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Hydroquinone, a Reactive Metabolite of Benzene, Reduces Macrophage-mediated Immune Responses  

Lee, Ji Yeon (School of Biotechnology and Bioengineering, Kangwon National University)
Kim, Joo Young (School of Biotechnology and Bioengineering, Kangwon National University)
Lee, Yong Gyu (School of Biotechnology and Bioengineering, Kangwon National University)
Shin, Won Cheol (School of Biotechnology and Bioengineering, Kangwon National University)
Chun, Taehoon (Division of Biotechnology, College of Life Sciences and Biotechnology, Korea University)
Rhee, Man Hee (College of Veterinary Medicine, Kyungpook National University)
Cho, Jae Youl (School of Biotechnology and Bioengineering, Kangwon National University)
Abstract
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)-${\alpha}$, interleukin (IL)-$1{\beta}$, 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 phoshorylation of Akt. Therefore, our data suggest that hydroquinone inhibits macrophage-mediated immune responses by modulating intracellular signaling and protective mechanisms.
Keywords
Akt; Cell-Cell Adhesion; Cytokines; Cytotoxic Molecules; Heme Oxygenase-1; Hydroquinone; Macrophages;
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