</a>, <a href="https://publications.waset.org/abstracts/search?q=Jyotsana%20%20Pandey"> Jyotsana Pandey</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Assessment of antioxidant status is an effective tool to appraise the presence of oxidative stress. A combination of assays can be used to evaluate the antioxidant status like serum catalase (CAT), superoxide dismutase (SOD) and monoamine oxidase (MAO). In human medicine pregnancy is known to be associated with oxidative stress. Oxidative stress produces harmful effects to the developing foetus. Several metabolic changes occur in the maternal body to meet the demand of energy of developing foetus. Due to these changes susceptibility of maternal body increases to oxidative stress. There is paucity of research work on this aspect in nondescript goats. Therefore, the present study was intended to appraise the oxidative stress in pregnant and non-pregnant non-descript goat. Blood samples were collected for serum separation in otherwise healthy pregnant and non-pregnant nondescript goats. Mean values of serum CAT, SOD and MAO were found on a higher side (p≤0.05) with serum SOD values showing a rise of 2.5 times higher than the control healthy value. Correlations among all the three parameters were found to be highly significant (p≤0.01) especially greatest in youngest group of pregnant animals. Illustration of result enlightened the veracity of bumped up production of free radicals in pregnant animals. Technical savoir-faire of oxidative stress supervision is essential for upholding of health status of foetus. The upshot of present study undoubtedly implied the development of oxidative stress in pregnant goats on the basis of altered antioxidant status. These findings conclude that initially the oxidative stress due to pregnancy is critically combated by the intricate defensive mechanism of natural antioxidant system of the body. It appears that this imbalance between oxidant and antioxidant must be checked in time to prevent cellular damage by regularly appraising the antioxidant status through laboratory methods. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=antioxidant" title="antioxidant">antioxidant</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=pregnancy" title=" pregnancy"> pregnancy</a>, <a href="https://publications.waset.org/abstracts/search?q=serum%20catalase" title=" serum catalase"> serum catalase</a> </p> <a href="https://publications.waset.org/abstracts/51343/appraisal-of-oxidative-stress-in-pregnant-and-non-pregnant-non-descript-goat-from-arid-tracts-in-india" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/51343.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">334</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4120</span> Night Shift Work as an Oxidative Stressor: A Systematic Review</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Madeline%20Gibson">Madeline Gibson</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Night shift workers make up an essential part of the modern workforce. However, night shift workers have higher incidences of late in life diseases and earlier mortality. Night shift workers are exposed to constant light and experience circadian rhythm disruption. Sleep disruption is thought to increase oxidative stress, defined as an imbalance of excess pro-oxidative factors and reactive oxygen species over anti-oxidative activity. Oxidative stress can damage cells, proteins and DNA and can eventually lead to varied chronic diseases such as cancer, diabetes, cardiovascular disease, Alzheimer’s and dementia. This review aimed to understand whether night shift workers were at greater risk of oxidative stress and to contribute to a consensus on this relationship. Twelve studies published in 2001-2019 examining 2,081 workers were included in the review. Studies compared both the impact of working a single shift and in comparisons between those who regularly work night shifts and only day shifts. All studies had evidence to support this relationship across a range of oxidative stress indicators, including increased DNA damage, reduced DNA repair capacity, increased lipid peroxidation, higher levels of reactive oxygen species, and to a lesser extent, a reduction in antioxidant defense. This research supports the theory that melatonin and the sleep-wake cycle mediate the relationship between shift work and oxidative stress. It is concluded that night shift work increases the risk for oxidative stress and, therefore, future disease. Recommendations are made to promote the long-term health of shift workers considering these findings. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=night%20shift%20work" title="night shift work">night shift work</a>, <a href="https://publications.waset.org/abstracts/search?q=coxidative%20stress" title=" coxidative stress"> coxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=circadian%20rhythm" title=" circadian rhythm"> circadian rhythm</a>, <a href="https://publications.waset.org/abstracts/search?q=melatonin" title=" melatonin"> melatonin</a>, <a href="https://publications.waset.org/abstracts/search?q=disease" title=" disease"> disease</a>, <a href="https://publications.waset.org/abstracts/search?q=circadian%20rhythm%20disruption" title=" circadian rhythm disruption"> circadian rhythm disruption</a> </p> <a href="https://publications.waset.org/abstracts/140453/night-shift-work-as-an-oxidative-stressor-a-systematic-review" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/140453.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">266</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4119</span> Sulforaphane Attenuates Fibrosis of Dystrophic Muscle in Mdx Mice via Nrf2-Mediated Inhibition of TGF-β/Smad Signaling</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Ruilin%20Xue"> Ruilin Xue</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Backgrounds: A few lines of evidence show that Sulforaphane (SFN) has anti-fibrosis effect in liver tissue via Nrf2-mediated inhibition of TGF-β/Smad signaling. However, its effects on muscular dystrophic fibrosis remain unknown. This work was undertaken to evaluate the effects of SFN on fibrosis in dystrophic muscle. Methods: 3-month-old male mdx mice were treated with SFN by gavage (2 mg/kg body weight per day) for 3 months. Gastrocnemius, tibial anterior and triceps brachii muscles were collected for related analysis. Fibrosis in skeletal muscles was analyzed by Sirius red staining. Histology and morphology of skeletal muscles were investigated by H&E staining. Moreover, the expressions of Nrf2, NQO1, HO-1, and TGF-β/Smad signaling pathway were detected by western blot, qRT-PCR, immunohistochemistry and immunofluorescence assays. Results: Our results demonstrated that SFN treatment significantly decreased and improved morphological features in mdx muscles. Moreover, SFN increased the expression of muscle phase II enzymes NQO1 and HO-1 and significantly decreased the expression of TGF-β1，p-smad2, p-smad3, α-SMA, fibronectin, collagen I, PAI-1, and TIMP-1 in Nrf2 dependent manner. Additionally, SFN significantly decreased the expression of CD45 and TNF-α. Conclusions: Collectively, these results show that SFN can ameliorate muscle fibrosis in mdx mice by Nrf2-induced inhibition of TGF-β/Smad signaling pathway, which indicate Nrf2 may be useful for the treatment of muscular dystrophy. