Differential induction of superoxide dismutase in core and penumbra regions after transient focal ischemia in the rat neocortex.
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.
Article: The protective effect of M40401, a superoxide dismutase mimetic, on post-ischemic brain damage in Mongolian gerbils.[show abstract] [hide abstract]
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.BMC Pharmacology 07/2003; 3:8.
Article: Effects of nimodipine and magnesium sulfate on endogenous antioxidant levels in brain tissue after experimental head trauma.[show abstract] [hide abstract]
ABSTRACT: To examine the effects of calcium antagonists nimodipine and magnesium sulfate (MgSO4) on tissue endogenous antioxidant levels, the authors studied superoxide dismutase (SOD) and glutathione peroxidase (GPx) levels in rabbit brain 1 hour after experimental head trauma. Forty New Zealand rabbits were anesthetized and randomly divided into four groups. Group 1 (n = 10) was the sham operated group. Group 2 (n = 10), the control group, received head trauma and no treatment. Group 3 (n = 10) received head trauma and intravenous (IV) 2 microgr/kg nimodipine. Group 4 (n = 10) received head trauma and IV 100 mg/kg MgSO4. Head trauma was delivered by performing a craniectomy over the right hemisphere and dropping a weight of 20 g from a height of 40 cm. In the right (traumatized) hemisphere, SOD and GPx decreased by 57.60% +/- 9.60% and 72.93% +/- 5.51% respectively from sham values. Magnesium sulfate, but not nimodipine, reduced the magnitude of decrease of SOD and GPx to 19.43% +/- 7.15% and 39.01% +/- 7.92% respectively from sham values. In the left (nontraumatized) hemisphere, MgSO4 increased SOD to 42.43% +/- 24.76% above sham values. The authors conclude that MgSO4 treatment inhibited the decrease in SOD and GPx levels in experimental brain injury.Journal of Neurosurgical Anesthesiology 08/2001; 13(3):227-32. · 2.23 Impact Factor