The effect of antioxidant carnosine on oxidative stress induced by ethanol in rat brain tissue

Ethanol may enhance the production of ROS through a number of mechanisms. Ethanol promotes oxidative stress in several organs. Brain and nervous system are more vulnerable to ethanol-induced oxidative damage than other organs. The brain is the tissue most vulnerable to oxidative damage because of its higher rate of oxidative metabolic activity, low antioxidant activity, non replicatory nature of neuronal cells, high membrane surface to cytoplasm ratio and high levels of transition metals. Carnosine is an endogenously synthesized dipeptide which is formed from (3- alanine and L-histidine. Excitable tissues such as brain and skeletal muscle contain high levels of carnosine and histidine-containing dipeptides. Many functions have preoviously been proposed for carnosine; these include antioxidant and free radical scavenger, physiological buffer, neurotransmitter, metal chelator, immunostimulator and wound healing agent. The antioxidant mechanism of carnosine is attributed to its chelating effect against metal ions, SOD-like activity, ROS and free radicals scavenging ability. In the current study, the oxidative stress induced by ethanol, the antioxidant effects of carnosine and the histological observations in the rat brain were investigated. The MDA levels in the ethanol group increased significantly according to the other groups (p<0,001). There was a significant decrease in the carnosine group with respect to the control group (p<0,05). The MDA levels were almost similiar in both of the ethanol+carnosine group and the control group. The protein carbonyl levels in the ethanol group were increased significantly compared with the other groups. There was no statistical significancy in the protein carbonyl levels between the other groups. The SOD activities increased only in the ethanol+carnösine group with respect to the control group (p<0,05). The effects of the dietary carnosine on the endojen carnosine were investigated in the ethanol (p<0,05), carnosine (p<0,005) and the ethanol+carnosine (p<0,001) groups. The tissue crnosine levels were increased significantly with respect to the control group-58- in ethanol, carnosine and the ethanol+ carnosine groups. Also, the carnosine levels in the caraosine group increased significantly compared with the ethanol group (p<0,005). With respect o the other groups, the carnosine levels were higher in the carnosine group. The effects of ethanol and carnosine on the brain tissues were observed histologically. In the ethanol group, an obvious edema in the vessel walls and vocuolization in piramidal cells were observed compared with the control and with the other groups. Though the histological observations at the carnosine group was almost the same with control group, a "slight edema was investigated in the cell walls. The glial cells were normal. The biochemical and histological results of the study were similiar with the studies in those the ethanol was an oxidant. According to the results, carnosine was an antioxidant ameliorating the oxidant effects of ethanol in the brain.