Journal
MOLECULAR AND CELLULAR NEUROSCIENCE
Volume 100, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2019.103408
Keywords
Stroke; Ischemia-reperfusion injury; Mitochondria; Complex I; Flavin; Riboflavin
Categories
Funding
- NIH USA [NS-100850]
- MRC UK [G1100051, MR/L007339/1]
- MRC [MR/L007339/1, G1100051] Funding Source: UKRI
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The purpose of this review is to integrate available data on the effect of brain ischemia/reperfusion (I/R) on mitochondrial complex I. Complex I is a key component of the mitochondrial respiratory chain and it is the only enzyme responsible for regenerating NAD(+) for the maintenance of energy metabolism. The vulnerability of brain complex I to I/R injury has been observed in multiple animal models, but the mechanisms of enzyme damage have not been studied. This review summarizes old and new data on the effect of cerebral I/R on mitochondrial complex I, focusing on a recently discovered mechanism of the enzyme impairment. We found that the loss of the natural cofactor flavin mononucleotide (FMN) by complex I takes place after brain I/R. Reduced FMN dissociates from the enzyme if complex I is maintained under conditions of reverse electron transfer when mitochondria oxidize succinate accumulated during ischemia. The potential role of this process in the development of mitochondrial I/R damage in the brain is discussed.
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