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• W2091258488 abstract "In this study, we have used isolated brain mitochondria to investigate the effects of superoxide anions (O 2 − ) on mitochondrial parameters related to apoptosis, such as swelling, potential, enzymatic activity, NAD(P)H, cytochrome c release, and caspase activity. Addition of the reactive oxygen species (ROS) generator KO 2 produced brain mitochondrial swelling, which was blocked by cyclosporin A (CSA), and which was Ca 2+ independent. Calcium induced mitochondrial swelling only at high concentrations and in the presence of succinate. This correlated with the increase in O 2 − production detected with hydroethidine in mitochondrial preparations exposed to Ca 2+ and the fact that ROS were required for Ca 2+ ‐induced mitochondrial swelling. Superoxide anions, but not Ca 2+ , decreased citrate synthase and dehydrogenase enzymatic activities and dropped total mitochondrial NAD(P)H levels. Calcium, but not O 2 − , triggered a rapid loss of mitochondrial potential. Calcium‐induced Δψ m dissipation was inhibited by Ruthenium Red, but not by CSA. Calcium‐ and superoxide‐induced mitochondrial swelling released cytochrome c and increased caspase activity from isolated mitochondria in a CS A‐sensitive manner. In summary, superoxide potently triggers mitochondrial swelling and the release of proteins involved in activation of postmitochondrial apoptotic pathways in the absence of mitochondrial depolarization. British Journal of Pharmacology (2003) 139 , 797–804. doi: 10.1038/sj.bjp.0705309" @default.
• W2091258488 created "2016-06-24" @default.
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• W2091258488 date "2003-06-01" @default.
• W2091258488 modified "2023-10-14" @default.
• W2091258488 title "Reactive oxygen species induce swelling and cytochrome<i>c</i>release but not transmembrane depolarization in isolated rat brain mitochondria" @default.
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• W2091258488 doi "https://doi.org/10.1038/sj.bjp.0705309" @default.
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