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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Oxidative stress and inhibition of oxidative phosphorylation induced by peroxynitrite and nitrite in rat brain subcellular fractions.
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Oxidative stress and inhibition of oxidative phosphorylation induced by peroxynitrite and nitrite in rat brain subcellular fractions.

机译：过氧化亚硝酸盐和亚硝酸盐诱导的大鼠脑亚细胞部分的氧化应激和氧化磷酸化的抑制作用。

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摘要

Nitrite and nitrate, two endogenous oxides of nitrogen, are toxic in vivo. Furthermore, the reaction of superoxide (produced by all aerobic cells) with nitric oxide (NO) generates peroxynitrite, a potent oxidizing agent, that can cause biological oxidative stress. Using subcellular fractions from rat brain hemispheres we studied oxidative stress induced by these nitrogen compounds with special emphasis on nitrite. The consumption of Vitamin C (ascorbate) and Vitamin E (alpha tocopherol), two of the important nutritional antioxidants, was followed in synaptosomes (nerve-ending particles) and mitochondria along with changes in parameters of mitochondrial oxidative phosphorylation. Nitrite, but not nitrate, oxidized ascorbate without oxidizing alpha tocopherol in both synaptosomes and mitochondria whereas peroxynitrite oxidized both ascorbate and alpha tocopherol. Functionally, both nitrite and peroxynitrite inhibited mitochondrial oxidative phosphorylation. Nitrite was less potent than peroxynitrite whenthe effects of equal concentrations of the two were compared. However, since nitrite is much more stable than peroxynitrite the impact of nitrite as an oxidant in vivo could be as much or even more significant than peroxynitrite. Nitrate would not have similar action unless it is reduced to nitrite. It is possible that nitrite may impair oxidative phosphorylation through modulating levels of nitric oxide, changing the activity of heme proteins or a mild uncoupling of mitochondria.
机译：亚硝酸盐和硝酸盐是氮的两种内源性氧化物，在体内有毒。此外，超氧化物（由所有需氧细胞产生）与一氧化氮（NO）反应生成过氧亚硝酸盐，这是一种强氧化剂，可引起生物氧化应激。使用来自大鼠脑半球的亚细胞部分，我们研究了由这些氮化合物引起的氧化应激，其中特别强调了亚硝酸盐。突触小体（神经末梢颗粒）和线粒体中维生素C（抗坏血酸）和维生素E（两种重要的抗氧化剂）的消耗量随线粒体氧化磷酸化参数的变化而变化。亚硝酸盐（而不是硝酸盐）氧化了抗坏血酸而不氧化突触小体和线粒体中的α-生育酚，而过氧亚硝酸盐氧化了抗坏血酸和α-生育酚。在功能上，亚硝酸盐和过氧亚硝酸盐都抑制线粒体的氧化磷酸化。当比较两种浓度相等的亚硝酸盐时，亚硝酸盐的效果不如过氧亚硝酸盐。但是，由于亚硝酸盐比过氧亚硝酸盐稳定得多，因此亚硝酸盐作为氧化剂在体内的影响可能与过氧亚硝酸盐相同甚至更大。除非将其还原为亚硝酸盐，否则硝酸盐不会具有类似的作用。亚硝酸盐可能通过调节一氧化氮的含量，改变血红素蛋白的活性或线粒体的轻度解偶联而损害氧化磷酸化。

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