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首页> 外文期刊>Toxicology in vitro: an international journal published in association with BIBRA >The role of selenium-dependent glutathione peroxidase (Se-GPx) against oxidative and genotoxic effects of mercury in haemocytes of mussel Mytilus galloprovincialis (Lmk.).
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The role of selenium-dependent glutathione peroxidase (Se-GPx) against oxidative and genotoxic effects of mercury in haemocytes of mussel Mytilus galloprovincialis (Lmk.).

机译:硒依赖性谷胱甘肽过氧化物酶(Se-GPx)对贻贝贻贝(Lmk。)血细胞中汞的氧化和遗传毒性作用的作用。

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摘要

This study investigated whether mercury (Hg) oxidative and genotoxic effects are related with its ability to inhibit selenium-dependent glutathione peroxidase (Se-GPx) activity in haemocytes of mussel Mytilus galloprovincialis. Se-GPx activity was measured both in Se-free cells' cytosolic fraction and in Se-treated cells, pre-treated with 4 microg/l of Se (as sodium selenite), before the exposure to the metal. Hg at concentrations ranged within 10 or 20 microg/l, thus representing the onset of Hg toxic effects, showed to inhibit Se-GPx activity in Se-free cells, followed by increased levels of superoxide anions (()O(2)(-)) and nitric oxide (NO) generation, lipid peroxidation and DNA damage as well. On the other hand, increased enzymatic activity and a significant attenuation of Hg toxicity were measured in Se-treated cells exposed to Hg in all cases. The results of the present study showed that inhibition of Se-GPx activity by Hg could promote a shift in the balance between oxidants and antioxidants in favor of oxidants, resulted in the enhancement of Hg-induced oxidative and genotoxic effects. In addition, Se bioavailability within phagocytic cells, such as haemocytes, could regulate the antioxidant role of Se-GPx, thus reinforcing haemocytes' immune system against toxic effects induced by pro-oxidants, such as Hg.
机译:这项研究调查了汞(Hg)的氧化和遗传毒性作用是否与其抑制贻贝贻贝贻贝血细胞中硒依赖性谷胱甘肽过氧化物酶(Se-GPx)活性的能力有关。在暴露于金属之前,在无硒细胞的细胞质分数和经4微克/升硒(亚硒酸钠)预处理的硒处理过的细胞中测量硒GPx活性。汞浓度在10或20微克/升之间,因此表示汞毒性作用的开始,显示抑制无硒细胞中Se-GPx活性,然后增加超氧阴离子(()O(2)(- )和一氧化氮(NO)的产生,脂质过氧化和DNA损伤。另一方面,在所有情况下,在经硒处理的暴露于汞的细胞中均检测到酶活性增强和汞毒性显着降低。本研究的结果表明,Hg抑制Se-GPx活性可以促进氧化剂和抗氧化剂之间的平衡转变,有利于氧化剂,从而增强了Hg诱导的氧化和遗传毒性作用。此外,吞噬细胞(如血细胞)中硒的生物利用度可以调节Se-GPx的抗氧化作用,从而增强血细胞的免疫系统,抵抗由前氧化剂(如汞)诱导的毒性作用。

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