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.
目的： 研究正己烷亚急性染毒对小鼠学习记忆及海马组织线粒体能量代谢的影响。 方法： 选择昆明种SPF级小鼠40只，采用简单随即分组方法根据不同染毒剂量分为低、中、高剂量染毒组和对照组，每组10只，采用灌胃方式进行正己烷染毒，低、中、高剂量染毒组每只小鼠分别给予浓度500、1 000、2 000 mg/kg正己烷0.2 ml/d灌胃；对照组给予食用油0.2 ml/d灌胃，1次/d，连续28 d。染毒结束后，各组进行Y型迷宫实验，以及海马组织ATP酶、线粒体呼吸链酶复合体Ⅰ~Ⅳ活力、线粒体融合基因（Mfn1、Mfn2）与分裂基因（Fis1）mRNA的测定，并进行统计学分析。 结果： 与对照组比较，除第1次实验低剂量染毒组错误反应次数外，低、中、高剂量染毒组第1、2次Y型迷宫实验结果均有差异，差异有统计学意义（P<0.05）。低、中、高剂量染毒组Na(+)-K(+)-ATP酶活力分别为（8.27±2.65）、（5.38±1.55）、（3.55±1.69）μmol/gprot/h，Ca(2+)-Mg(2+)-ATP酶活力分别为（10.32±2.96）、（7.19±1.94）、（4.49±1.33）μmol/g prot/h。与对照组比较，中、高剂量染毒组海马组织Na(+)-K(+)-ATP酶、Ca(2+)-Mg(2+)-ATP酶活力均明显降低，差异有统计学意义（P<0.05）。与对照组比较，各剂量染毒组的复合体Ⅰ、Ⅱ、Ⅲ、Ⅳ酶活力均降低，Mfn1 mRNA、Mfn2 mRNA表达均明显降低，差异有统计学意义（P<0.05）。 结论： 正己烷亚急性染毒可导致小鼠海马组织线粒体呼吸链酶复合体活力的降低，并进而可能通过ATP酶活力下降及线粒体融合-分裂失衡而导致线粒体的能量代谢紊乱，可能导致小鼠学习记忆能力下降。.
Keywords: Adenosine triphosphatase; Administration of toxicant; Hexane; Hippocampus; Learning; Memory; Mice; Mitochondrion.