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• W575884678 abstract "Cerebral ischemia is known to produce excessive reactive oxygen species (ROS) in mitochondria, and these radicals initiate radical chain reactions, causing cellular macromolecule damage and also promote mitochondrial apoptosis pathway, ultimately leading to cell death. However, little is known about the mitochondrial functional change after ischemia. We studied expression of cytochrome c oxidase (COX), a terminal, rate-limiting enzyme of the respiratory chain to generate ATP, after global cerebral ischemia in rats. Immunofluorescent staining and Western blot were performed to investigate the spatial and temporal changes in two important COX subunits, mitochondria-encoded COX subunit I (COX I) and nucleus-encoded COX subunit IV (COX IV). In normal condition, these subunits have to be precisely regulated in a 1 : 1 stoichiometry to assemble functional COX holoenzyme. In this study, a massive increase in COX I, which is disproportionate to COX IV was observed at 1 and 6 h after lethal ischemia, preceding delayed neuronal death. In contrast to lethal ischemia, mild sublethal ischemia did not elicit obvious alteration in COX I and IV. This aberrant increase in COX I may be an early sign of delayed neuronal death or may predict later electron transport chain dysfunction to generate ATP." @default.
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• W575884678 date "2013-02-01" @default.
• W575884678 modified "2023-09-28" @default.
• W575884678 title "REMARKABLE INCREASE OF CYTOCHROME C OXIDASE SUBUNIT I AFTER GLOBAL CEREBRAL ISCHEMIA" @default.
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