Article

Differential induction of superoxide dismutase in core and penumbra regions after transient focal ischemia in the rat neocortex.

Department of Neurological Surgery, Health Sciences Center, University of Virginia, Charlottesville 22908, USA.
Neuroscience Letters (impact factor: 2.11). 11/1997; 235(1-2):29-32. DOI:10.1016/S0304-3940(97)00707-6 pp.29-32
Source: PubMed

ABSTRACT Oxygen free radicals are postulated to participate in the pathogenesis of ischemic brain injury. The present study investigated the response of the endogenous antioxidant enzyme, superoxide dismutase (SOD), in a model of transient focal ischemia in the rat neocortex. SOD activity was increased significantly in the penumbra region at 6-24 h postischemia, while no significant changes in SOD activity were observed in either the core region or striatum. These results indicate that endogenous antioxidant activity is differentially affected by the intensity of ischemic challenge and suggest that the regional effects of oxygen free radicals may vary substantially following ischemia-reperfusion.

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    Article: The protective effect of M40401, a superoxide dismutase mimetic, on post-ischemic brain damage in Mongolian gerbils.
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    ABSTRACT: Overproduction of free radical species has been shown to occur in brain tissues after ischemia-reperfusion injury. However, most of free radical scavengers known to antagonize oxidative damage (e.g. superoxide dismutase, catalase), are unable to protect against ischemia-reperfusion brain injury when given in vivo, an effect mainly due to their difficulty to gain access to brain tissues. Here we studied the effect of a low molecular weight superoxide dismutase mimetic (M40401) in brain damage subsequent to ischemia-reperfusion injury in Mongolian gerbils. In animals undergoing ischemia-reperfusion injury, neuropathological and ultrastructural changes were monitored for 1-7 days either in the presence or in the absence of M40401 after bilateral common carotid artery occlusion (BCCO). Administration of M40401 (1-40 mg/kg, given i.p. 1 h after BCCO) protected against post-ischemic, ultrastructural and neuropathological changes occurring within the hippocampal CA1 area. The protective effect of M40401 was associated with a significant reduction of the levels of malondialdehyde (MDA; a marker of lipid peroxidation) in ischemic brain tissues after ischemia-reperfusion. Taken together, these results demonstrate that M40401 provides protective effects when given early after the induction of ischemia-reperfusion of brain tissues and suggest the possible use of such compounds in the treatment of neurological dysfunction subsequent to cerebral flow disturbances.
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