Bolcsak L E, Nerland D E
Toxicol Appl Pharmacol. 1983 Jul;69(3):363-8. doi: 10.1016/0041-008x(83)90259-4.
Mice were injected sc with benzene or one of its metabolites, phenol, catechol, or hydroquinone. The ability of these compound to inhibit erythropoiesis was quantified by measuring the incorporation of 59Fe into developing erythrocytes. Benzene decreased 59Fe incorporation into developing erythrocytes in a dose-dependent manner. Maximum inhibition was observed when benzene was administered 48 hr prior to initiation of the 59Fe uptake test. The three metabolites of benzene also significantly inhibited 59Fe incorporation when they were administered 48 hr prior to initiation of 59Fe uptake assay. The degree of inhibition observed with the metabolites was not as great as that observed with benzene. Coadministration of the microsomal mixed-function oxidase inhibitor, 3-amino-1,2,4-triazole, abolished the erythropoietic toxicity of benzene and phenol but had no effect on the catechol- or hydroquinone-induced toxicity.
给小鼠皮下注射苯或其代谢产物之一苯酚、儿茶酚或对苯二酚。通过测量59Fe掺入发育中的红细胞来定量这些化合物抑制红细胞生成的能力。苯以剂量依赖的方式降低了59Fe掺入发育中的红细胞。在开始59Fe摄取试验前48小时给予苯时观察到最大抑制作用。当在开始59Fe摄取试验前48小时给予苯的三种代谢产物时,它们也显著抑制了59Fe的掺入。观察到的代谢产物的抑制程度不如苯观察到的程度大。微粒体混合功能氧化酶抑制剂3-氨基-1,2,4-三唑的共同给药消除了苯和苯酚的红细胞生成毒性,但对儿茶酚或对苯二酚诱导的毒性没有影响。