Protective mechanisms of melatonin on caprine spleen injury induced by cadmium (Cd): an in vitro study

Abstract

Current study explores the potential mechanisms of melatonin on cadmium-induced spleen tissue injury of goat. Spleen tissues were incubated with different concentrations (50, 100, 200, 400 and 600 µM) of cadmium acetate (Cd), respectively and the lipid peroxidation of the tissue was measured. It was found that Cd at the level of 400 µM induced maximum spleen damage among other concentrations. Thus, Cd 400 µM was selected to examine whether melatonin treatment can protect against this damage. The results showed that Cd increased the oxidative stress in the spleen tissue either by elevating pro-oxidant enzymes, or, by suppressing the variety of antioxidant enzymes and thus, to increase the intracellular reactive oxygen species (ROS). Melatonin treatment at the concentrations of 0.25, 0.5 and 1 mM significantly reduced all these alterations, respectively. At the level of cellular organelles, Cd caused mitochondrial morphological and functional injuries. These include mitochondrial surface distortion and inhibitions of glycolytic, Krebs cycle, and respiratory chain enzymes. Melatonin at a concentration of 0.5 mM almost completely preserved Cd induced mitochondrial pathological alterations. Cd pollution is a cause of serious health hazard world wide, particularly in the developing areas and currently, there is no specific remedy for Cd toxicities. The results suggest that melatonin is a promising therapeutic agent to combat Cd-induced oxidative stress and it deserves further investigation clinically.