Mitigative role of melatonin and α-tocopherol against mercury-induced genotoxicity.

The present study was conducted to elucidate the protective effect of melatonin (MLT) and α-tocopherol on mercury-induced genotoxicity in human blood cultures. The in vitro effects of inorganic mercury added to human lymphocytes on the cell-cycle proliferative index (CCPI)/proliferation replicative index (PRI) and sister chromatid exchange (SCE) using fluorescence plus Giemsa staining were examined. A significant increase occurred in SCE per metaphase (SCE/chromosome and SCE/cell) and inhibition of proliferative kinetics, which resulted in a decline of the replicative index, in comparison to the controls. Treated lymphocyte cultures also exhibited a reduction in %M1 and %M2 metaphase plates, but an increase in %M3 metaphase plates was noticed. Adding α-tocopherol and MLT individually and in combination indicated a mitigative effect by reducing the genotoxic potential of treated cultures. The percent amelioration for all the three parameters, namely, frequency of SCE, SCE/plate and SCE/chromosome as well as CCPI, was comparatively high with MLT and α-tocopherol in combination than MLT followed by α-tocopherol. The percent mitigation was better in combined antioxidant additions to toxicant-exposed cultures, compared to MLT, whereas the percent mitigation by α-tocopherol alone was less for average generation time and population doubling time, respectively.

Melatonin protection on mercury-exerted brain toxicity in the rat.

The effect of melatonin on the neurotoxicity induced by mercuric chloride was studied. Adult rats were fed orally with two different doses of mercuric chloride (2 mg; 4 mg/kg body weight) to evaluate brain toxicity with respect to cerebral hemisphere, cerebellum, and medulla oblongata regions for 60 days with or without supplementation with melatonin (5 mg/kg body weight) intraperitoneally. The results suggest that the graded doses of mercury elicit the depletion of enzymatic activities, such as adenosine triphosphatase, succinate dehydrogenase, phosphorylase, alkaline phosphatase, acid phosphatase, altered glycogen, total protein, and lipid peroxidation levels in the cerebral hemisphere, cerebellum, and medulla oblongata of the brain, thereby affecting their respective functions. Blood glucose and mercury levels increased, followed by a reduction in body and organ weights. All these effects seemed to be severe in the cerebral hemisphere of the brain. Further affected indices were, to some extent, maintained in the brain of animals cotreated with melatonin, showing its protective role against mercury-exerted neurotoxicity.