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=sulforaphane" title="sulforaphane">sulforaphane</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a>, <a href="https://publications.waset.org/abstracts/search?q=TGF-%CE%B2%2Fsmad%20signaling" title=" TGF-β/smad signaling"> TGF-β/smad signaling</a>, <a href="https://publications.waset.org/abstracts/search?q=duchenne%20muscular%20dystrophy" title=" duchenne muscular dystrophy"> duchenne muscular dystrophy</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title=" fibrosis"> fibrosis</a> </p> <a href="https://publications.waset.org/abstracts/19674/sulforaphane-attenuates-fibrosis-of-dystrophic-muscle-in-mdx-mice-via-nrf2-mediated-inhibition-of-tgf-vsmad-signaling" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/19674.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">441</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4118</span> Relationship of Oxidative Stress to Elevated Homocysteine and DNA Damage in Coronary Artery Disease Patients</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Shazia%20Anwer%20Bukhari">Shazia Anwer Bukhari</a>, <a href="https://publications.waset.org/abstracts/search?q=Madiha%20Javeed%20Ghani"> Madiha Javeed Ghani</a>, <a href="https://publications.waset.org/abstracts/search?q=Muhammad%20Ibrahim%20Rajoka"> Muhammad Ibrahim Rajoka</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Objective: Biochemical, environmental, physical and genetic factors have a strong effect on the development of coronary disease (CAD). Plasma homocysteine (Hcy) level and DNA damage play a pivotal role in its development and progression. The aim of this study was to investigate the predictive strength of an oxidative stress, clinical biomarkers and total antioxidant status (TAS) in CAD patients to find the correlation of homocysteine, TOS and oxidative DNA damage with other clinical parameters. Methods: Sixty confirmed patients with CAD and 60 healthy individuals as control were included in this study. Different clinical and laboratory parameters were studied in blood samples obtained from patients and control subjects using commercially available biochemical kits and statistical software Results: As compared to healthy individuals, CAD patients had significantly higher concentrations of indices of oxidative stress: homocysteine (P=0.0001), total oxidative stress (TOS) (P=0.0001), serum cholesterol (P=0.04), low density lipoprotein cholesterol (LDL) (P=0.01), high density lipoprotein-cholesterol (HDL) (P=0.0001), and malondialdehyde (MDA) (P=0.001) than those of healthy individuals. Plasma homocysteine level and oxidative DNA damage were positively correlated with cholesterol, triglycerides, systolic blood pressure, urea, total protein and albumin (P values= 0.05). Both Hcy and oxidative DNA damage were negatively correlated with TAS and proteins. Conclusion: Coronary artery disease patients had a significant increase in homocysteine level and DNA damage due to increased oxidative stress. In conclusion, our study shows a significantly increase in lipid peroxidation, TOS, homocysteine and DNA damage in the erythrocytes of patients with CAD. A significant decrease level of HDL-C and TAS was observed only in CAD patients. Therefore these biomarkers may be useful diagnosis of patients with CAD and play an important role in the pathogenesis of CAD. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=antioxidants" title="antioxidants">antioxidants</a>, <a href="https://publications.waset.org/abstracts/search?q=coronary%20artery%20disease" title=" coronary artery disease"> coronary artery disease</a>, <a href="https://publications.waset.org/abstracts/search?q=DNA%20damage" title=" DNA damage"> DNA damage</a>, <a href="https://publications.waset.org/abstracts/search?q=homocysteine" title=" homocysteine"> homocysteine</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=malondialdehyde" title=" malondialdehyde"> malondialdehyde</a>, <a href="https://publications.waset.org/abstracts/search?q=8-Hydroxy-2%E2%80%99deoxyguanosine" title=" 8-Hydroxy-2’deoxyguanosine"> 8-Hydroxy-2’deoxyguanosine</a> </p> <a href="https://publications.waset.org/abstracts/33536/relationship-of-oxidative-stress-to-elevated-homocysteine-and-dna-damage-in-coronary-artery-disease-patients" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/33536.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">485</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4117</span> Erythrophagocytic Role of Mast Cells in vitro and in vivo during Oxidative Stress</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Priyanka%20Sharma">Priyanka Sharma</a>, <a href="https://publications.waset.org/abstracts/search?q=Niti%20Puri"> Niti Puri</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Anemia develops when blood lacks enough healthy erythrocytes. Past studies indicated that anemia, inflammatory process, and oxidative stress are interconnected. Erythrocytes are continuously exposed to reactive oxygen species (ROS) during circulation, due to normal aerobic cellular metabolism and also pathology of inflammatory diseases. Systemic mastocytosis and genetic depletion of mast cells have been shown to affect anaemia. In the present study, we attempted to reveal whether mast cells have a direct role in clearance or erythrophagocytosis of normal or oxidatively damaged erythrocytes. Murine erythrocytes were treated with tert-butyl hydroperoxidase (t-BHP), an agent that induces oxidative damage and mimics in vivo oxidative stress. Normal and oxidatively damaged erythrocytes were labeled with carboxyfluorescein succinimidyl ester (CFSE) to track erythrophagocytosis. We show, for the first time, direct erythrophagocytosis of oxidatively damaged erythrocytes in vitro by RBL-2H3 mast cells as well as in vivo by murine peritoneal mast cells. Also, activated mast cells, as may be present in inflammatory conditions, showed a significant increase in the uptake of oxidatively damaged erythrocytes than resting mast cells. This suggests the involvement of mast cells in erythrocyte clearance during oxidative stress or inflammatory disorders. Partial inhibition of phagocytosis by various inhibitors indicated that this process may be controlled by several pathways. Hence, our study provides important evidence for involvement of mast cells in severe anemia due to inflammation and oxidative stress and might be helpful to circumvent the adverse anemic disorders. