Abstract: ObjectiveTo explore vie effect of MnCl₂ exposure on energy metabolism and oxidative damage of mitochondria in rat brain and vie preventive effect of NAC.Methods24 Wistar rats were randomly divided into control group (NaCI),MnCl₂ group,NAC pretreatment group by body weight.The rats were given injection for 21d.The animals in all groups were decapitated and vie samples of striatum and cortex were collected.Mitochondria were prepared using differential centrifugation.The activities of aconitase,mitochondrial complex I,vie level of MDA,GSH and mitochondrion membrane potential were investigated.ResultsCompared with vie control group,vie activities of aconitase(18.64nmol/min·mg pro), mitochondrial complex I〔48.92 nmol/(min·mgpro)〕in MnCl₂ group were significantly decreased.The level of MDA〔37.98 (nmol/g·pro)〕in MnCl₂ group was significantly increased.The level of GSH〔3.99 mol/(g·pro)〕in MnCl₂ group was significantly decreased.The mitochondrion membrane potential(Light density was 25.54)in MnCl₂ group was significantly decreased(P<0.05).Compared with MnCl₂ group,vie activities of aconitase〔22.95 nmol/(min·mgpro)〕,mitochondrial complex I〔66.89 nmol/(min·mgo pro)〕in NAC pretreated group were significantly increased.The level of MDA〔31.44 nmol/(g·pro)〕in NAC pretreated group was significantly decreased.The level of GSH〔5.56μmol/(g·pro)〕in NAC pretreated group was significantly increased.The mitochondrion membrane potential(Light density was 37.71)in NAC pretreated group was significantly increased(P<0.05).ConclusionManganese could induce vie decline of energy metabolism and cause oxidative damage of mitochondria in rat brain.And vie change could be prevented by pre-treating with NAC.