期刊
BIOCHEMISTRY-MOSCOW
卷 84, 期 11, 页码 1411-1423出版社
MAIK NAUKA/INTERPERIODICA/SPRINGER
DOI: 10.1134/S0006297919110154
关键词
stroke; ischemia-reperfusion injury; mitochondria; complex I; flavin; thiols; nitrosation
资金
- NIH [NS-100850]
- MRC UK [G1100051, MR/L007339/1]
Ischemic stroke and neonatal hypoxic-ischemic encephalopathy are two of the leading causes of disability in adults and infants. The energy demands of the brain are provided by mitochondrial oxidative phosphorylation. Ischemia/reperfusion (I/R) affects the production of ATP in brain mitochondria, leading to energy failure and death of the affected tissue. Among the enzymes of the mitochondrial respiratory chain, mitochondrial complex I is the most sensitive to I/R; however, the mechanisms of its inhibition are poorly understood. This article reviews some of the existing data on the mitochondria impairment during I/R and proposes two distinct mechanisms of complex I damage emerging from recent studies. One mechanism is a reversible dissociation of natural flavin mononucleotide cofactor from the enzyme I after ischemia. Another mechanism is a modification of critical cysteine residue of complex I involved into the active/deactive conformational transition of the enzyme. I describe potential effects of these two processes in the development of mitochondrial I/R injury and briefly discuss possible neuroprotective strategies to ameliorate I/R brain injury.
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