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=mast%20cells" title="mast cells">mast cells</a>, <a href="https://publications.waset.org/abstracts/search?q=anemia" title=" anemia"> anemia</a>, <a href="https://publications.waset.org/abstracts/search?q=erythrophagocytosis" title=" erythrophagocytosis"> erythrophagocytosis</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidatively%20damaged%20erythrocytes" title=" oxidatively damaged erythrocytes"> oxidatively damaged erythrocytes</a> </p> <a href="https://publications.waset.org/abstracts/78116/erythrophagocytic-role-of-mast-cells-in-vitro-and-in-vivo-during-oxidative-stress" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/78116.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">254</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4116</span> Effect of Oxidative Stress from Smoking on Erythrocyte Phosphatidylserine Externalization</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ratchaneewan%20Maneemaroj">Ratchaneewan Maneemaroj</a>, <a href="https://publications.waset.org/abstracts/search?q=Paveena%20Noisuwan"> Paveena Noisuwan</a>, <a href="https://publications.waset.org/abstracts/search?q=Chonlada%20Lakhonphon"> Chonlada Lakhonphon</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The smoking is one of the major risk factors in Non-Communicable Disease. Free radicals from cigarette smoke can cause oxidative stress. The oxidative insults can lead to red blood cell (RBC) senescence and are involved in the clearance of red blood cells. The objective of the present study is to assess the association between smoke, oxidative stress evaluated with serum Malondialdehyde (MDA) level and phosphatidylserine (PS) externalization (biomarker of RBC senescence) evaluated with annexin V binding. A total of sixty-four male volunteers aged 25-60 years old were recruited in this study. MDA was measured by colorimetric method. Annexin V binding was detected by flow cytometry. Our results show that there was a significant increase in MDA levels in cigarette smokers as compared to non-smokers (p < 0.001). However, there was no significant different between annexin V binding (% gate) in cigarette smokers and non-smokers (p = 0.978). These results provide evidence of free radical from smoking is associated with oxidative damage to erythrocytes. However, our results suggest that PS externalization is unlikely to have a role in RBC senescence pathway of stressed erythrocytes from cigarette smoke. The other biomarker of RBC senescence should be determined on cigarette smoker erythrocytes. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=malondialdehyde" title="malondialdehyde">malondialdehyde</a>, <a href="https://publications.waset.org/abstracts/search?q=phosphatidylserine" title=" phosphatidylserine"> phosphatidylserine</a>, <a href="https://publications.waset.org/abstracts/search?q=RBC%20senescence" title=" RBC senescence"> RBC senescence</a>, <a href="https://publications.waset.org/abstracts/search?q=annexin%20V" title=" annexin V"> annexin V</a> </p> <a href="https://publications.waset.org/abstracts/28190/effect-of-oxidative-stress-from-smoking-on-erythrocyte-phosphatidylserine-externalization" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/28190.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">437</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4115</span> Effects of Benzo(k)Fluoranthene, a Polycyclic Aromatic Hydrocarbon, on DNA Damage and Oxidative Stress in Marine Gastropod Morula Granulata</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Jacky%20Bhagat">Jacky Bhagat</a>, <a href="https://publications.waset.org/abstracts/search?q=Baban%20S%20Ingole"> Baban S Ingole</a> </p> <p class="card-text"><strong>Abstract:</strong></p> In this study, in vivo experiments were carried out to investigate the effects of a toxic polycyclic aromatic hydrocarbon (PAH), benzo(k)fluoranthene (B[k]F), on marine gastropod, Morula granulata collected from Goa, west coast of India. Snails were exposed to different concentrations of B(k)F (1, 10, 25 and 50 µg/L) for 96 h. The genotoxic effects were evaluated by measuring DNA strand breaks using alkaline comet assay and oxidative stress were measured with the help of battery of biomarkers such as superoxide dismutase (SOD) catalase (CAT), glutathione-s-transferase (GST), and lipid peroxidation (LPO). Concentration-dependent increase in percentage tail DNA (TDNA) was observed in snails exposed to B(k)F. Exposure concentrations above 1 µg/L of B(k)F, showed significant increase in SOD activity and LPO value in snails. After 96 h, SOD activity were found to be doubled for 50 µg/L of B(k)F with reference to control. Significant increase in CAT and GST activity was observed at all exposure conditions at the end of the exposure time. Our study showed that B(k)F induces oxidative stress in snails which further lead to genotoxic damage. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=benzo%28k%29fluoranthene" title="benzo(k)fluoranthene">benzo(k)fluoranthene</a>, <a href="https://publications.waset.org/abstracts/search?q=comet%20assay" title=" comet assay"> comet assay</a>, <a href="https://publications.waset.org/abstracts/search?q=gastropod" title=" gastropod"> gastropod</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a> </p> <a href="https://publications.waset.org/abstracts/39775/effects-of-benzokfluoranthene-a-polycyclic-aromatic-hydrocarbon-on-dna-damage-and-oxidative-stress-in-marine-gastropod-morula-granulata" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/39775.