Protective effects of oral melatonin against cadmium-induced neurotoxicity in Wistar rats

Abstract

The aim of this study was to investigate the effects of oral melatonin on oxidative/antioxidative parameters and histopathological changes in the hippocampal tissue of Cd-exposed Wistar rats, including malondialdehyde (MDA), glutathione (GSH), tumour necrosis factor-alpha (TNF-α), interleukin (IL-6 and IL-10), and gamma-aminobutyric acid (GABA) levels and catalase (CAT), superoxide dismutase (SOD), and acetylcholinesterase (AChE) activities. Thirty-two male Wistar rats were divided randomly into four groups as follows: untreated control (n=8), cadmium (Cd) (n=8), melatonin (Mlt) (n=8), and Cd+Mlt (CdMlt) (n=8). Cd (2 mg/kg) was administered orally by gastric gavage three times a week and Mlt (100 mg/kg) five times a week. The control group received standard feed and water only. After four weeks of treatment, the animals were decapitated and tissue samples taken for biochemical and histopathological evaluations. Mlt caused a significant increase in GSH levels and SOD and CAT activities in the CdMlt group compared to the Cd group. Tissue TNF-α and IL-6 levels were significantly higher in the Cd group than other groups (P<0.05). This effect was significantly countered by Mlt in the CdMlt group (P<0.05). GABA concentrations were significantly higher in the Mlt than other groups (P<0.05). Our findings clearly evidence the protective effects of melatonin against Cd-induced neurotoxicity in rats.