Neuroprotective and Ameliorative Effect of Caffeic Acid On Antioxidant and Acetylcholine Status of Mercury Intoxicated Rats

Author(s): Manogaran Manju and Ganesan Jagadeesan*

Abstract: Mercury (Hg), a well-known environmental and industrial hazard, exerts a number of toxic effects in humans and animals. And also it acts as a neurotoxin. In the present experimental study, the antioxidant and acetylcholine property of mercury intoxicated brain tissue of rat was investigated. And withdrawal effects of mercury toxicity in the brain tissue with the help of caffeic acid treatments were also investigated. Caffeic acid at a concentration of 5 mg/kg body weight, accelerate the oxidation of neurotoxicity induced by HgCl2 (1.29mg/kg Body weight of the animal). The aim of this study was to investigate the protective potential of Caffeic acid against Hgcl2 induced brain damage. The antioxidant activities of caffeic acid concentration were mainly due to the scavenging of lipid peroxide in this system. The oxidant mechanism for caffeic acid is most likely due to the strong reducing power and weak metal chelating ability. During the Hgcl2 treatment, the mercury toxicants mainly induced the toxicity in the brain tissues or rats to exhibit elevated level of lipid peroxidation (LOP). At the same time the level of enzymic antioxidants Superoxide dismutase (SOD), Catalase (CAT), and glutathione peroxidase (GPx), AchE activity and non-enzymic antioxidants reduced glutathion (GSH) were significantly decreased in brian tissues. But during the recovery period (Caffeic acid treatment on mercury intoxicated animal), are enhances the not only the GSH levels, and also promote the AchE activities. It leads to protects cell damage against neurotoxicity induced by mercuric chloride. Histological and histopathogical observation are also supporting these findings by the way of restoration of brain level or nearl normal level. Thus, result of the present study caffeic acid exhibited potent antioxidant, neuroprotective activities on HgCl2 induced neurotoxicity in rats.

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