Seppäläinen A M, Savolainen H
Neurotoxicology. 1982 Jul;3(1):36-43.
Vinyltoluene is a less volatile homologue of styrene, a neurotoxic chemical. Sixty male Wistar rats were exposed to vinyltoluene vapor at 50, 100 or 300 ppm solvent concentrations 6 h daily, 5 days a week for up to 15 weeks. Twenty control rats were similarly sham exposed. Motor conduction velocity of the tail nerve decreased significantly after exposure for 12 weeks to 100 or 300 ppm and the amplitude of evoked motor action potential decreased also. This effect was reproducible in another series of 15 rats exposed to similar concentrations for 11 weeks. Acid proteinase activity in the cerebral homogenate increased at 8 weeks in 300-ppm rats and at 15 weeks in 100-ppm rats. Succinate dehydrogenase activity was below the control range in all exposed groups. Two small protein fractions appeared in the electrophoretograms of axons taken from exposed rats at the end of the experiment; these fractions occurred near the origin and between the two main fractions of the typical axon pattern. Electrophysiological changes typical of axonal degeneration and a change in the axonal proteins coincided in rats exposed to 100 or 300 ppm of vinyltoluene, while exposure to 50 ppm had no electrophysiological effects.
乙烯基甲苯是苯乙烯挥发性较低的同系物,苯乙烯是一种神经毒性化学物质。60只雄性Wistar大鼠每天暴露于溶剂浓度为50、100或300 ppm的乙烯基甲苯蒸气中6小时,每周5天,持续长达15周。20只对照大鼠同样进行假暴露。暴露12周后,100或300 ppm组大鼠的尾神经运动传导速度显著下降,诱发运动动作电位的幅度也下降。在另一组15只暴露于相似浓度11周的大鼠中,这种效应可重现。300 ppm组大鼠在8周时、100 ppm组大鼠在15周时,脑匀浆中的酸性蛋白酶活性增加。所有暴露组的琥珀酸脱氢酶活性均低于对照范围。实验结束时,从暴露大鼠提取的轴突电泳图中出现了两个小蛋白质组分;这些组分出现在原点附近以及典型轴突模式的两个主要组分之间。暴露于100或300 ppm乙烯基甲苯的大鼠出现了典型的轴突变性电生理变化以及轴突蛋白变化,而暴露于50 ppm则没有电生理效应。