神经毒性杀虫药剂对家蝇头部环腺苷酸含量的影响

THE EFFECT OF NEUROTOXIC INSECTCIDES ON THE cAMP LEVEL IN HOUSEFLY BRAINS

本文报道用七类20种神经毒性杀虫药剂处理家蝇(Musca dcmestica vicina),发现引起环腺苷酸(cAMP)增加的药剂有:DDT、菊酯类和甲脒类,而BHC、狄氏剂、有机磷、氨基甲酸酯、沙蚕毒素均没有影响。并做了DDT、溴氰菊酯和杀虫脒中毒0—8小时内cAMP变化的时间曲线,以及DDT中毒0—8小时内腺苷酸环化酶(ACE)活性的时间曲线。结果表明:DDT中毒1小时引起cAMP达一峰值,2小时后回到原位;2—8小时内持续而缓慢的上升;乙酰胆碱酯酶活性曲线与此基本一致,但2—8小时内活性增加不大。溴氰菊酯中毒引起cAMP变化的时间曲线与DDT的基本一致,只是第二次cAMP上升更高二些。杀虫脒引起cAMP的时间变化曲线是0.5小时达一峰值,1小时基本回到原位,2—4小时有一个上升较快、较高的峰。我们认为,DDT引起cAMP值的第一次上升是激活了ACE造成的,第二次上升可能与钙调蛋白和磷酸二酯酶有关。杀虫脒引起cAMP值上升,是因为激活了章鱼胺激性的ACE。

Neurotoxic insecticides affect the level of cyclic adenosine 3', 5'-monophosphate (cAMP) in nervous tissues of insects. Three categories of insecticides among the seven we used stimulated the production of cAMP in the heads of housefly: DDT, pyrethroids (Deltamethrin, Sumicidin, Allethrin, Permethrin) and form-amidines (Chlordimeform, Dan-jia-mi, DCPM and a metabolite of Chlordimeform). But BHC, Dieldrin, organophosphorus compounds (Paiathion, Systox, Dimethoate, Trichlorfon), carba.mat.es (Carbaryl, Aldicarb) and ncreistoxin (Padan, Sha-chong shuang) had little effects. The time courses of the change in cAMP contents after treatments with DDT, Deltamethrin and Chlordimeform were studied. We also investignted the time course of adenylate cyclase (ACE) activity during DDT poisoning. The results showed: (1) DDT caused an rise and fall in cAMP content within 2 hours. The rise and fall ran parallel with the induction curve of ACE activity. In 2-8 hours, cAMP showed a second slower rise, but an obvious change of ACE activity was not observed. (2) Deltamethrin showed the same changs as DDT, except that the second rise of cAMP was even more prominent. (3) Chlordimeform also caused a rise and fall of cAMP ievel within 1 hr. In 2-4 hrs, a second and more prominent rise occurredThe biphasic change of cAMP content after treatment with DDT, and Deltamethrin was due to the induction of tyrosine decarboxylase, resulting in the formations of tyramine which consequently β-hydroxylated to octopamine; both of them activated ACE. The second rise seemed to have little relation with ACE and might be the results of inhibition of phosphodiesterase. The first rise of cAMP content after Chlordimeform treatment was caused by Chlordimeform itself, while the second rise was caused by its metabolite, desmethyl-Chlordimeform, which had greater effect. Chlordimeform and desmethyl-Chlordimeform are both agonists of the octopami-nergic ACE.