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首页> 外文期刊>Journal of environmental pathology, toxicology and oncology: official organ of the International Society for Environmental Toxicology and Cancer >Protective Role of Zinc in Ameliorating Arsenic-Induced Oxidative Stress and Histological Changes in Rat Liver
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Protective Role of Zinc in Ameliorating Arsenic-Induced Oxidative Stress and Histological Changes in Rat Liver

机译:锌在减轻砷诱导的大鼠肝脏氧化应激和组织学变化中的保护作用

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The aim of present work was to gain insight into the role of dietary zinc in ameliorating the adverse effects caused by arsenic on rat liver. Male Wistar rats received arsenic alone in the form of sodium arsenite in drinking water at a dose level of 100 ppm, zinc alone in the form of zinc sulfate in drinking water at a dose level of 227 mg/L, or arsenic + zinc treatments in the combined group for a total duration of 3 months. Arsenic treatment resulted in a significant increase in lipid peroxidase (LPO); however, glutathione (GSH) levels and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and catalase (CAT) were found to be significantly decreased following arsenic treatment. Furthermore, arsenic treatment resulted in a significant decrease in hepatic zinc levels. Histological studies showed well-differentiated signs of focal hepatitis, lobular inflammation, prominent hepatocyte degeneration, and severe periportal necrosis. Administration of zinc to arsenic-treated rats significantly decreased the level of LPO but increased the level of GSH compared with arsenic-treated rats. Further, the zinc level and activities of SOD, GPx, GR, and CAT were found to be significantly increased following zinc treatment. The administration of zinc to arsenic-treated rats caused signs of improvement in liver histoarchitecture, but a few focal areas of degeneration and necrosis were still occasionally seen. In conclusion, the results of this study suggest that zinc can be beneficial against arsenic-induced hepatotoxicity in rats.
机译:当前工作的目的是深入了解饮食中锌在缓解砷对大鼠肝脏造成的不良影响中的作用。雄性Wistar大鼠以100 ppm的剂量在饮用水中单独接受亚砷酸钠形式的砷,以227 mg / L的剂量在饮用水中单独接受以硫酸锌形式的锌,或在大鼠体内接受砷+锌处理。合并后的组总共3个月。砷处理导致脂质过氧化物酶(LPO)明显增加;然而,发现砷处理后谷胱甘肽(GSH)水平和超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GPx),谷胱甘肽还原酶(GR)和过氧化氢酶(CAT)的活性显着降低。此外,砷处理导致肝锌水平显着下降。组织学研究显示局灶性肝炎,小叶炎症,突出的肝细胞变性和严重的门静脉周围坏死的迹象明显不同。与用砷处理的大鼠相比,向用砷处理的大鼠施用锌显着降低了LPO的水平,但增加了GSH的水平。此外,发现锌处理后锌水平和SOD,GPx,GR和CAT的活性显着增加。给砷处理过的大鼠服用锌引起肝脏组织结构改善的迹象,但仍偶尔观察到一些局灶性的变性和坏死区域。总而言之,这项研究的结果表明锌可能对砷诱导的大鼠肝毒性有益。

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