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">344</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4114</span> Effect of Zinc-Lysine on Growth, Photosynthesis, Oxidative Stress and Antioxidant System and Chromium Uptake in Rice under Cr Stress</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Shafaqat%20Ali">Shafaqat Ali</a>, <a href="https://publications.waset.org/abstracts/search?q=Afzal%20Hussain"> Afzal Hussain</a>, <a href="https://publications.waset.org/abstracts/search?q=Muhammad%20Rizwan"> Muhammad Rizwan</a>, <a href="https://publications.waset.org/abstracts/search?q=Longhua%20Wu"> Longhua Wu </a> </p> <p class="card-text"><strong>Abstract:</strong></p> Chromium (Cr) is one of the widespread and toxic trace elements present in the agricultural land. Chromium can enter into the food chain mainly through agricultural crops grown on Cr-contaminated soils such as rice (Oryza sativa L.). The current study was done to evaluate the effects of increasing concentrations foliar applied zinc (Zn) chelated with lysine (Zn-lys) (0, 10, 20, and 30 mg L⁻¹) on rice biomass, photosynthesis, oxidative stress, key antioxidant enzyme activities and Cr uptake under increasing levels of Cr in the soil (0, 100, 500 mg kg⁻¹). Cr-induced toxicity reduced the height of plants, biomass, chlorophyll contents, gas exchange parameters, and antioxidant enzyme activities while increased the Cr concentrations and oxidative stress (malondialdehyde, electrolyte leakage, and H₂O₂) in shoots and roots than control plants. Foliar application of Zn-lys increased the plant growth, photosynthesis, Zn concentrations, and enzyme activities in rice seedlings. In addition, Zn-lys reduced the Cr concentrations and oxidative stress compared to the respective Cr treatments alone. The present results indicate that foliar Zn-lys stimulates the antioxidant defense system in rice, increase the rice growth while reduced the Cr concentrations in plants by promoting the Zn uptake and photosynthesis. Taken together, foliar spray of Zn-lys chelate can efficiently be employed for improving plant growth and Zn contents while reducing Cr concentration in rice grown in Cr-contaminated and Zn-deficient soils. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=antioxidants" title="antioxidants">antioxidants</a>, <a href="https://publications.waset.org/abstracts/search?q=chromium" title=" chromium"> chromium</a>, <a href="https://publications.waset.org/abstracts/search?q=zinc-lysine" title=" zinc-lysine"> zinc-lysine</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=photosynthesis" title=" photosynthesis"> photosynthesis</a>, <a href="https://publications.waset.org/abstracts/search?q=tolerance" title=" tolerance"> tolerance</a> </p> <a href="https://publications.waset.org/abstracts/76594/effect-of-zinc-lysine-on-growth-photosynthesis-oxidative-stress-and-antioxidant-system-and-chromium-uptake-in-rice-under-cr-stress" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/76594.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">194</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4113</span> Fluoride-Induced Stress and Its Association with Bone Developmental Pathway in Osteosarcoma Cells</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Deepa%20Gandhi">Deepa Gandhi</a>, <a href="https://publications.waset.org/abstracts/search?q=Pravin%20K.%20Naoghare"> Pravin K. Naoghare</a>, <a href="https://publications.waset.org/abstracts/search?q=Amit%20Bafana"> Amit Bafana</a>, <a href="https://publications.waset.org/abstracts/search?q=Krishnamurthi%20Kannan"> Krishnamurthi Kannan</a>, <a href="https://publications.waset.org/abstracts/search?q=Saravanadevi%20Sivanesana"> Saravanadevi Sivanesana</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Oxidative stress is known to depreciate normal functioning of osteoblast cells. Present study reports oxidative/inflammatory signatures in fluoride exposed human osteosarcoma (HOS) cells and its possible association with the genes involved in bone developmental pathway. Microarray analysis was performed to understand the possible molecular mechanisms of stress-mediated bone lose in HOS cells. Cells were chronically exposed with sub-lethal concentration of fluoride. Global gene expression is profiling revealed 34 up regulated and 2598 down-regulated genes, which were associated with several biological processes including bone development, osteoblast differentiation, stress response, inflammatory response, apoptosis, regulation of cell proliferation. Microarray data were further validated through qRT-PCR and western blot analyses using key representative genes. Based on these findings, it can be proposed that chronic exposure of fluoride may impair bone development via oxidative and inflammatory stress. The present finding also provides important biological clues, which will be helpful for the development of therapeutic targets against diseases related bone. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=bone" title="bone">bone</a>, <a href="https://publications.waset.org/abstracts/search?q=HOS%20cells" title=" HOS cells"> HOS cells</a>, <a href="https://publications.waset.org/abstracts/search?q=microarray" title=" microarray"> microarray</a>, <a href="https://publications.waset.org/abstracts/search?q=stress" title=" stress"> stress</a> </p> <a href="https://publications.waset.org/abstracts/40877/fluoride-induced-stress-and-its-association-with-bone-developmental-pathway-in-osteosarcoma-cells" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/40877.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">377</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4112</span> Imipramine Ameliorate Altered Biochemical Parameter and Oxidative Damage in Depression</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=D.%20S.%20Mohale">D. S. Mohale</a>, <a href="https://publications.waset.org/abstracts/search?q=A.V.%20Chandewar"> A.V. Chandewar </a> </p> <p class="card-text"><strong>Abstract:</strong></p> Study was undertaken to investigate the effect of imipramine on various biochemical parameters and oxidative stress markers in short and long term depression on rats. Rats were subjected for short (21 days) and long term (84 days) social isolation for and checked for depression on force swim test and tail suspension method. Various markers of oxidative stress like lipid peroxidation (LPO), reduced glutathione (GSH), Supersoxide dismutase (SOD), catalase (CAT) and biochemical parameters like Serum glutamate oxaloacetate transaminase (SGOT), Serum glutamate pyruate transaminase (SGPT), and blood glucose were determined in depressed, control, imipramine and Vitamin E treated group. The rats displayed an increase in depression on force swim test and tail suspension method relative to control. There was significant increase in the level of LPO and decrease in the levels of GSH, SOD and CAT after short and long term depression. Increased oxidative stress in depression which may leads to alteration of biochemical parameters. Treatment with imipramine an tricyclic antidepressant significantly decreases in level of LPO, SGOT, SGPT and increase in the levels of GSH, SOD and CAT in long term depression. