Abou-Donia M B, Graham D G, Abdo K M, Komeil A A
Toxicology. 1979 Nov;14(3):229-43. doi: 10.1016/0300-483x(79)90005-2.
Subchdronic administration of S,S,S-tributyl phosphorotrithioate (DEF) caused 3 toxicologic effects in hens, depending upon route of administration. Small delay oral doses (0.5--20 mg/kg) of DEF produced ataxia, which progressed to paralysis and death in some birds. Large daily oral doses (40 and 80 mg/kg) caused a 'late acute' effect 4 days after administration. The clinical signs of the late acute effect were identical to those produced by n-butyl mercaptan (nBM), a hydrolytic product of DEF, and were not relieved by atropine sulfate. The late acute effect of DEF overlapped with the clinical signs of delayed neurotoxicity. These hens died early, and while one hen showed histopathological lesions in peripheral nerves, another showed unequivocal lesions in the central nervous system. Topical application of daily doses of DEF consistently produced delayed neurotoxicity in the absence of late acute poisonining and was characterized by degeneration of the central and peripheral nerve tissues. Orally administered DEF was rapidly metabolized in the gastrointestinal tract to nBM, which apparently caused the late acute toxic effect. Topically administered DEF, which was not subjected to gastrointestinal tract hydrolysis, caused delayed neurotoxicity but did not produce a late acute effect.
根据给药途径的不同,亚慢性给予三硫代磷酸 S,S,S-三丁酯(DEF)会在母鸡身上产生三种毒理学效应。小剂量延迟口服 DEF(0.5--20 毫克/千克)会导致共济失调,在某些鸟类中会发展为麻痹和死亡。大剂量每日口服(40 和 80 毫克/千克)会在给药后 4 天产生“迟发性急性”效应。迟发性急性效应的临床症状与 DEF 的水解产物正丁硫醇(nBM)产生的症状相同,且不能被硫酸阿托品缓解。DEF 的迟发性急性效应与迟发性神经毒性的临床症状重叠。这些母鸡早期死亡,一只母鸡在外周神经出现组织病理学损伤,另一只在中枢神经系统出现明确损伤。每日局部应用 DEF 在没有迟发性急性中毒的情况下持续产生迟发性神经毒性,其特征是中枢和外周神经组织变性。口服的 DEF 在胃肠道中迅速代谢为 nBM,这显然导致了迟发性急性毒性效应。局部给药的 DEF 未经过胃肠道水解,会导致迟发性神经毒性,但不会产生迟发性急性效应。