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It is known that oxidative stress and mitochondrial dysfunction plays an important role in animal models of brain ischemia. The present study was undertaken to test whether oral supplementation of coenzyme Q (CoQ) could protect against transient cerebral ischemia-induced mitochondrial damage in the rat brain. Rats were divided into four groups: 1- control; 2- ischemia-reperfusion; 3- CoQ before ischemia; 4- CoQ after ischemia. Transient cerebral ischemia was induced with three vessel occlusion (3-VO) for 50 min. CoQ (200 mg/kg/day, p.o.) was administered for 30 days before ischemia and/or for 30 days after ischemia. Brain mitochondria were used for the determination of oxidative phosphorylation (OXPHOS). Moreover, the concentrations of CoQ and tocopherols, and formation of TBARS were measured in brain mitochondria and in plasma. Ischemia-reperfusion injury revealed significant impairment of OXPHOS, decreased concentrations of brain and plasma endogenous antioxidants and increased formation of TBARS in plasma. When compared with ischemia-reperfusion group, preventive supplementation of CoQ was ineffective. However, positive effect of therapeutic CoQ supplementation was detected in RCI (P<0.001), S3 (p<0.05) and in OPR (P<0.05), as well as in the concentration of coenzyme Q9 in brain mitochondria (P<0.05) and of α-tocopherol (P<0.01) in plasma. This suggests that the protection of CoQ10 involve increased resistance to oxidative stress, when supplemented during reperfusion.
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Author(s): Horeck J Aliev G Gvozdjkov A Kucharsk J Vanov O
Rat, three-vessel occlusion, coenzyme Q10, endogenous antioxidants, TBARS