The present study targeted the brain mitochondria dysfunction in Swiss albino mice through carbon tetrachloride intoxication and its treatment with Zingerone. It is proposed that brain mitochondria is the main organelle responsible for oxidative stress by producing reactive oxygen species (ROS). Swiss albino mice were divided into four groups; Group-1 was control; Group-2 was carbon tetrachloride (CCl4) toxic (1.5mg kg-1 bm i.p two days in a week.); Group-3 was pretreated with Zingerone (100 mg kg-1 b.m) a day before the administration of CCl4 and Group-4 was only Zingerone (100 mg kg-1 bm) given orally for 15days once in a day. At the end of the experiment mice were sacrificed and mitochondria were isolated from brain. Isolated brain mitochondria were further analyzed for oxidative stress marker. Thiobarbituric acid reactive substance (TBARS) content was increased significantly by CCl4 administration in Group-II as compared to the control Group-I, while the antioxidant (GSH) and other antioxidant enzyme GPx , GR, and CAT was depleted significantly in CCl4 treated Group-II as compare to control Group-I. Zingerone protected the toxicity of brain mitochondria by reducing the lipid peroxidation and enhancing the antioxidant enzyme in Group-III and there was no significant changes were noticed in Group-IV as compared to Group-I. Overall results showed the potential effects of Zingerone in protecting the neuronal cell loss by oxidative stress. Thus, the present study indicated that the Zingerone may be used as the potential therapeutic tools for the prevention of CCl4 induced brain mitochondrial toxicity.
Brain Mitochondria, Carbon tetrachloride, Oxidative stress, Zingerone
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