Cheung S C, Nerland D E, Sonnenfeld G
Department of Microbiology and Immunology, School of Medicine, University of Louisville, Ky.
Oncology. 1989;46(5):335-8. doi: 10.1159/000226743.
Murine L-929 cells were treated with benzene or a series of benzene metabolites, washed and then interferon-alpha/beta was induced with polyriboinosinic-polyribocytidylic acid. Exposure of the cells to benzene or phenol, a monocyclic metabolite of benzene, did not affect interferon-alpha/beta induction. However, exposure of the cells to p-benzoquinone, hydroquinone or catechol, dihydroxy- and diketo-metabolites of benzene, resulted in a severe inhibition of interferon-alpha/beta production. There was no significant loss of viability of the cell cultures. Additional studies with p-benzoquinone indicated that inhibition of interferon-alpha/beta was reversible and could be abrogated by addition of reduced glutathione to the cell cultures.
将小鼠L-929细胞用苯或一系列苯代谢物处理，洗涤后用聚肌苷酸-聚胞苷酸诱导α/β干扰素。将细胞暴露于苯或苯的单环代谢物苯酚中，不影响α/β干扰素的诱导。然而，将细胞暴露于对苯醌、氢醌或儿茶酚（苯的二羟基和二酮代谢物）中，会导致α/β干扰素产生受到严重抑制。细胞培养物的活力没有明显损失。对苯醌的进一步研究表明，α/β干扰素的抑制是可逆的，并且可以通过向细胞培养物中添加还原型谷胱甘肽来消除。
