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目的研究阿维菌素对大鼠神经系统的神经毒性作用以及对大鼠大脑皮层中神经代谢酶的影响,探讨阿维菌素的神经毒性作用机制。方法将健康清洁级成年Wistar大鼠72只按体重随机分为高(5 mg/kg)、低剂量(2.5 mg/kg)阿维菌素染毒组和溶剂对照组(生理盐水),每组24只,雌雄各半。采用经口灌胃方式染毒,隔日灌胃1次,共染毒3次,灌胃剂量为20 ml/kg。在染毒结束后第7、14和21天,称量各组大鼠体重和大脑重量,并计算大脑系数。按照试剂盒使用说明书测定大脑皮层中乳酸脱氢酶(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。结果高剂量阿维菌素染毒组大鼠染毒后出现明显兴奋症状,表现为烦躁,多动,互相厮打,至染毒后第7天时,兴奋症状基本消失,而表现出一定的抑制症状,如闭目静卧,四肢无力,站立不稳等。低剂量阿维菌素染毒组的症状表现不明显。各阿维菌素染毒组体重、大脑重量及其间大脑系数比较,差异均无统计学意义(P>0.05)。与溶剂对照组比较,各阿维菌素染毒组大脑皮层中乳酸脱氢酶(LDH)、谷氨酰胺合成酶(GS)和肌酸激酶(CK)活力较高,钙调神经磷酸酶(CaN)活力较低,差异多有统计学意义(P<0.05或P<0.01)。不同性别大鼠各检测指标间比较,差异均无统计学意义(P>0.05)。结论阿维菌素可通过改变神经代谢酶活力而对大鼠神经系统产生毒性作用。
Aim To investigate the neurotoxic effect of abamectin on the nervous system of rats and its effect on the neuro-metabolic enzymes in the cerebral cortex of rats and to explore the neurotoxic mechanism of abamectin. Methods Healthy clean adult Wistar rats were randomly divided into 72 higher (5 mg / kg), low dose (2.5 mg / kg) avermectin exposed and solvent control group (saline), each 24, male and female half. Using oral gavage exposure, gavage once every other day, a total of three poisoning, intragastric dose of 20 ml / kg. On the 7th, 14th and 21st days after the end of the treatment, the body weight and brain weight of each group were weighed, and the cerebral coefficient was calculated. Determination of the cerebral cortex of lactate dehydrogenase (LDH) according to the kit instructions for use, glutamine synthetase (GS), creatine kinase (CK) and the phosphatase calcineurin (of CaN) activity. Results The rats in high dose avermectin group showed obvious excitement symptoms after being exposed to the drugs. The symptoms were irritability, hyperactivity and mutual fighting, and the symptoms of excitement disappeared on the 7th day after exposure , Such as blindfolded lying, limb weakness, standing instability and so on. Low-dose avermectin group showed no obvious symptoms. There was no significant difference in body weight, brain weight and cerebral coefficient among the avermectin-treated groups (P> 0.05). Compared with the solvent control group, the activities of lactate dehydrogenase (LDH), glutamine synthase (GS) and creatine kinase (CK) in cerebral cortex of each avermectin-treated group were higher than those of the control group. Calcineurin CaN) activity was lower, the difference was statistically significant (P <0.05 or P <0.01). There was no significant difference between the detection indexes of different sex rats (P> 0.05). Conclusion Abamectin can produce toxic effects on the nervous system in rats by changing the activity of neurotransmitter enzymes.