{"title":"Curcumin protects against cadmium-induced germ cell death in the testis of rats.","authors":"Yamin Li, Lu Yang, Ping Su, Na Chen","doi":"10.1093/toxres/tfae082","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Cadmium (Cd) has been shown to disrupt the reproductive system. In this study, we evaluated the protective effects of Curcumin (Cur) against Cd-induced reproductive toxicity.</p><p><strong>Methods: </strong>Exploring the role of Cur in Cd-treated rat models.</p><p><strong>Results: </strong>The study demonstrated that Cd treatment impaired the seminiferous epithelium, leading to increased apoptosis of germ cells. Interestingly, pretreatment with Cur ameliorated the histological damage and decreased the germ cell apoptosis induced by Cd. Furthermore, after Cd exposure, B-cell lymphoma-2 expression was significantly decreased while Bax expression was increased. Pretreatment of rats with Cur protected against germ cell apoptosis by improving the expression of B-cell lymphoma-2 and reducing Bax. Additionally, Cd treatment increased reactive oxygen species, resulting in a decrease in antioxidant enzymes. However, pretreatment of rats with Cur followed by Cd administration led to a substantial decrease in reactive oxygen species levels and increased activities of antioxidant enzymes. Ultrastructural investigations revealed that damage to the mitochondrial structure was significantly ameliorated by Cur pretreatment in Cd-treated rats. Notably, Cur significantly activated the peroxisome proliferator-activated receptor gamma coactivator 1a/Sirtuins-3 signaling pathway.</p><p><strong>Conclusions: </strong>Overall, our data suggest that Cd induces germ cell apoptosis through mitochondrial-induced oxidative stress, but Cur pretreatment offers strong protection against Cd-induced reproductive toxicity.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":null,"pages":null},"PeriodicalIF":2.2000,"publicationDate":"2024-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11149375/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/toxres/tfae082","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/4/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"TOXICOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction: Cadmium (Cd) has been shown to disrupt the reproductive system. In this study, we evaluated the protective effects of Curcumin (Cur) against Cd-induced reproductive toxicity.
Methods: Exploring the role of Cur in Cd-treated rat models.
Results: The study demonstrated that Cd treatment impaired the seminiferous epithelium, leading to increased apoptosis of germ cells. Interestingly, pretreatment with Cur ameliorated the histological damage and decreased the germ cell apoptosis induced by Cd. Furthermore, after Cd exposure, B-cell lymphoma-2 expression was significantly decreased while Bax expression was increased. Pretreatment of rats with Cur protected against germ cell apoptosis by improving the expression of B-cell lymphoma-2 and reducing Bax. Additionally, Cd treatment increased reactive oxygen species, resulting in a decrease in antioxidant enzymes. However, pretreatment of rats with Cur followed by Cd administration led to a substantial decrease in reactive oxygen species levels and increased activities of antioxidant enzymes. Ultrastructural investigations revealed that damage to the mitochondrial structure was significantly ameliorated by Cur pretreatment in Cd-treated rats. Notably, Cur significantly activated the peroxisome proliferator-activated receptor gamma coactivator 1a/Sirtuins-3 signaling pathway.
Conclusions: Overall, our data suggest that Cd induces germ cell apoptosis through mitochondrial-induced oxidative stress, but Cur pretreatment offers strong protection against Cd-induced reproductive toxicity.
介绍:镉(Cd)已被证明会破坏生殖系统。本研究评估了姜黄素(Cur)对镉诱导的生殖毒性的保护作用:方法:探索姜黄素在镉处理大鼠模型中的作用:结果:研究表明,镉处理损害了大鼠的曲细精管上皮,导致生殖细胞凋亡增加。有趣的是,用 Cur 预处理可改善组织学损伤并减少 Cd 诱导的生殖细胞凋亡。此外,在接触镉后,B细胞淋巴瘤-2的表达明显减少,而Bax的表达却增加了。通过改善 B 细胞淋巴瘤-2 的表达和降低 Bax 的表达,用 Cur 对大鼠进行预处理可防止生殖细胞凋亡。此外,镉处理会增加活性氧,导致抗氧化酶减少。然而,先用 Cur 对大鼠进行预处理,然后再给大鼠施用镉,则可大幅降低活性氧水平,并提高抗氧化酶的活性。超微结构研究显示,镉处理大鼠的线粒体结构损伤在 Cur 预处理后得到明显改善。值得注意的是,Cur能明显激活过氧化物酶体增殖激活受体γ辅助激活剂1a/Sirtuins-3信号通路:总之,我们的数据表明,镉可通过线粒体诱导的氧化应激诱导生殖细胞凋亡,但Cur预处理可有效防止镉诱导的生殖毒性。