Wells M S, Nerland D E
Department of Pharmacology and Toxicology, School of Medicine, University of Louisville, KY 40292.
Toxicol Lett. 1991 Apr;56(1-2):159-66. doi: 10.1016/0378-4274(91)90102-c.
Benzene is metabolized to one or more hematotoxic species. Saturation of benzene metabolism could limit the production of toxic species. Saturation of phase II enzymes involved in the conjugation of the phenolic metabolites of benzene also could affect the hematotoxicity of benzene. To investigate the latter possibility, we exposed male Swiss mice, via the inhalation route, to various concentrations of benzene for 6 h per day for 5 days. Following termination of the final exposure the mice were killed and the levels of phenylsulfate and phenylglucuronide in the blood determined. Spleen weights were recorded and the number of white blood cells counted. At low benzene exposure concentrations phenylsulfate is the major conjugated form of phenol in the blood. At high exposure concentrations, phenylglucuronide is the predominant species. The reductions in spleen weight and white blood cell numbers correlated with the concentration of phenylsulfate in the blood, but are most probably not causally related.
苯会代谢为一种或多种血液毒性物质。苯代谢的饱和可能会限制毒性物质的产生。参与苯酚类代谢物结合的Ⅱ相酶的饱和也可能影响苯的血液毒性。为了研究后一种可能性，我们通过吸入途径让雄性瑞士小鼠每天暴露于不同浓度的苯中，每天暴露6小时，持续5天。在最后一次暴露结束后，处死小鼠并测定血液中硫酸苯酯和苯葡糖醛酸的水平。记录脾脏重量并计数白细胞数量。在低苯暴露浓度下，硫酸苯酯是血液中酚的主要结合形式。在高暴露浓度下，苯葡糖醛酸是主要的物质。脾脏重量和白细胞数量的减少与血液中硫酸苯酯的浓度相关，但很可能没有因果关系。
