Hypoxia accelerates nitric oxide-dependent inhibition of mitochondrial complex I in activated macrophages
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Hypoxia accelerates nitric oxide-dependent inhibition of mitochondrial complex I in activated macrophages.
Excess production of nitric oxide (NO) is implicated in the development of multiple organ failure, with a putative mechanism involving direct mitochondrial inhibition, predominantly affecting complex I. The persistent effects of NO on complex I may be mediated through S-nitrosylation and/or nitration. The temporal contribution of these chemical modifications to the inhibition of respiration and...
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ژورنال
عنوان ژورنال: AJP: Regulatory, Integrative and Comparative Physiology
سال: 2004
ISSN: 0363-6119,1522-1490
DOI: 10.1152/ajpregu.00504.2004