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=depression" title="depression">depression</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=lipid%20peroxidation" title=" lipid peroxidation"> lipid peroxidation</a>, <a href="https://publications.waset.org/abstracts/search?q=reduced%20glutathione" title=" reduced glutathione"> reduced glutathione</a> </p> <a href="https://publications.waset.org/abstracts/23137/imipramine-ameliorate-altered-biochemical-parameter-and-oxidative-damage-in-depression" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/23137.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">501</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4111</span> Diallyl Trisulfide Protects the Rat Liver from CCl4-Induced Injury and Fibrogenesis by Attenuating Oxidative Stress</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Xiao-Jing%20Zhu">Xiao-Jing Zhu</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Zhou"> Liang Zhou</a>, <a href="https://publications.waset.org/abstracts/search?q=Shi-Zhong%20Zheng"> Shi-Zhong Zheng</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Various studies have shown that diallyl trisulfide (DATS) can protect the liver injury, and DATS has a strong antioxidant property. The aim of this study is to evaluate the in vivo role of DATS in protecting the liver against injury and fibrogenesis and further explores the underlying mechanisms. Our results demonstrated that DATS protected the liver from CCl4-caused injury by suppressing the elevation of ALT and AST activities, and by improving the histological architecture of the liver. Treatment with DATS or colchicine improved the liver fibrosis by sirius red staining and immunofluorescence. In addition, immunohistochemistry, western blot, and RT-PCR analyses indicated that DATS inhibited HSC activation. Furthermore, DATS attenuated oxidative stress by increasing glutathione and reducing lipid peroxides and malondialdehyde. These findings suggest that the protective effect of DATS on CCl4-caused liver injury and liver fibrogenesis was, at least partially, attributed to its antioxidant activity. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=liver%20fibrogenesis" title="liver fibrogenesis">liver fibrogenesis</a>, <a href="https://publications.waset.org/abstracts/search?q=liver%20injury" title=" liver injury"> liver injury</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=DATS" title=" DATS"> DATS</a> </p> <a href="https://publications.waset.org/abstracts/2858/diallyl-trisulfide-protects-the-rat-liver-from-ccl4-induced-injury-and-fibrogenesis-by-attenuating-oxidative-stress" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/2858.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">430</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4110</span> Beneficial Effects of Curcumin against Stress Oxidative and Mitochondrial Dysfunction Induced by Trinitrobenzene Sulphonic Acid in Colon </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Souad%20Mouzaoui">Souad Mouzaoui</a>, <a href="https://publications.waset.org/abstracts/search?q=Bahia%20Djerdjouri"> Bahia Djerdjouri</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Oxidative stress is one of the main factors involved in the onset and chronicity of inflammatory bowel disease (IBD). In this study, we investigated the beneficial effects of a potent natural antioxidant, curcumin (Cur) on colitis and mitochondrial dysfunction in trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Rectal instillation of the chemical irritant TNBS (30 mg kg-1) induced the disruption of distal colonic architecture and a massive inflammatory cells influx to the mucosa and submucosa layers. Under these conditions, daily administration of Cur (25 mg kg-1) efficiently decreased colitis scores in the inflamed distal colon by reducing leukocyte infiltrate as attested by reduced myeloperoxidase (MPO) activity. Moreover, the levels of nitrite, an end product of inducible NO synthase activity (iNOS) and malonyl dialdehyde (MDA), a marker of lipid peroxidation increased in a time depending manner in response to TNBS challenge. Conversely, the markers of the antioxidant pool, reduced glutathione (GSH) and catalase activity (CAT) were drastically reduced. Cur attenuated oxidative stress markers and partially restored CAT and GSH levels. Moreover, our results expanded the effect of Cur on TNBS-induced colonic mitochondrial dysfunction. In fact, TNBS induced mitochondrial swelling and lipids peroxidation. These events reflected in the opening of mitochondrial transition pore and could be an initial indication in the cascade process leading to cell death. TNBS inhibited also mitochondrial respiratory activity, caused overproduction of mitochondrial superoxide anion (O2-.) and reduced level of mitochondrial GSH. Nevertheless, Cur reduced the extent of mitochondrial oxidative stress induced by TNBS and restored colonic mitochondrial function. In conclusion, our results showed the critical role of oxidative stress in TNBS-induced colitis. They highlight the role of colonic mitochondrial dysfunction induced by TNBS, as a potential source of oxidative damages. Due to its potent antioxidant properties, Cur opens a promising therapeutic approach against oxidative inflammation in IBD. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=colitis" title="colitis">colitis</a>, <a href="https://publications.waset.org/abstracts/search?q=curcumin" title=" curcumin"> curcumin</a>, <a href="https://publications.waset.org/abstracts/search?q=mitochondria" title=" mitochondria"> mitochondria</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=TNBS" title=" TNBS"> TNBS</a> </p> <a href="https://publications.waset.org/abstracts/1767/beneficial-effects-of-curcumin-against-stress-oxidative-and-mitochondrial-dysfunction-induced-by-trinitrobenzene-sulphonic-acid-in-colon" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/1767.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">253</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4109</span> Safety Assessment and Prophylactic Efficacy of Moringa stenopetala Leaf Extract Through Mitigation of Oxidative Stress in BV-2 Microglial Cell</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Stephen%20Adeniyi%20Adefegha">Stephen Adeniyi Adefegha</a>, <a href="https://publications.waset.org/abstracts/search?q=Vitor%20Mostardeiro"> Vitor Mostardeiro</a>, <a href="https://publications.waset.org/abstracts/search?q=Vera%20Maria%20Morsch"> Vera Maria Morsch</a>, <a href="https://publications.waset.org/abstracts/search?q=Ademir%20F.