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Abnormal accumulation of Ca²⁺ and exposure to pro‐apoptotic proteins, such as Bax, is believed to stimulate mitochondrial generation of reactive oxygen species (ROS) and contribute to neural cell death during acute ischemic and traumatic brain injury, and in neurodegenerative diseases, e.g. Parkinson's disease. However, the mechanism by which Ca²⁺ or apoptotic proteins stimulate mitochondrial ROS production is unclear. We used a sensitive fluorescent probe to compare the effects of Ca²⁺ on H₂O₂ emission by isolated rat brain mitochondria in the presence of physiological concentrations of ATP and Mg²⁺ and different respiratory substrates. In the absence of respiratory chain inhibitors, Ca²⁺ suppressed H₂O₂ generation and reduced the membrane potential of mitochondria oxidizing succinate, or glutamate plus malate. In the presence of the respiratory chain Complex I inhibitor rotenone, accumulation …