Redox-dependent loss of flavin by mitochondria complex I is different in brain and heart

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Increased Succinate Accumulation Induces ROS Generation in In Vivo Ischemia/Reperfusion-Affected Rat Kidney Mitochondria

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Accumulation of Succinate in Cardiac Ischemia Primarily Occurs via Canonical Krebs Cycle Activity

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The dependence of brain mitochondria reactive oxygen species production on oxygen level is linear, except when inhibited by antimycin A

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Reverse electron transfer results in a loss of flavin from mitochondrial complex I: Potential mechanism for brain ischemia reperfusion injury

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Ischaemic accumulation of succinate controls reperfusion injury through mitochondrial ROS

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The Oxygen Free Radicals Originating from Mitochondrial Complex I Contribute to Oxidative Brain Injury Following Hypoxia-Ischemia in Neonatal Mice

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