%20Morel"> Ademir F. Morel</a>, <a href="https://publications.waset.org/abstracts/search?q=Ivana%20Beatrice%20Manica%20Da%20Cruz"> Ivana Beatrice Manica Da Cruz</a>, <a href="https://publications.waset.org/abstracts/search?q=Sabrina%20Somacal%20Maria%20Rosa%20Chitolina%20Schetinger"> Sabrina Somacal Maria Rosa Chitolina Schetinger</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Moringa stenopetala is often consumed as food and used in folkloric medicine for the management of several diseases. Purpose: This study was set up in order to assess the effect of aqueous extract of Moringa stenopetala on cell viability and oxidative stress biomarkers in BV-2 microglial cells. Aqueous extracts of M. stenopetala were prepared, lyophilized and reconstituted in 0.5% dimethylsulphoxide (DMSO). Cells were treated with M. stenopetala extracts (0.1 - 100 µg/ml) for cell viability and nitric oxide (NO) production tests. However, M. stenopetala extract (50 µg/ml) was used in the treatment of cells for the determination of protein carbonyl content and reactive oxygen species (ROS) level. Incubation of BV-2 microglia cell with M. stenopetala extract maintained cell viability, diminished NO and ROS levels, and reduced protein carbonyl contents Chlorogenic acid, rutin, kaempferol and quercetin derivatives were the main phenolic compounds identified in M. stenopetala leaf extract. These phenolic compounds present in M. stenopetala may be responsible for the mitigation of oxidative stress in BV-2 microglial cells. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title="oxidative stress">oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=BV-2%20microglial%20cell" title=" BV-2 microglial cell"> BV-2 microglial cell</a>, <a href="https://publications.waset.org/abstracts/search?q=Moringa%20stenopetala" title=" Moringa stenopetala"> Moringa stenopetala</a>, <a href="https://publications.waset.org/abstracts/search?q=cell%20viability" title=" cell viability"> cell viability</a>, <a href="https://publications.waset.org/abstracts/search?q=antioxidant" title=" antioxidant"> antioxidant</a> </p> <a href="https://publications.waset.org/abstracts/157189/safety-assessment-and-prophylactic-efficacy-of-moringa-stenopetala-leaf-extract-through-mitigation-of-oxidative-stress-in-bv-2-microglial-cell" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/157189.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">110</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4108</span> Modulation of Isoprenaline-Induced Myocardial Damage by Atorvastatin</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Dalia%20Atallah">Dalia Atallah</a>, <a href="https://publications.waset.org/abstracts/search?q=Lamiaa%20Ahmed"> Lamiaa Ahmed</a>, <a href="https://publications.waset.org/abstracts/search?q=Hala%20Zaki"> Hala Zaki</a>, <a href="https://publications.waset.org/abstracts/search?q=Mahmoud%20Khattab"> Mahmoud Khattab</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Isoprenaline (ISO) administration induces myocardial damage via oxidative stress and endothelial dysfunction. Atorvastatin (ATV) treatment improves both oxidative stress and endothelial dysfunction yet recent studies have reported a pro-oxidant effect upon ATV administration on both clinical and experimental studies. The present study was directed to investigate the effect of ATV pre-treatment and treatment on ISO-induced myocardial damage. Methods: Male rats were divided into five groups (n = 10). Rats were given ISO (5mg/kg/day, i.p.) for one week with or without ATV (10mg/kg/day, p.o.). ATV was given either as pre-treatment for one week before its co-administration with ISO for another week or as a treatment for two weeks at the end of the ISO administration. At the end of the experiment, the electrocardiographic examination was done and blood was isolated for the estimation of plasma creatine kinase MB (CK-MB) activity. Rats were then sacrificed and the whole ventricles were isolated for histological examination and the estimation of lipid peroxides as malondialdehyde (MDA) level, reduced glutathione (GSH) level, catalase activity, total nitrate-nitrite (NOx), as well as the estimation of both endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) protein expression. Results: ISO-induced myocardial damage showed a significant elevation in ST segment, an increase in CK-MB activity, as well as increased oxidative stress biomarkers. Also, ISO-treated rats showed a significant decrease in myocardial NOx level and eNOS as well as degeneration in the myocardium. ATV pre-treatment didn’t show any protection to ISO-treated rats. On the other hand, ATV treatment showed a significant decrease in both the elevated ST wave and CK-MB activity. Moreover, ATV Treatment succeeded to improve oxidative stress biomarkers, tissue NOx, and eNOS protein expression, as well as amelioration of the histological alterations. Conclusion: Pre-treatment with ATV failed to protect against ISO-induced damage. This might suggest a synergistic pro-oxidant effect upon administration of the pro-oxidant ISO along with ATV as demonstrated by the increased oxidative stress and endothelial dysfunction. On the other side, ATV treatment succeeded to significantly improve oxidative stress biomarkers, endothelial dysfunction and myocardial degeneration. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=atorvastatin" title="atorvastatin">atorvastatin</a>, <a href="https://publications.waset.org/abstracts/search?q=endothelial%20dysfunction" title=" endothelial dysfunction"> endothelial dysfunction</a>, <a href="https://publications.waset.org/abstracts/search?q=isoprenaline" title=" isoprenaline"> isoprenaline</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a> </p> <a href="https://publications.waset.org/abstracts/14947/modulation-of-isoprenaline-induced-myocardial-damage-by-atorvastatin" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/14947.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">446</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4107</span> Oxidative Stress Markers in Sports Related to Training</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=V.%20Antevska">V. Antevska</a>, <a href="https://publications.waset.org/abstracts/search?q=B.%20Dejanova"> B. Dejanova</a>, <a href="https://publications.waset.org/abstracts/search?q=L.%20Todorovska"> L. Todorovska</a>, <a href="https://publications.waset.org/abstracts/search?q=J.