During cerebral ischemic cascade, a unifying factor which leads to
mitochondrial dysfunctions is lack of
oxygen followed by decrease in
ATP production. The present study demonstrates the effect of
selenium pretreatment (0.1 mg/kg as
sodium selenite, i.p, 7 days) on
cerebral ischemia-induced altered levels of mitochondrial
ATP content, intracellular
calcium (Ca(i)(2+)) in synaptosomes, expression of heat stress
protein (Hsp70) and
caspase-3 activity in hippocampus followed by neurobehavioral deficits and histopathological changes in Wistar rats.
Cerebral ischemia was induced for 2 h followed by reperfusion for 22 h. It was observed that levels of (Ca(i)(2+)), Hsp70 and
caspase-3 activity were significantly (p<0.01-0.001) higher with a marked decrease in
ATP level in hippocampus of ischemic group as compared to
sham values. Subsequently, a marked change was observed in neurobehavioral activities in ischemic animals as compared to control one. As a result of
selenium pretreatment, a significant (p<0.05-0.001) trend of restoration was observed in the level of
ATP, (Ca(i)(2+)), Hsp70,
caspase-3 and behavioral outputs as compared to ischemic group. Histopathological analysis confirmed the protective effect of
selenium against
cerebral ischemia induced histological alterations as evidenced by lesser
edema formation and separation of cells with minimal microglial cell infiltration in
selenium pretreated group as compared to ischemic animals. The present study suggests that
selenium may be able to salvage the ischemic penumbral zone neurons, thereby limiting ischemic cell death.