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首页> 外文OA文献 >Nitric oxide protects against cellular damage and cytotoxicity from reactive oxygen species.
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Nitric oxide protects against cellular damage and cytotoxicity from reactive oxygen species.

机译：一氧化氮可保护细胞免受活性氧的损害和细胞毒性。

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Nitric oxide, NO, which is generated by various components of the immune system, has been presumed to be cytotoxic. However, NO has been proposed to be protective against cellular damage resulting during ischemia reperfusion. Along with NO there is often concomitant formation of superoxide/hydrogen peroxide, and hence a synergistic relationship between the cytotoxic effects of nitric oxide and these active oxygen species is frequently assumed. To study more carefully the potential synergy between NO and active oxygen species in mammalian cell cytotoxicity, we utilized either hypoxanthine/xanthine cell cytotoxicity, we utilized either hypoxanthine/xanthine oxidase (a system that generates superoxide/hydrogen peroxide) or hydrogen peroxide itself. NO generation was accomplished by the use of a class of compounds known as "NONOates," which release NO at ambient temperatures without the requirement of enzyme activation or biotransformation. When Chinese hamster lung fibroblasts (V79 cells) were exposed to hypoxanthine/xanthine oxidase for various times or increasing amounts of hydrogen peroxide, there was a dose-dependent decrease in survival of V79 cells as measured by clonogenic assays. However, in the presence of NO released from (C2H5)2N[N(O)NO]-Na+ (DEA/NO), the cytotoxicity resulting from superoxide or hydrogen peroxide was markedly abrogated. Similarly, primary cultures of rat mesencephalic dopaminergic cells exposed either to hydrogen peroxide or to hypoxanthine/xanthine oxidase resulted in the degradation of the dopamine uptake and release mechanism. As was observed in the case of the V79 cells, the presence of NO essentially abrogated this peroxide-mediated cytotoxic effect on mesencephalic cells.
机译：一氧化氮（NO）是由免疫系统的各种成分产生的，被认为具有细胞毒性。然而，已经提出NO可以防止缺血再灌注期间引起的细胞损伤。与NO一起经常会形成超氧化物/过氧化氢，因此一氧化氮与这些活性氧的细胞毒性作用之间通常存在协同关系。为了更仔细地研究哺乳动物细胞毒性中NO和活性氧之间的潜在协同作用，我们利用了次黄嘌呤/黄嘌呤细胞的细胞毒性，我们利用了次黄嘌呤/黄嘌呤氧化酶（产生超氧化物/过氧化氢的系统）或过氧化氢本身。通过使用称为“ NONOates”的一类化合物完成NO的生成，该化合物在环境温度下释放NO而无需酶活化或生物转化。当中国仓鼠肺成纤维细胞（V79细胞）多次暴露于次黄嘌呤/黄嘌呤氧化酶或过氧化氢量增加时，通过克隆形成测定法测定，V79细胞的存活率呈剂量依赖性下降。但是，在存在从（C2H5）2N [N（O）NO] -Na +（DEA / NO）释放的NO的情况下，由过氧化物或过氧化氢引起的细胞毒性被显着消除。类似地，暴露于过氧化氢或次黄嘌呤/黄嘌呤氧化酶的大鼠中脑多巴胺能细胞的原代培养导致多巴胺摄取和释放机制的降解。如在V79细胞中观察到的，NO的存在基本上消除了过氧化物介导的对中脑细胞的细胞毒性作用。

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