Cheung S C, Nerland D E, Sonnenfeld G
Department of Microbiology and Immunology, School of Medicine, University of Louisville, KY 40292.
J Natl Cancer Inst. 1988 Sep 7;80(13):1069-72. doi: 10.1093/jnci/80.13.1069.
We exposed spleen cells from female Swiss/Webster mice to benzene and benzene metabolites to determine the effects of such exposure on interferon gamma induction by concanavalin A. Exposing the cells to benzene or phenol did not affect interferon gamma production, but exposing them to p-benzoquinone, catechol, or hydroquinone significantly inhibited interferon gamma production. Cell viability, as determined by trypan blue viability staining, was not influenced by the chemical treatment. When interferon gamma production was inhibited, the inhibition was dose dependent. The time of optimum production of interferon gamma after exposure to concanavalin A was not affected by treatment of the cells with p-benzoquinone. These data indicate the importance of dihydroxy and diketo metabolites as immunotoxic derivatives of benzene.
我们将雌性瑞士/韦伯斯特小鼠的脾细胞暴露于苯和苯代谢物中，以确定这种暴露对伴刀豆球蛋白A诱导γ干扰素的影响。将细胞暴露于苯或苯酚中不会影响γ干扰素的产生，但将它们暴露于对苯醌、邻苯二酚或氢醌中会显著抑制γ干扰素的产生。通过台盼蓝活力染色测定的细胞活力不受化学处理的影响。当γ干扰素的产生受到抑制时，这种抑制是剂量依赖性的。暴露于伴刀豆球蛋白A后γ干扰素的最佳产生时间不受对苯醌处理细胞的影响。这些数据表明二羟基和二酮代谢物作为苯的免疫毒性衍生物的重要性。