%20Pluncevic"> J. Pluncevic</a>, <a href="https://publications.waset.org/abstracts/search?q=E.%20Sivevska"> E. Sivevska</a>, <a href="https://publications.waset.org/abstracts/search?q=S.%20Petrovska"> S. Petrovska</a>, <a href="https://publications.waset.org/abstracts/search?q=S.%20Mancevska"> S. Mancevska</a>, <a href="https://publications.waset.org/abstracts/search?q=I.%20Karagjozova"> I. Karagjozova</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Introduction: The aim of this study was to optimise the laboratory oxidative stress (OS) markers in soccer players. Material and methods: In a number of 37 soccer players (21±3 years old) and 25 control subjects (sedenters), plasma samples were taken for d-ROMs (reactive oxygen metabolites) and NO (nitric oxide) determination. The d-ROMs test was performed by measurement of hydroperoxide levels (Diacron, Italy). For NO determination the method of nitrate enzyme reduction with the Greiss reagent was used (OXIS, USA). The parameters were taken after the training of the soccer players and were compared with the control group. Training was considered as maximal exercise treadmill test. The criteria of maximum loading for each subject was established as >95% maximal heart rate. Results: The level of d-ROMs was found to be increased in the soccer players vs. control group but no significant difference was noticed. After the training d-ROMs in soccer players showed increased value of 299±44 UCarr (p<0.05). NO showed increased level in all soccer players vs. controls but significant difference was found after the training 102±29 μmol (p<0.05). Conclusion: Due to these results we may suggest that the measuring these OS markers in sport medicine may be useful for better estimation and evaluation of the training program. More oxidative stress should be used to clarify optimization of the training intensity program. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress%20markers" title="oxidative stress markers">oxidative stress markers</a>, <a href="https://publications.waset.org/abstracts/search?q=soccer%20players" title=" soccer players"> soccer players</a>, <a href="https://publications.waset.org/abstracts/search?q=training" title=" training"> training</a>, <a href="https://publications.waset.org/abstracts/search?q=sport" title=" sport"> sport</a> </p> <a href="https://publications.waset.org/abstracts/10708/oxidative-stress-markers-in-sports-related-to-training" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/10708.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">447</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4106</span> Protective Effect of Celosia Argentea Leaf Extract on Cadmium Induced Toxicity and Oxidative Stress in Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sulyman%20Abdulhakeem%20Olarewaju">Sulyman Abdulhakeem Olarewaju</a>, <a href="https://publications.waset.org/abstracts/search?q=S.%20O.%20Malomo"> S. O. Malomo</a>, <a href="https://publications.waset.org/abstracts/search?q=M.%20T.%20Yakubu"> M. T. Yakubu</a>, <a href="https://publications.waset.org/abstracts/search?q=J.%20O.%20Akolade"> J. O. Akolade</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The ameliorative effect of Celosia argentea var. cristata leaf extract against cadmium (Cd) induced oxidative stress and toxicity in selected tissues of rats was investigated. Toxicity coupled with oxidative stress was induced in rats by oral administration of Cd (8 mg/kg b. wt). Preliminary quantitative phytochemical and in vitro antioxidant analyses showed that the methanolic extract of C. argentea leaves was constituted by polyphenols (5.72%), saponins (3.20%), tannins (0.65%) and cadenolides (0.006%). IC50 of 9800, 7406, and 45.04 μg/ml were recorded for inhibition of linoleic acid oxidation, 2, 2-diphenyl-1-picrylhydrazyl and hydrogen peroxide radicals respectively. Simultaneous administration of C. argentea leaf extract with Cd significantly attenuated Cd-induced elevation of serum enzyme markers such as aspartate and alanine transaminase, alkaline and acid phosphatase as well as γ-glutaryltransferase in a dose-dependent fashion, while their reduced level in the liver were significantly increased. Higher levels of enzymatic antioxidants; superoxide dismutase and catalase activities were observed in the liver, brain, kidney and testes of the Cd-induced rats treated with C. argentea extract, while lipid peroxidation expressed in malondialdehyde concentrations were lower when compared to values in rats administered Cd only. Other Cd-induced toxicity and stress markers in the serum viz. reduced uric acid and albumin levels as well as elevated total and unconjugated bilirubin were attenuated by the extract and their values compared favorably with those animals co-administered cadmium with ascorbic acid. Data from the study showed that oral administration of extract from the leaf C. argentea may ameliorate Cd-induced oxidative stress and toxicity in rats. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=toxicity" title="toxicity">toxicity</a>, <a href="https://publications.waset.org/abstracts/search?q=cadmium" title=" cadmium"> cadmium</a>, <a href="https://publications.waset.org/abstracts/search?q=celosia" title=" celosia"> celosia</a>, <a href="https://publications.waset.org/abstracts/search?q=antioxidants" title=" antioxidants"> antioxidants</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a> </p> <a href="https://publications.waset.org/abstracts/27502/protective-effect-of-celosia-argentea-leaf-extract-on-cadmium-induced-toxicity-and-oxidative-stress-in-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/27502.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">346</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4105</span> Bioactivity Profiling of Botswana’s Medicinal Ethnobotany With Potential to Mitigate Oxidative Stress</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Daniel%20Motlhanka">Daniel Motlhanka</a>, <a href="https://publications.waset.org/abstracts/search?q=Neo%20Kerebotswe"> Neo Kerebotswe</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The strong and long history of use of medicinal plants in Botswana to address existing and emerging health threats provides undebatable evidence for their potential as innovative therapeutic tools. The prevalence of emerging health threats, such as COVID-19 and hard-to-treat non-communicable diseases, warrants the scientific community to revisit and exploit ethnopharmacology for its potential as a source of therapeutic tools. Many studies conducted on bioactivity-guided bioassays of ethnobotanical resources have proved a number of health beneficial properties of these plants, such as free radical scavenging, anti-inflammatory, antimicrobial and, most importantly, the capability of medicinal plants to alleviate oxidative stress. In this work, a number of medicinal plants used in Botswana traditional medicine were investigated for both their free radical scavenging capability and total phenolic contents using the Free Radical Scavenging Power (FRSP) and Folin Ciocalteau (FC) method. At 100 micrograms/ml all the studied plants expressed above 90% Scavenging power and expressed total phenolic contents between 5000- 8890 mg/L.GAE. These plants are promising tools for engineering active therapeutic tools against life-threatening diseases of oxidative stress origin. