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首页> 外文期刊>Chemosphere >Hexavalent chromium-induced toxic effects on the antioxidant levels, histopathological alterations and expression of Nrf2 and MT2 genes in the branchial tissue of Ctenopharyngodon idellus
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Hexavalent chromium-induced toxic effects on the antioxidant levels, histopathological alterations and expression of Nrf2 and MT2 genes in the branchial tissue of Ctenopharyngodon idellus

机译:六价铬对中叶ten牙分支组织中抗氧化剂水平,组织病理学改变以及Nrf2和MT2基因表达的毒性作用

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Ability of hexavalent chromium to accumulate and induce oxidative stress has been studied in the gills of Ctenopharyngodon idellus, with the resulting damage in the form of altered endogenous antioxidant enzyme activity and, histopathology in the tissue. The fish were exposed to 5.3 (Cl) and 10.63 mg/L (C2) of hexavalent chromium and were scrutinised on 15th, 30th and 45th day of toxicant exposure. Oxidative stress studied in terms of lipid peroxidation and glutathione levels and the antioxidant enzymes activity also exhibited alterations. The histopathological modifications in gills announced lesions in the form of hyperplasia, aneurysm, lamellar fusion, focal proliferation, epithelial degeneration and necrosis with loss of lamellae, bringing irreversible damage on 45th day with mean degree of tissue change value of 100.35 +/- 10.69. Bioaccumulation of chromium, and increased anomalies in branchial tissue exhibited damage in concentration and time-dependent manner. The ultrastructural anomalies in the cellular morphology in the epithelial cells of filaments and lamellae, exhibited pleomorphic nuclei, swollen mitochondria, extensive vacuolation and loss of microridges in pavement cells. The tissue also displayed altered regulation of Nrf2 and Mt2 following Cr(VI) exposure with maximum downregulation on 45th day by 61 and 53%, respectively. PCA generated two principal components, PCI (GSH, GST, CAT and SOD) and PC2 (DTC, MDA and Cr(VI) concentration). Thus, it can be concluded that accumulation of Cr(VI) induces alteration in the gene expression of Nrf2 and Mt2 leading to the development of oxidative stress, ensuing various pathological changes creating hindrance in fish survival. (C) 2019 Elsevier Ltd. All rights reserved.
机译:研究了六价铬在chromium牙ten的accu中积累和诱导氧化应激的能力,其结果以组织中内源性抗氧化酶活性和组织病理学改变的形式受到损害。将鱼暴露于5.3(Cl)和10.63 mg / L(C2)的六价铬中,并在有毒物质暴露的第15、30和45天进行仔细检查。根据脂质过氧化和谷胱甘肽水平以及抗氧化酶活性研究的氧化应激也表现出变化。 g的组织病理学改变以增生,动脉瘤,板层融合,局灶性增生,上皮变性和坏死的形式宣布病变,并丧失片状细胞,在第45天造成不可逆的损害,平均组织变化值为100.35 +/- 10.69。铬的生物富集以及分支组织中异常的增多表现出浓度和时间依赖性的破坏。细丝和薄层上皮细胞的细胞形态中的超微结构异常表现为多形核,线粒体肿胀,广泛的空泡化和路面细胞中的微孔缺失。 Cr(VI)暴露后,该组织还显示出对Nrf2和Mt2的调节改变,在第45天分别最大下调了61%和53%。 PCA产生两个主要成分,PCI(GSH,GST,CAT和SOD)和PC2(DTC,MDA和Cr(VI)浓度)。因此,可以得出结论,Cr(VI)的积累会诱导Nrf2和Mt2基因表达的改变,从而导致氧化应激的发展,从而导致各种病理变化,从而阻碍鱼类的生存。 (C)2019 Elsevier Ltd.保留所有权利。

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