Attenuation of focal cerebral ischemic injury in transgenic mice overexpressing CuZn superoxide dismutase.

摘要: Oxygen-derived free radicals have been implicated in the pathogenesis of vasogenic edema and infarction caused by ischemia reperfusion injury. In earlier studies, exogenously supplied liposome-entrapped CuZn superoxide dismutase (CuZn-SOD) ameliorated ischemic brain rats following focal cerebral ischemia. To ascertain directly role SOD protection against radical-induced injury, we measured infarct size water content 24 hr nontransgenic mice transgenic bearing human SOD1 gene. These 3.1-fold higher cellular CuZn-SOD activity than do their littermates. We also antioxidant levels (reduced glutathione reduced ascorbate) contralateral cortex, surrounding striatum. Infarct were significantly decreased compared with mice. Reduced ascorbate hemisphere, but cortex striatum results indicate that increased endogenous reduces level damage support concept play an important