Section of Animal Biology, Department of Biology, Faculty of Sciences, University of Patras, 26 500 Patras, Greece.
Toxicol In Vitro. 2010 Aug;24(5):1363-72. doi: 10.1016/j.tiv.2010.04.008. Epub 2010 Apr 18.
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.
本研究探讨了汞（Hg）的氧化和遗传毒性效应与其抑制贻贝血细胞中硒依赖型谷胱甘肽过氧化物酶（Se-GPx）活性的能力之间的关系。在暴露于金属之前，用 4μg/l 的硒（以亚硒酸钠形式）预处理，分别测量了无硒细胞胞质部分和经硒处理的细胞中的 Se-GPx 活性。Hg 的浓度范围在 10 或 20μg/l 之间，这代表 Hg 毒性作用的开始，结果表明 Hg 抑制了无硒细胞中的 Se-GPx 活性，随后导致超氧阴离子（()O(2)(-))和一氧化氮（NO）生成增加、脂质过氧化和 DNA 损伤。另一方面，在所有情况下，暴露于 Hg 的经硒处理的细胞中测量到的酶活性增加和 Hg 毒性的显著减弱。本研究的结果表明，Hg 抑制 Se-GPx 活性可能会导致氧化剂和抗氧化剂之间的平衡向氧化剂倾斜，从而增强 Hg 诱导的氧化和遗传毒性效应。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对氧化剂（如 Hg）引起的毒性作用的抵抗力。
