Aldridge W N, Dinsdale D, Nemery B, Verschoyle R D
Fundam Appl Toxicol. 1985 Dec;5(6 Pt 2):S47-60. doi: 10.1016/0272-0590(85)90114-9.
The pharmacokinetics (disposal curves) of trimethyl and triethyl phosphorothioates have been determined. The concentrations to which the lung has been exposed at the LD50 dose of different chemical structures have been compared with the dose administered to the animal; the variation of LD50 of different chemical structures is little reduced. The in vitro kinetics of the reaction of O,S,S-trimethyl phosphorodithioate or O,O,S-triethyl phosphorothioate with plasma cholinesterase and carboxylesterase and brain acetylcholinesterase have been determined. The relation between inhibition and circulating concentrations in vivo have been examined. Changes in Clara cells reported by others seem to be physiological rather than pathological. O,S,S-Trimethyl phosphorodithioate is metabolised by rat lung and liver slices and microsomes. From these studies and the effect of various pretreatments of the rats on toxicity to the lung, it is probable that the proximal toxin is produced in the lung by oxidative attack on the alkylthio moeity of the compounds.
已测定了三甲基硫代磷酸酯和三乙基硫代磷酸酯的药代动力学（消除曲线）。将不同化学结构的半数致死剂量下肺所接触的浓度与给予动物的剂量进行了比较；不同化学结构的半数致死量变化减小幅度不大。已测定了O,S,S-三甲基二硫代磷酸酯或O,O,S-三乙基硫代磷酸酯与血浆胆碱酯酶、羧酸酯酶以及脑乙酰胆碱酯酶反应的体外动力学。已研究了体内抑制作用与循环浓度之间的关系。其他人报道的克拉拉细胞变化似乎是生理性的而非病理性的。O,S,S-三甲基二硫代磷酸酯可被大鼠肺和肝切片及微粒体代谢。从这些研究以及大鼠的各种预处理对肺毒性的影响来看，很可能近端毒素是由化合物的烷硫基部分在肺中受到氧化攻击而产生的。
