Zitting A, Savolainen H
Arch Toxicol. 1980 Dec;46(3-4):295-304. doi: 10.1007/BF00310447.
Male Wistar rats were exposed to thermo-oxidative degradation products of heated poly(acrylonitrile-butadiene-styrene) (ABS). The exposures were conducted once, three times or ten times (5 nights/week, 6 h/night) in the nighttime. The degradation products included styrene, various nitriles, aldehydes, acids, and a significant aerosol fraction. The oxygen concentration in the exposure chamber was constantly above 20%. The shortest exposures caused a significant reduction of the 0-deethylation activity in lung and kidney but not in liver, as well as a decrease in tissue reduced glutathione concentration in liver and kidney but not in lung. These effects well-nigh disappeared during the two-week exposure. In these rats the cerebral glutathione was below the control range. Superoxide dismutase activity increased in liver and brain during the three-day exposure. In liver the activity reached the control value after the two-week exposure but the cerebral activity was significantly lower than in controls. The complex mixture of noxious compounds in the ABS fumes does not readily allow identification of causative agents. Nitrile-dependent histotoxic, peroxidative and reactive metabolite mediated mechanisms may be involved.
将雄性Wistar大鼠暴露于加热的聚（丙烯腈 - 丁二烯 - 苯乙烯）（ABS）的热氧化降解产物中。暴露在夜间进行一次、三次或十次（每周5晚，每晚6小时）。降解产物包括苯乙烯、各种腈类、醛类、酸类以及大量气溶胶成分。暴露室内的氧气浓度持续高于20%。最短时间的暴露导致肺和肾中0 - 脱乙基化活性显著降低，但肝脏中未出现这种情况，同时肝脏和肾中组织还原型谷胱甘肽浓度降低，但肺中未降低。在两周的暴露期间，这些影响几乎消失。在这些大鼠中，大脑中的谷胱甘肽低于对照范围。在三天的暴露期间，肝脏和大脑中的超氧化物歧化酶活性增加。在肝脏中，两周暴露后活性达到对照值，但大脑中的活性显著低于对照组。ABS烟雾中有害化合物的复杂混合物不容易确定致病因素。可能涉及腈依赖性组织毒性、过氧化和反应性代谢物介导的机制。
