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目的探讨阿维菌素对大鼠毒性作用特点和神经毒性作用机制。方法成年Wistar大鼠72只,雌雄各半,随机分为3组。经口灌胃给予阿维菌素原药,剂量分别为5,2.5 mg/kg和阴性对照组(溶剂对照);隔日染毒共3次,在染毒后7,14和21 d测定动物体重、小脑的脏器系数,小脑中乳酸脱氢酶(LDH)、谷氨酰胺合成酶(GS)、肌酸激酶(CK)以及钙调神经磷酸酶(CaN)活力。结果阿维菌素染毒后对大鼠体重增长和小脑脏器系数无影响,但可引起运动失调;染毒后21 d时,5.0 mg/kg组大脑皮层中LDH、GS、CK以及CaN活力分别为(1.508±0.084),(299.849±33.563)U/(g.prot),(7.635±0.377)U/ml,(0.699±0.043)μmolpi/(mg.pro),与对照组比较LDH活力无明显改变,GD、CK活力明显增加,CaN活力明显下降(P<0.05)。结论阿维菌素可以造成小脑内神经代谢酶活力改变而引起运动失调。
Objective To investigate the toxic effects of avermectin on rats and the mechanism of neurotoxicity. 72 adult Wistar rats, male and female, were randomly divided into three groups. The avermectin was given orally by gavage at doses of 5 and 2.5 mg / kg and negative control (solvent control) respectively. The rats were exposed to a total of 3 doses on the following day. The body weight of animals was measured at 7, 14 and 21 d , Organ coefficient of the cerebellum, lactate dehydrogenase (LDH), glutamine synthetase (GS), creatine kinase (CK) and calcineurin (CaN) activity in the cerebellum. Results Abamectin had no effect on body weight gain and cerebellar organ coefficient after exercise, but it could cause dyskinesia. At 21 d after exposure, the activities of LDH, GS, CK and CaN in the cerebral cortex of 5.0 mg / kg group (1.508 ± 0.084), (299.849 ± 33.563) U / (g.prot), (7.635 ± 0.377) U / ml and (0.699 ± 0.043) μmolpi / (mg.pro), respectively. Compared with the control group, Significantly changed, GD, CK activity increased significantly, CaN activity decreased significantly (P <0.05). Conclusion Abamectin can cause dyskinesia caused by the change of activity of nerve metabolic enzymes in the cerebellum.