Regulation of hydrogen peroxide production by brain mitochondria by calcium and Bax.

摘要: Abnormal accumulation of Ca 2+ and exposure to pro-apoptotic proteins, such as Bax, is believed stimulate mitochondrial generation reactive oxygen species (ROS) contribute neural cell death during acute ischemic traumatic brain injury, in neurodegenerative diseases, e.g. Parkinson’s disease. However, the mechanism by which or apoptotic proteins ROS production unclear. We used a sensitive fluorescent probe compare effects on H2O2 emission isolated rat mitochondria presence physiological concentrations ATP Mg different respiratory substrates. In absence chain inhibitors, suppressed reduced membrane potential oxidizing succinate, glutamate plus malate. Complex I inhibitor rotenone, stimulated this stimulation was associated with release cytochrome c. malate, c formation were human recombinant full-length Bax BH3 domain peptide. These results indicate that ,C either inhibits stimulates production, depending substrate effect potential. peptide due insensitive changes