Kreiling R, Laib R J, Bolt H M
Institut für Arbeitsphysiologie, Universität Dortmund, F.R.G.
Toxicol Lett. 1988 Jun;41(3):209-14. doi: 10.1016/0378-4274(88)90056-2.
B6C3F1 mice, Sprague-Dawley and Wistar rats were exposed to 1,3-butadiene in a closed exposure system. Exposure concentrations were kept above 2000 ppm to ensure saturation of butadiene metabolism in both species (Vmax conditions). Hepatic non-protein sulfhydryl (NPSH) content was determined in butadiene-exposed animals (and air-exposed controls) after exposures for 0, 7 and 15 h. Depletion of hepatic NPSH content was different for the species and strains investigated. In mice, hepatic NPSH content declined to about 20% after 7 h and was further depleted to about 4% at 15 h when signs of acute toxicity were observed. After a 7 h exposure of rats to butadiene, hepatic NPSH content was depleted to about 65% (Wistar) or 80% (Sprague-Dawley) of the corresponding controls but remained practically stable after a 15 h exposure to butadiene. The time-courses of depletion by butadiene of hepatic NPSH support previous findings on differences in butadiene metabolism between rats and mice and offer an additional explanation for the considerable species differences observed in the toxicity and carcinogenicity of this compound.
将B6C3F1小鼠、斯普拉格-道利大鼠和Wistar大鼠置于密闭暴露系统中，使其暴露于1,3-丁二烯。暴露浓度保持在2000 ppm以上，以确保两种动物体内丁二烯代谢均达到饱和状态（Vmax条件）。在暴露0、7和15小时后，测定丁二烯暴露动物（以及空气暴露对照组）的肝脏非蛋白巯基（NPSH）含量。所研究的物种和品系肝脏NPSH含量的耗竭情况各不相同。在小鼠中，7小时后肝脏NPSH含量降至约20%，15小时时进一步降至约4%，此时观察到急性毒性迹象。大鼠暴露于丁二烯7小时后，肝脏NPSH含量降至相应对照组的约65%（Wistar大鼠）或80%（斯普拉格-道利大鼠），但在暴露于丁二烯15小时后基本保持稳定。丁二烯导致肝脏NPSH耗竭的时间进程支持了先前关于大鼠和小鼠丁二烯代谢差异的研究结果，并为该化合物在毒性和致癌性方面观察到的显著物种差异提供了额外解释。
