Sch?nfeld and Reiser recently hypothesized that fatty acid â-oxidation is a source of oxidative stress in the brain. To test this hypothesis, we inhibited brain mitochondrial â-oxidation with methyl palmoxirate (MEP) and measured oxidative polyunsaturated fatty acid (PUFA) metabolites in the rat brain. Upon MEP treatment, levels of several nonenzymatic auto-oxidative PUFA metabolites were reduced with few effects on enzymatically derived metabolites. Our finding confirms the hypothesis that reduced fatty acid â-oxidation decreases oxidative stress in the brain and â-oxidation inhibitors may be a novel therapeutic approach for brain disorders associated with oxidative stress.
Animals Asphyxia