Weitman S D, Vodicnik M J, Lech J J
Fundam Appl Toxicol. 1986 Jan;6(1):155-61. doi: 10.1016/0272-0590(86)90271-x.
The mechanism of enhanced parathion/paraoxon toxicity during pregnancy was examined. Enhanced toxicity following exposure to paraoxon in the pregnant mouse as determined by cholinesterase suppression was observed at 0.10 and 0.58 mg/kg after ip administration on Day 19 of gestation. However, there were no significant differences in cholinesterase activity between pregnant animals and virgin controls after either po or iv paraoxon. Higher systemic and lower hepatic levels of parathion were demonstrated in pregnant mice following ip administration of parathion (5 mg/kg). Data herein also suggest that during pregnancy, larger quantities of paraoxon bypass initial liver detoxification after ip dosing. The mechanism of increased toxicity of parathion/paraoxon during pregnancy may result from alterations in absorption from the peritoneal cavity.
研究了孕期对硫磷/对氧磷毒性增强的机制。在妊娠第19天腹腔注射后，通过胆碱酯酶抑制作用测定，妊娠小鼠接触对氧磷后在0.10和0.58mg/kg剂量下观察到毒性增强。然而，口服或静脉注射对氧磷后，妊娠动物与未孕对照动物的胆碱酯酶活性无显著差异。腹腔注射对硫磷（5mg/kg）后，妊娠小鼠体内对硫磷的全身水平较高而肝脏水平较低。本文数据还表明，孕期腹腔注射给药后，大量对氧磷绕过了肝脏的初始解毒过程。孕期对硫磷/对氧磷毒性增加的机制可能是腹腔吸收改变所致。
