Hydroquinone, a Reactive Metabolite of Benzene, Inhibits NF-kappaB in Primary Human CD4+ T Lymphocytes

Authors: Pyatt, D.W.; Stillman, W.S.; Irons, R.D.

Source: Toxicology and Applied Pharmacology, Volume 149, Number 2, April 1998 , pp. 178-184(7)

Publisher: Academic Press

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Abstract:

Hydroquinone (HQ), a reactive metabolite of benzene, is present in cigarette smoke and is known to inhibit mitogen-stimulated activation of both T and B lymphocytes. Despite extensive study, the underlying mechanism for HQ's immunotoxicity is not clear. NF-kappaB is a transcription factor known to regulate the expression of a number of genes critical for normal T cell activation. We therefore hypothesized that NF-kappaB might be involved in HQ-induced immunosuppression. In this study, we demonstrate that 1 muM HQ inhibits tumor necrosis factor alpha induced activation of NF-kappaB in primary human CD4+ T cells. This inhibition is not accompanied by a loss in viability, and HQ-treated T cells maintain other active signaling pathways throughout the exposure duration. Additionally, the inhibition of NF-kappaB is reversible as HQ-treated T cells regain normal functioning after 72 h in culture. HQ does not appear to alter NF-kappaB directly as preincubation of nuclear extracts with HQ does not diminish activity of this protein. We further demonstrate that 1 muM HQ inhibits intracellular IL-2 production in T cells stimulated with phorbol ester but does not alter surface expression of CD25 (the alpha-subunit of the IL-2 receptor). These data suggest that NF-kappaB may be an important molecular mediator of HQ's (and benzene's) immunotoxicity. Copyright 1998 Academic Press.

Document Type: Research Article

Affiliations: School of Pharmacy

Publication date: April 1, 1998

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