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• W2114521612 startingPage "565" @default.
• W2114521612 abstract "In diseases associated with neuronal degeneration, such as Alzheimer's or cerebral ischemia, the cytosolic Ca2+ concentration ([Ca2+]cyt) is pathologically elevated. It is still unclear, however, under which conditions Ca2+ induces either apoptotic or necrotic neuronal cell death. Studying respiration and morphology of rat brain mitochondria, we found that extramitochondrial [Ca2+] above 1 M causes reversible release of cytochrome c, a key trigger of apoptosis. This event was NO-independent but required Ca2+ influx into the mitochondrial matrix. The mitochondrial permeability transition pore (PTP), widely thought to underlie cytochrome c release, was not involved. In contrast to noncerebral tissue, only relatively high [Ca2+] (is approximately equal to 200 M) opened PTP and ruptured mitochondria. Our findings might reflect a fundamental mechanism to protect postmitotic neuronal tissue against necrotic devastation and inflammation." @default.
• W2114521612 created "2016-06-24" @default.
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• W2114521612 date "2001-01-19" @default.
• W2114521612 modified "2023-09-26" @default.
• W2114521612 title "Distinct Ca²⁺thresholds determine cytochrome c release or permeability transition pore opening in brain mitochondria" @default.
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• W2114521612 doi "https://doi.org/10.1096/fj.00-0551fje" @default.
• W2114521612 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11259368" @default.
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