有机磷酸酯诱导迟发性神经毒性及其对神经毒性酯酶（NTE）活性影响的动态研究

STUDIES ON THE DELAYED NEUROPATHY INDUCED BY ORGANOPHOSPHATE AND ITS INFLUENCE ON THE ACTIVITY OF NEUROPATHY TRAGET ENZYME(NTE)

以成年产卵来航母鸡为试验动物，研究了三甲基苯基磷酸酯（Ｔｒｉ－ｏ－ＣｒｅｓｙｌＰｈｏｓ－ｐｈａｔｅ，ＴＯＣＰ）诱导的迟发性神经毒性．试验发现，母鸡口服ＴＯＣＰ（７５０ｍｇ／ｋｇ）后，经过大约８－１０ｄ的潜伏期开始出现中毒症状，其表现为以步态失调为主要特征的运动障碍呈进行性加重，至第２１ｄ开始便发展为瘫痪，对鸡脑神经病损靶标酯酶（ＮｅｕｒｏｐａｔｈｙＴａｒｇｅｔＥｎｚｙｍｅ，ＮＴＥ）活性的测定表明，有机械诱导的迟发性神经毒性（Ｏｒｇａｎｏｐｈｏｓｐｈａｔｅ－ＩｎｄｕｃｅｄＤｅｌａｙｅｄＰｏｌｙｎｅｕｒｏｐａｔｈｙ，ＯＰＩＤＰ）与ＮＴＥ活性抑制之间的关系不平行，其毒性症状的轻重与ＮＴＥ活性被抑制的强弱也不呈正相关，很可能，在给药后２４ｈ，体内ＯＰＩＤＰ已被触发，此外，实验观察到给予ＴＯＣＰ后被试鸡的体重明显下降。

A study on delayed neuropathy induced by tri-o-cresyl phosphate(TOCP)in adult lay-ing white Leghorn hens has been carried out.. The results showed that the clinical symptomcan not be seen until 8-10 days after the treatment of a single oral 750 mg/kg dose ofTOCP, and its main feature is ataxia in progress,Almost dosed hens became paralysis at 3weeks after dosing. The activity of neuropathy target enzyme(NTE)of dosed hen brainwas inhibited and the maximum inhibition at 3 days(the inhibition rate is 91;15%,P<0.01),and then NTE activity was somewhat recovered,but the inhibition rate is 74.87%(P<0.01)at 1 week and 8.22%at 4 weeks,respectively. Therefore,the relationship be-tween the inhibition of NTE and organophosphate-induced delayed polyneuropathy(OPIDP)is not positive. It is possible that OPIDP had been triggered in the hen at 24 hoursafter treatment with TOCP,In addition,the decrease of body weight of the hens had alsobeen observed in the experiment.