Nickel is a potential neurotoxic
pollutant. Oxidative stress is supposed to be involved in the mechanism underlying
nickel-induced neurotoxicity.
Melatonin has efficient protective effects against various oxidative damages in nervous system. The purpose of this study was to investigate whether
melatonin could efficiently protect against neurotoxicity induced by
nickel. Here, we exposed primary cultured cortical neurons and mouse
neuroblastoma cell lines (neuro2a) to different concentrations of
nickel chloride (NiCl(2)) (0.125, 0.25, 0.5, and 1 mm) for 12 hr or 0.5 mm NiCl(2) for various periods (0, 3, 6, 12, and 24 hr). We found that
nickel significantly increased
reactive oxygen species production and caused the loss of cell viability both in cortical neurons and neuro2a cells. In addition,
nickel exposure obviously inhibited the mitochondrial function, disrupted the mitochondrial membrane potential (DeltaPsim), reduced
ATP production, and decreased
mitochondrial DNA (
mtDNA) content. However, each of these oxidative damages was efficiently attenuated by
melatonin pretreatment. These protective effects of
melatonin may be attributable to its roles in reducing oxidative stress and improving mitochondrial function in
nickel-treated nerve cells. Our results suggested that
melatonin may have great pharmacological potential in protecting against the adverse effects of
nickel in the nervous system.