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- W2021504443 abstract "The physical law of diffusion imposes O 2 concentration gradients from the plasma membrane to the center of the cell. The present study was undertaken to determine how such intracellular radial gradients of O 2 affect the fate of isolated single cardiomyocytes. In single rat cardiomyocytes, mitochondrial respiration was moderately elevated by an oxidative phosphorylation uncoupler to augment the intracellular O 2 gradient. At physiological extracellular O 2 levels (2–5%), decreases in myoglobin O 2 saturation and increases in NADH fluorescence at the center of the cell were imaged (anoxic cell core) while the mitochondrial membrane potential (ΔΨ m ) and ATP levels at the anoxic cell core were relatively sustained. In contrast, treatment with 0.5 mM iodoacetamide (IA) to inhibit creatine kinase (CK) resulted in depletion of both ΔΨ m and ATP at the anoxic cell core. Even at normal extracellular Po 2 , actively respiring cardiomyocytes developed rigor contracture followed by necrotic cell death. Furthermore, such rigor was remarkably accelerated by IA, whereas cell injury was perfectly rescued by mitochondrial F 1 F o inhibition by oligomycin. These results suggest that increases in radial gradients of O 2 potentially promote cell death through the reverse action of F 1 F o in mitochondria located at the anoxic cell core. However, in the intact cardiomyocyte, the CK-mediated energy flux from the subsarcolemmal space may sustain ΔΨ m at the cell core, thus avoiding uncontrolled consumption of ATP that can lead to necrotic cell death. Mitochondria at the anoxic core can cause necrotic cell death in cardiomyocytes at physiological extracellular Po 2 ." @default.
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- W2021504443 date "2008-06-01" @default.
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- W2021504443 title "Anoxic cell core can promote necrotic cell death in cardiomyocytes at physiological extracellular Po2" @default.
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- W2021504443 doi "https://doi.org/10.1152/ajpheart.00168.2008" @default.
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