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作 者:郁东[1] 徐旭东[1] 周永田[1] 谢林[1] 杜景云[2] 刘正亮[1] 闫伟[3] 徐明怡[1]
机构地区:[1]山东省职业卫生与职业病防治研究院,山东济南250002 [2]山东省医学科学院,山东济南250002 [3]山东中医药大学,山东济南250002
出 处:《环境与健康杂志》2006年第5期409-412,共4页Journal of Environment and Health
摘 要:目的观察HgCl2对SD大鼠胫神经的影响。方法SD大鼠70只,雌雄各半,随机分为4组:急性毒理学实验组(40只)、高、低剂量连续染毒组、对照组(各10只雌雄各半)。急性毒理学实验组分4个剂量组,分别一次染毒HgCl221.5、46.4、100.0、215mg/kg,按霍恩法求出HgCl2经口灌胃LD50。高、低剂量连续染毒组按17mg/kg(1/4LD50)和8.5mg/kg(1/8LD50)分别经口灌胃HgCl2溶液,每天1次,对照组每天1次经口灌胃2ml生理盐水,连续灌胃(20±4)d,建立亚急性汞中毒动物模型后,高、低剂量各组和对照组均处死雄鼠,留雌鼠作药物干预实验。用二巯基丙磺酸钠(DMPS)按28mg/kg腹腔注射驱汞2个疗程。造模后和驱汞后,分别用透射电镜观察大鼠胫神经超微结构。同时测定尿汞和尿微量白蛋白。结果SD大鼠经口灌胃LD50为68.1mg/kg。高剂量染汞组中有7只出现汞中毒,其中2只大鼠(雌雄各1只)出现疼痛表现。低剂量组中有6只出现汞中毒,无疼痛大鼠。高、低剂量组大鼠于驱汞前后尿汞、尿微量白蛋白含量均高于对照组(P<0.05,P<0.01)。汞中毒大鼠胫神经出现脱髓鞘及轴索的改变,DMPS驱汞2个疗程未能阻止神经病变进展。结论亚急性HgCl2中毒可以导致SD大鼠胫神经变性。Objective To study the adverse effect of mercury on the tibial nerves of rats. Methods Seventy SD rats (35 females, 35 males, weighed 160-200 g) were randomly divided into 4 groups. 40 rats in group 1 were used to test the acute toxicity of HgCl2, 10 rats in group 2 were given HgC12 by garage at 17 mg/kg(1/4 LD50) daily, in group 3 the dose was 8.5 mg/kg(1/8 LD50), 10 rats in group 4 were treated with 0.9% saline 2 ml by gavage daily, the experimental duration was (20±4) days. When the model had been developed, all the male rats were killed and the female rats in group 2 and 3 were given the chelator (DMPS) by intraperitoneal injection at 28 mg/kg for 2 periods of treatment, then were killed and the tibial nerves were examined with the electronic microscope. Resdts The oral LD50 of HgCl2 was 68.1 mg/kg. Seven rats in group 2 (7/10) were poisoned and two of them got pain manifestation. Six rats in group 3(6/10) were poisoned. Myelinoclasis and the changed axons were found in the tibial nerves of poisoned rats and it was more serious in the rats with pain. The chelator(DMPS) did not relieve the change. Conclusion Sub-acute poisoning of HgCl2 can induce degeneration of tibial nerves in SD rats.
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