Effect of manganese chloride exposure on liver and brain mitochondria function in rats

Manganese (Mn) is an essential trace element found in many enzymes. As is the case for many essential trace elements, excessive Mn is toxic. Individuals suffering from manganese toxicity exhibit several symptoms, which are similar to those frequently observed in cases of Parkinson's disease. In this investigation, we studied the effect of manganese chloride (7.5, 15.0, and 30.0 mg/kg body weight) on mitochondrial function and attempted to ascertain the mechanism of manganese-induced mitochondrial dysfunction. The production of reactive oxygen species in mitochondria of rat liver and brain was assayed using 2',7'-dichlorofluorescin diacetate, and the activities of respiratory chain enzymes were examined spectrophotometrically. Monoamine oxidase (MAO) activity was assayed by measuring reduction of benzylamine. Manganese and calcium content in mitochondria were determined by atomic absorption spectrophotometry. These results indicate that manganese chloride (MnCl2) can decrease MAO activity and inhibit the respiratory chain. Manganese can accumulate in mitochondria and inhibit efflux of calcium. There is a significant inverse correlation between the amount of superoxide radicals and the specific activities of the mitochondria enzymes. Mitochondrial function was significantly affected in both males and females.