In vitro effect of manganese chloride exposure on energy metabolism and oxidative damage of mitochondria isolated from rat brain.

Manganese (Mn) is an essential trace element for human nutrition but also a toxicant when humans are exposed to high concentration. Occupational exposures to excess levels of Mn are known to cause manganism in humans. Mn is known to induce mitochondrial dysfunction in excessive dose, however the mechanisms underlying its action are not elucidated clearly. To determine the possible role of energy metabolism and oxidative stress in Mn-induced mitochondria injury, isolated mitochondria were exposed to different concentrations of MnCl(2) (5, 50, 500, 1000μmol/L), aconitase and mitochondrial complex I activities, MDA and GSH contents, MMP were investigated. In addition, effects of NAC (500μmol/L) were studied at 500μmol/L MnCl(2). Dose-dependent inhibition of aconitase and mitochondrial complex I activities, increase of MDA content, decrease of GSH content and MMP were observed. Further investigation indicated NAC pre-treatment significantly reversed toxic effect of MnCl(2). The results indicated that manganese could dose-dependently induce the decline of energy metabolism and cause oxidative damage of mitochondria isolated from rat brain, and this change could be prevented by pre-treating with NAC.