Abstract
Aluminum is a ubiquitous element with known toxicity for both human and experimental animals. It has been implicated in the pathogenesis of several diseases. The present study investigates the possible hepatoprotective role of melatonin in modulating the toxicity and the oxidative stress induced by chronic exposure to aluminum chloride (AlCl3) in the liver of male rats. 40 male rats were divided into four groups (10 rats each): vehicle control group treated with alcoholic saline, AlCl3 group treated with 20 mg/kg of AlCl3, melatonin group treated with 5 mg/kg of melatonin, and melatonin+ AlCl3 group treated with the previous doses of both AlCl3 and melatonin. Rats were treated orally once daily for 30 consecutive days. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin, total lipids, total cholesterol, triglycerides, glucose and total proteins were measured in the plasma to assess the liver functioning. Liver specimens were also collected for histopathological examination and also for assessment of hepatic level of malondialdehyde (MDA), reduced glutathione (GSH) in addition to the activity of glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT). The results showed that the oral administration of AlCl3 caused significant (p<0.05) increases in the plasma level of the ALT, AST, ALP, total bilirubin, total lipids, total cholesterol, triglycerides and glucose while the level of total proteins was found to be decreased. Moreover, AlCl3 induced oxidative stress as indicated by a significant increase in the level of MDA with a concomitant decrease in the GSH content as well as in the activity of GPx, SOD and CAT in the liver tissue. Histological examination for liver sections revealed marked necrosis and degeneration of hepatocytes, centrilobular necrosis, congestion of the central vein, vacuolization of cytoplasm, infiltration of inflammatory cells, dilatation and congestion of the blood sinusoids. Pretreatment with melatonin in AlCl3-treated rats alleviated the previously mentioned alterations in the biochemical and oxidative stress parameters and restored their values toward the normal value of the control group. Moreover, it improved to a large extent the histological changes induced by AlCl3 in such a way that more or less normal architecture of the liver was observed. Therefore, the data obtained in the present study confirmed the deleterious effects of AlCl3 in the liver. Moreover, it can be concluded that these effects could be overcome or, at least, significantly minimized by the administration of melatonin. [Wessam M. Abdel-Wahab. AlCl3-Induced Toxicity and Oxidative Stress in Liver of Male Rats: Protection by Melatonin. Life Sci J 2012; 9(4): 1173-1182] (ISSN: 1097-8135). http://www.lifesciencesite.com. 174