首页> 外文期刊>Brazilian Archives of Biology and Technology >Vitamin E and Sodium Selenite Against Mercuric Chloride-Induced Lung Toxicity in the Rats
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Vitamin E and Sodium Selenite Against Mercuric Chloride-Induced Lung Toxicity in the Rats

机译:维生素E和亚硒酸钠对抗氯化汞诱导的大鼠肺毒性

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The aim of the present study was to elucidate the possible protective role of vitamin E and / or sodium selenite on mercuric chloride-induced oxidative stress and histopathological changes in the lung tissue of the rats. Adult male albino Wistar rats were exposed to mercuric chloride (1.0 mg/kg day) for four weeks. Treatment with mercuric chloride led to oxidative stress by enhancing MDA level and also decreasing superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) and glutathione S transferaz (GST) activities. However, mercuric chloride exposure resulted in histopathological changes in the lung tissue in the rats. MDA level and SOD, CAT GPx and GST activities and histopathological changes modulated in concomitantly supplementation of vitamin E (100 mg/kg day) and /or sodium selenite (0.25 mg/kg day) to mercuric chloride-treated groups.
机译:本研究的目的是阐明维生素E和/或亚硒酸钠对氯化汞诱导的大鼠氧化应激和组织病理学变化的可能保护作用。成年雄性白化Wistar大鼠暴露于氯化汞(1.0 mg / kg每天)持续四个星期。氯化汞处理通过提高MDA含量并降低超氧化物歧化酶(SOD),过氧化氢酶(CAT)谷胱甘肽过氧化物酶(GPx)和谷胱甘肽S transferaz(GST)活性而导致氧化应激。但是,氯化汞暴露导致大鼠肺组织的组织病理学改变。 MDA水平和SOD,CAT GPx和GST活性以及组织病理学变化通过向氯化汞治疗组同时补充维生素E(每天100 mg / kg)和/或亚硒酸钠(每天0.25 mg / kg)来调节。

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