一氧化氮、过氧亚硝酸盐和S-亚硝基硫醇对线粒体呼吸复合体I的抑制作用。
Inhibition of mitochondrial respiratory complex I by nitric oxide, peroxynitrite and S-nitrosothiols.
作者信息
Brown Guy C, Borutaite Vilmante
机构信息
Department of Biochemistry, University of Cambridge, Tennis Court Road, Cambridge CB2 1QW, UK.
出版信息
Biochim Biophys Acta. 2004 Jul 23;1658(1-2):44-9. doi: 10.1016/j.bbabio.2004.03.016.
NO or its derivatives (reactive nitrogen species, RNS) inhibit mitochondrial complex I by several different mechanisms that are not well characterised. There is an inactivation by NO, peroxynitrite and S-nitrosothiols that is reversible by light or reduced thiols, and therefore may be due to S-nitrosation or Fe-nitrosylation of the complex. There is also an irreversible inhibition by peroxynitrite, other oxidants and high levels of NO, which may be due to tyrosine nitration, oxidation of residues or damage of iron sulfur centres. Inactivation of complex I by NO or RNS is seen in cells or tissues expressing iNOS, and may be relevant to inflammatory pathologies, such as septic shock and Parkinson's disease.
一氧化氮（NO）或其衍生物（活性氮物质，RNS）通过几种尚未完全明确的不同机制抑制线粒体复合体I。NO、过氧亚硝酸盐和S-亚硝基硫醇可导致失活，这种失活可被光或还原型硫醇逆转，因此可能是由于该复合体的S-亚硝基化或铁-亚硝基化。过氧亚硝酸盐、其他氧化剂和高浓度的NO也会导致不可逆抑制，这可能是由于酪氨酸硝化、残基氧化或铁硫中心受损。在表达诱导型一氧化氮合酶（iNOS）的细胞或组织中可观察到NO或RNS使复合体I失活，这可能与炎症性疾病有关，如脓毒性休克和帕金森病。
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