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KMID : 0578320070230020198
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Molecules and Cells
2007 Volume.23 No. 2 p.198 ~ p.206
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Hydroquinone, a Reactive Metabolite of Benzene, Reduces Macrophage-mediated Immune Responses
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Lee Ji-Yeon
Kim Joo-Young
Lee Yong-Gyu
Shin Won-Cheol
Chun Tae-Hoon
Rhee Man-Hee
Cho Jae-Youl
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Abstract
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Hydroquinone is a toxic compound and a major benzene metabolite. We report that it strongly inhibits the activation of macrophages and associated cells. Thus, it suppressed the production of proinflammatory cytokines [tumor necrosis factor (TNF)-?, interleukin (IL)-1?, IL-3, IL-6, IL-10, IL-12p40, IL-23], secretion of toxic molecules [nitric oxide (NO) and reactive oxygen species (ROS)] and the activation and expression of CD29 as judged by cell-cell adhesion and surface staining experiments. The inhibition was due to the induction of heme oxygenase (HO)-1 in LPS-activated macrophages, since blocking HO-1 activity with ZnPP, an HO-1 specific inhibitor, abolished hydroquinone’s NO inhibitory activity. In addition, hydroquinone and inhibitors (wortmannin and LY294002) of the phosphatidylinositol-3 kinase (PI3K)/Akt pathway had very similar inhibitory effects on LPS-induced and CD29-mediated macrophage responses, including the pho-shorylation of Akt. Therefore, our data suggest that hydroquinone inhibits macrophage-mediated immune re-sponses by modulating intracellular signaling and protective mechanisms.
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KEYWORD
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Akt, Cell-Cell Adhesion, Cytokines, Cytotoxic Molecules, Heme Oxygenase-1, Hydroquinone, Macrophages
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