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首页> 外文期刊>American Journal of Physiology >Oxidative and nitrosative stress in acute renal ischemia.
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Oxidative and nitrosative stress in acute renal ischemia.

机译：急性肾缺血中的氧化和亚硝化应激。

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摘要

Generation of reactive oxygen species and nitric oxide in hypoxia-reperfusion injury may form a cytotoxic metabolite, peroxynitrite, which is capable of causing lipid peroxidation and DNA damage. This study was designed to examine the contribution of oxidative and nitrosative stress to the renal damage in ischemic acute renal failure (iARF). iARF was initiated in rats by 45-min renal artery clamping. This resulted in lipid peroxidation, DNA damage, and nitrotyrosine modification confirmed both by Western and immunohistochemical analyses. Three groups of animals were randomly treated with an inhibitor of inducible nitric oxide synthase (NOS), L-N(6)-(1-iminoethyl)lysine (L-Nil), cell-permeable lecithinized superoxide dismutase (SOD), or both. Each treatment resulted in amelioration of renal dysfunction, as well as reduced nitrotyrosine formation, lipid peroxidation, and DNA damage, thus suggesting that peroxynitrite rather than superoxide anion is responsible for lipid peroxidation and DNA damage. Therefore, in a separate series of experiments, a scavenger of peroxynitrite, ebselen, was administered before the reperfusion period. This treatment resulted in a comparable degree of amelioration of iARF. In conclusion, the present study provides the first attempt to elucidate the role of peroxynitrite in initiation of the cascade of lipid peroxidation and DNA damage to ischemic kidneys. The results demonstrate that L-Nil, lecithinized SOD, and ebselen treatments improve renal function due to their suppression of peroxynitrite production or its scavenging, consequently preventing lipid peroxidation and oxidative DNA damage.
机译：缺氧-再灌注损伤中活性氧和一氧化氮的产生可能形成细胞毒性代谢产物过氧亚硝酸盐，其能够引起脂质过氧化和DNA损伤。本研究旨在检查氧化性和亚硝化应激对缺血性急性肾衰竭（iARF）肾损害的贡献。通过大鼠45分钟的肾动脉夹闭来启动iARF。 Western和免疫组织化学分析均证实了脂质过氧化，DNA损伤和硝基酪氨酸修饰。三组动物随机接受诱导型一氧化氮合酶（NOS），L-N（6）-（1-亚氨基乙基）赖氨酸（L-Nil）抑制剂，可渗透细胞的卵磷脂超氧化物歧化酶（SOD）或两者的抑制剂治疗。每种治疗均可以改善肾功能不全，并减少硝基酪氨酸的形成，脂质过氧化和DNA损伤，因此表明脂质过氧化和DNA损伤是过氧亚硝酸盐而不是超氧阴离子所致。因此，在单独的一系列实验中，在再灌注期之前施用过氧亚硝酸盐清除剂ebselen。该处理导致iARF的改善程度相当。总之，本研究提供了首次尝试阐明过氧亚硝酸盐在引发脂质过氧化和对缺血性肾脏的DNA损伤的级联中的作用。结果表明，L-Nil，卵磷脂SOD和依布硒啉治疗可抑制过氧亚硝酸盐的产生或清除，从而改善肾脏功能，从而防止脂质过氧化和DNA氧化损伤。

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