General Physiology and Biophysics Vol.34, No.4, p.415–424, 2015

This study aimed to investigate the potential effects of melatonin on aluminium-induced toxicity in a rat model using a set of biochemical, inflammatory, oxidant, lipid profile criteria and hepatic integrity (verified by hematoxylin-eosin staining). The results indicated that AlCl3 administration during 60 days (100 mg/kg b.w.) significantly increased the activities of transaminases AST and ALT by 46% (p < 0.001) and 21% (p < 0.01), lactate dehydrogenase (LDH) by 30% (p < 0.001), the levels of bilirubin by 85% (p < 0.001), total cholesterol by 115% (p < 0.001), triglycerides by130% (p < 0.001), LDL-cholesterol by 413% (p < 0.001), oxidized LDL (oxLDL) by 51% (p < 0.01) and apolipoprotein B100 (apoB100) by 63% (p < 0.001), as compared to controls. The inflammatory markers (TNF-α, IL-2, and IL-6) were significantly increased (p < 0.001), associated to higher lipid peroxidation (TBARS) level. Also, both plasma HDL-cholesterol level and hepatic LDL receptors (p < 0.01) expression and antioxidant protein (SOD, CAT, and GPx) activities are decreased.

Those physiological disturbances were, however, noted to alleviate following the co-administration of melatonin (10 mg/kg b.w.). Overall, the present study is the first to provide evidence on the anti-inflammatory, anti-oxidant, anti-lipidic and, hence, therapeutic effects of melatonin with regard to the control and prevention of aluminium-intoxication.