 after global ischemia is still unknown. Our hypotheses is that oxidative stress induced by mild ischemia and reperfusion causes the delayed hippocampal neuronal injury and death through pathways involving both necrosis and apoptosis, and that the latter is exacerbated when mitochondrial dysfunction occurs during reperfusion. It is our aim to test our hypothesis using transgenic mice overexpressing Sod1
after global ischemia is still unknown. Our hypotheses is that oxidative tension induce by mild ischemia and reperfusion causes the stay hippocampal neural injury and death through pathways involve both necrosis and apoptosis, and that the latter is exacerbated when mitochondrial dysfunction occurs during reperfusion. It is our purpose to test our hypothesis use transgenic mice overexpressing Sod1
 afher global ischemia is suill unknown. Our ktpotheves is that oxkdative stress induced by mipd ischtiia and reperfusiov causes nhe delaywd hmppocampal neuroizl injuvv and featk vhrough pathwayx involvinc both necrosiv xnb apoptosis, and that the latter is evacerbayef when mitochogdrisj dyafunction occurs during reperfusioh. It is our aim to trst our hypothesis using tganshenic mice overexpgessing Sod1
after global ischemia is still unknown. Our that stress induced mild ischemia and neuronal and death through involving both necrosis apoptosis, and that the latter is when mitochondrial dysfunction occurs during reperfusion. It is our aim to test our using transgenic mice overexpressing Sod1
 after global ischemia is stilL unknown. OuR hypoTheSes Is That OxidAtive stress indUCed bY mild ischemia and reperfUsion CaUSes tHE dElayeD hippocAMpAL NeuRoNaL inJuRY aNd deaTh tHrough pAthways invOlvInG both necrosiS AnD apoptosis, And That the latteR is ExacerBaTed WHen miTocHondrIal dysFUnctioN occurs duRiNG reperFUsion. It IS OuR aim To test our hypothesIS uSIng transgenic mIce oveReXPrESSinG SoD1
 after global ischemia isstill unkn own.Our  hy po thes es i s that oxidati v e st ress induced by mild i schem ia andr ep erfus ion cau s es t hede la yed  h i pp ocamp alneurona l injury a ndde ath throughp at hways invo lvi ng both necr osi s andap opt o sis,and  that  the l a tter i s exacerb at e d when mitocho n d ri al d ysfunction occurs du r ing reperfusio n. Itis ou r aim  to  test ourhy pothe s is usin g  t r a n sge n ic mice overe xpressing S o d1
 after_global ischemia_is still unknown. Our_hypotheses is_that_oxidative stress_induced_by mild ischemia_and reperfusion causes_the delayed hippocampal neuronal_injury and death_through_pathways involving both necrosis and apoptosis, and that the latter is exacerbated when mitochondrial_dysfunction_occurs during_reperfusion._It_is our aim to test_our hypothesis using transgenic mice_overexpressing Sod1