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[Effects on learning and memory and mitochondrial energy metabolism in hippocampus of mice by subacute exposure to n-hexane].

Objective: To study the effects on learning and memory, mitochondrial energy metabolism and ATPase activity of hippocampus in mice with subacute exposure to n-hexane. Methods: The SPF 40 Kunming mice were randomly divided into low, middle and high dose groups and control groups according to different dosages. Each group consisted of 10 mice. The mice were given n-hexane by gavage, the mice in the low, middle and high dose groups were given 0.2 ml/d of n-hexane at concentrations of 500, 1000 and 2000 mg/kg respectively, while the mice in the control group were given 0.2 ml/d of cooking oil once a day for 28 days. The y-type maze test, the activity of ATP Enzyme, mitochondrial respiratory chain enzyme complex Ⅰ-IV, the mrna of mitochondrial fusion gene (MFn1, Mfn2) and fission gene (FIs1) in brain tissues were performed. Results: Except for the wrong reaction times of low-dose exposure group in the first test, there existed significantly different in the first and second Y-maze tests in exposure groups and control group (P<0.05) ; in low, middle and high-dose group, the Na(+)-K(+)-ATPase activities were (8.27±2.65) , (5.38±1.55) , (3.55±1.69) μmol/gprot/h, and Ca(2+)-Mg(2+)-ATPase activities were (10.32±2.96) , (7.19±1.94) and (4.49±1.33) μmol/gprot/h, respectively. Compared with those in control group, the activities of Na(+)-K(+)-ATPase and Ca(2+)-Mg(2+)-ATPase decreased significantly in middle-dose group and high-dose group (P<0.05) . Compared with those in control group, the activities of mitochondrial respiratory chain enzyme complex I-IV in each dose group were significantly decreased (P<0.05) . The expressions of Mfn1mRNA and Mfn2mRNA in each dose group was significantly lower than those in control group (P<0.05) . Conclusion: Subacute exposure to n-hexane can result in the decrease of activities of mitochondrial respiratory chain enzyme complex in hippocampus of mice, which may lead to the disorder of mitochondrial energy metabolism by the decrease of ATPase activity and the imbalance of mitochondrial fusion-division, which must be one of the mechanisms of impairment of learning and memory of mice induced by n-hexane.