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title="oxidative stress">oxidative stress</a>, <a href="https://publications.waset.org/abstracts/search?q=non-communicable%20diseases" title=" non-communicable diseases"> non-communicable diseases</a>, <a href="https://publications.waset.org/abstracts/search?q=total%20phenolics" title=" total phenolics"> total phenolics</a>, <a href="https://publications.waset.org/abstracts/search?q=ethnobotanicals" title=" ethnobotanicals"> ethnobotanicals</a> </p> <a href="https://publications.waset.org/abstracts/186011/bioactivity-profiling-of-botswanas-medicinal-ethnobotany-with-potential-to-mitigate-oxidative-stress" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/186011.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">49</span> </span> </div> </div> <ul class="pagination"> <li class="page-item disabled"><span class="page-link">&lsaquo;</span></li> <li class="page-item active"><span class="page-link">1</span></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=Nrf2%20oxidative%20stress&page=2">2</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=Nrf2%20oxidative%20stress&page=3">3</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=Nrf2%20oxidative%20stress&page=4">4</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=Nrf2%20oxidative%20stress&page=5">5</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=Nrf2%20oxidative%20stress&page=6">6</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=Nrf2%20oxidative%20stress&page=7">7</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=Nrf2%20oxidative%20stress&page=8">8</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=Nrf2%20oxidative%20stress&page=9">9</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=Nrf2%20oxidative%20stress&page=10">10</a></li> <li class="page-item disabled"><span class="page-link">...</span></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=Nrf2%20oxidative%20stress&page=137">137</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=Nrf2%20oxidative%20stress&page=138">138</a></li> <li class="page-item"><a class="page-link" href="https://publications.waset.org/abstracts/search?q=Nrf2%20oxidative%20stress&page=2" rel="next">&rsaquo;</a></li> </ul> </div> </main> <footer> <div id="infolinks" class="pt-3 pb-2"> <div class="container"> <div style="background-color:#f5f5f5;" class="p-3"> <div class="row"> <div class="col-md-2"> <ul class="list-unstyled"> About <li><a href="https://waset.org/page/support">About Us</a></li> <li><a href="https://waset.org/page/support#legal-information">Legal</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/WASET-16th-foundational-anniversary.pdf">WASET celebrates its 16th foundational anniversary</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Account <li><a href="https://waset.org/profile">My Account</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Explore <li><a href="https://waset.org/disciplines">Disciplines</a></li> <li><a href="https://waset.org/conferences">Conferences</a></li> <li><a href="https://waset.org/conference-programs">Conference Program</a></li> <li><a href="https://waset.org/committees">Committees</a></li> <li><a href="https://publications.waset.org">Publications</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Research <li><a href="https://publications.waset.org/abstracts">Abstracts</a></li> <li><a href="https://publications.waset.org">Periodicals</a></li> <li><a href="https://publications.waset.org/archive">Archive</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Open Science <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Science-Philosophy.pdf">Open Science Philosophy</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Science-Award.pdf">Open Science Award</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Society-Open-Science-and-Open-Innovation.pdf">Open Innovation</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Postdoctoral-Fellowship-Award.pdf">Postdoctoral Fellowship Award</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Scholarly-Research-Review.pdf">Scholarly Research Review</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Support <li><a href="https://waset.org/page/support">Support</a></li> <li><a href="https://waset.org/profile/messages/create">Contact Us</a></li> <li><a href="https://waset.org/profile/messages/create">Report Abuse</a></li> </ul> </div> </div> </div> </div> </div> <div class="container text-center"> <hr style="margin-top:0;margin-bottom:.3rem;"> <a href="https://creativecommons.org/licenses/by/4.0/" target="_blank" class="text-muted small">Creative Commons Attribution 4.0 International License</a> <div id="copy" class="mt-2">© 2024 World Academy of Science, Engineering and Technology</div> </div> </footer> <a href="javascript:" id="return-to-top"><i class="fas fa-arrow-up"></i></a> <div class="modal" id="modal-template"> <div class="modal-dialog"> <div class="modal-content"> <div class="row m-0 mt-1"> <div class="col-md-12"> <button type="button" class="close" data-dismiss="modal" aria-label="Close"><span aria-hidden="true">×</span></button> </div> </div> <div class="modal-body"></div> </div> </div> </div> <script src="https://cdn.waset.org/static/plugins/jquery-3.3.1.min.js"></script> <script src="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/js/bootstrap.bundle.min.js"></script> <script src="https://cdn.waset.org/static/js/site.js?v=150220211556"></script> <script> jQuery(document).ready(function() { /*jQuery.get("https://publications.waset.org/xhr/user-menu", function (response) { jQuery('#mainNavMenu').append(response); });*/ jQuery.get({ url: "https://publications.waset.org/xhr/user-menu", cache: false }).then(function(response){ jQuery('#mainNavMenu').append(response); }); }); </script> </body> </html>