ABSTRACT
Under normal physiological aerobic conditions, brain mitochondria generate adenosine triphosphate through the electron transport chain that contains five multi-subunit enzyme complexes (I to V) (Mitchell, 1979). During mitochondrial respiration, superoxide radicals are produced in the complex I (reduced nicotinamide-adenine dinucleotide dehydrogenase) and in the complex III (ubiquinone-cytochrome b-c1) (Turrens and Boveris, 1980; Turrens et al., 1985; Turrens and McCord, 1990). However, superoxide radicals are rapidly dismutated by intramitochondrial manganese superoxide dismutase (MnSOD) or extra mitochondrial CuZn-SOD, respectively. The reaction product, H2O2, is then converted to H2O and O2 by glutathione peroxidase or by catalase. Ischemia and reperfusion cause an increased production of H2O2 and hydroxyl radicals, primarily due to the increased production of superoxide concomitant with insufficient antioxidant scavenger activities (Cao et al., 1988).
