Coppock R W, Mostrom M S, Khan A A, Stair E L
Environmental Toxicology Research, Alberta Environmental Centre, Vegreville, Canada.
Vet Hum Toxicol. 1995 Dec;37(6):576-9.
Nonpesticide phosphate esters induce delayed neurotoxicity in cattle. The most common exposures are to complex mixtures of triaryl phosphate used in lubricating oils. Oral ingestion is most common, but dermal exposures have also occurred. Clinical signs of cholinesterase (ChE) inhibition may or may not be seen. Depending on the biochemical targets, the percent reduction in blood ChE is variable and can be < 30% of normal activity. Organophosphate ester-induced delayed neurotoxicity cannot be predicted by inhibition of blood ChEs. Signs of delayed neurotoxicity occur 2 to 25 d after exposure; these signs are neurologic deficiencies of the antigravity muscles and the muscles of the urinary bladder and larynx. Affected cattle may dribble urine and some may be mute. Signs of ChE inhibition generally are not observed in animals with neurological deficiencies. Pathologic findigs are axonopathy and myelin degeneration of nerves with long axons located in both the peripheral and central nervous systems. In the spinal cord, location of the affected nerve tracts is variable. Degenerative changes occur in motor neurons. Calves are less susceptible to organophosphate ester-induced delayed neurotoxicity than cows. A dose of 500 mg triaryl phosphate/kg body weight will produce complete paralysis in a mature cow in 26 d.
非农药类磷酸酯可引起牛的迟发性神经毒性。最常见的接触途径是接触润滑油中使用的三芳基磷酸酯的复杂混合物。经口摄入最为常见，但也有经皮肤接触的情况。可能会出现或不出现胆碱酯酶（ChE）抑制的临床症状。根据生化靶点的不同，血液中ChE降低的百分比各不相同，可能低于正常活性的30%。有机磷酸酯诱导的迟发性神经毒性不能通过血液ChE的抑制来预测。迟发性神经毒性的症状在接触后2至25天出现；这些症状是抗重力肌肉以及膀胱和喉部肌肉的神经功能缺陷。受影响的牛可能会滴尿，有些可能会失声。在有神经功能缺陷的动物中一般观察不到ChE抑制的症状。病理发现为位于外周和中枢神经系统的长轴突神经的轴突病和髓鞘变性。在脊髓中，受影响神经束的位置各不相同。运动神经元会发生退行性变化。犊牛比母牛对有机磷酸酯诱导的迟发性神经毒性更不敏感。500毫克三芳基磷酸酯/千克体重的剂量会在26天内使成年母牛完全瘫痪。
