首页> 外文期刊>Free radical research >Antioxidant enzyme activity and lipid peroxidation in liver of female rats co-exposed to lead and cadmium: Effects of vitamin E and Mn(2+).
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Antioxidant enzyme activity and lipid peroxidation in liver of female rats co-exposed to lead and cadmium: Effects of vitamin E and Mn(2+).

机译:铅和镉共同暴露的雌性大鼠肝脏中的抗氧化酶活性和脂质过氧化作用:维生素E和Mn(2+)的影响。

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The oxidative status of liver of female rats exposed to lead acetate and cadmium acetate either alone or in combination at a dose of 0.05?mg/kg body wt intraperitoneally for 15 days was studied. After the administration of lead alone, the activity of superoxide dismutase (SOD) decreased in liver, whereas no changes were observed in catalase (CAT) activity, and glutathione (GSH) and thiobarbituric acid (TBARS) levels. Cadmium exposure and combined exposure to lead and cadmium led to decrease in GSH content and increased TBARS levels. Moreover, animals exposed to either cadmium alone or in combination with lead showed a decrease in SOD activity and an increase in CAT activity. The in vitro experiments showed that vitamin E failed to restore the antioxidant enzyme activities in metal treated postmitochondrial supernatant fraction of liver. But Mn(2+) ions protected the mitochondria from lipid peroxidation and could completely restore Mn-superoxide dismutase (Mn-SOD) activity following metal intoxication. The results of this study indicate that despite the ability of lead and cadmium to induce oxidative stress the effect in liver is not intensified by combined exposure to both lead and cadmium. The observed changes in various oxidative stress parameters in the liver of rats co-exposed to lead and cadmium may result from an independent effect of lead and /cadmium and also from their interaction such as changes in metal accumulation and content of essential elements like Cu, Zn and Fe. These results suggest that when lead and cadmium are present together in similar concentrations, cadmium mediates major effects due to its more reactive nature.
机译:研究了雌性大鼠腹膜内暴露于乙酸铅和乙酸镉的腹膜内或腹腔注射剂量为0.05?mg / kg体重15天的肝脏的氧化状态。单独施用铅后,肝脏中的超氧化物歧化酶(SOD)活性下降,而过氧化氢酶(CAT)活性,谷胱甘肽(GSH)和硫代巴比妥酸(TBARS)的水平未见变化。镉暴露以及铅和镉的联合暴露导致GSH含量降低和TBARS水平升高。而且,单独暴露于镉或与铅联合暴露的动物表现出SOD活性降低和CAT活性增加。体外实验表明,维生素E不能恢复金属处理的肝线粒体后上清液中的抗氧化酶活性。但是Mn(2+)离子保护线粒体免受脂质过氧化作用,并且可以在金属中毒后完全恢复Mn-超氧化物歧化酶(Mn-SOD)活性。这项研究的结果表明,尽管铅和镉具有诱导氧化应激的能力,但同时接触铅和镉并不能增强肝脏的作用。铅和镉共暴露的大鼠肝脏中各种氧化应激参数的变化可能是由于铅和镉的独立作用以及它们之间的相互作用所致,例如金属积累的变化和诸如铜,锌和铁。这些结果表明,当铅和镉以相似的浓度同时存在时,镉由于其更具反应性的性质而起主要作用。

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