Protective Effect of Resveratrol against Spleen Toxicity of Nicotine in Male Rat: Antioxidant and Histopathological Approaches

Abstract

Nicotine is a tertiary amine, nicotine can freely cross the biological membranes of body organs. During smoking, nicotine is rapidly absorbed into the circulatory system, and blood concentration of nicotine rise quickly during and peak at the completion of cigarette smoking. Resveratrol is a compound is a member of a group of plant compounds called polyphenol which possess a free radical scavenger that increases the activity of several antioxidant enzymes. The study aimed to evaluate the influence of Resveratrol (Res) in rat with Nicotine (Nic) induced spleen toxicity, by evaluating the biochemical and histopathological changes. The experiment was carried out on four groups of male rats as follows; group 1 served as a control group, group 2 was treated with Nic (2.5 mg kg^-1) in physiological saline, group 3 was received Res (20 mg Kg^-1), group 4 was treated with combination of Nic (2.5 mg Kg^-1) and Res (20 mg Kg^-1). The results indicated that Nic increased lipid peroxidation, Myloperoxidase, xanthine oxidase, nitrite level, TOS level and decrease the antioxidant enzymes as well as decrease the thiol and G6PD levels . A serious congestion and stasis, correlated with congested red pulp and numerous secondary lymphoid follicles were observed. All the lymphatic nodules appeared smaller with multiple variable sized reactive germinal centers with peripherally located central arteriole in the animals treated with Nic. Nic/Res treatments improve all the oxidative damage and the histopathological changes. In the light of the present results, it is evident that Res was able to reduce the toxic effect of Nic in rat. Conclusion: Resveratrol had found to effect on antioxidant parameters of the spleen tissue. The present study indicates that a decrease in the antioxidant status is one of the main factors contributing to Nicotine toxicity to the spleen. Res treatment found to remove the continuously generated free radicals, to prevent the endogenous antioxidant enzymes decrease and act to prevent oxidative cell damage induced by Nic.