Hydroquinone, a reactive metabolite of benzene, reduces macrophage-mediated immune responses

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)-1beta, IL-3, IL-6, IL-10, IL-1...

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Bibliographic Details
Published in:Molecules and cells 2007, 23(2), , pp.198-206
Main Authors: Lee, Ji Yeon, Kim, Joo Young, Lee, Yong Gyu, Shin, Won Cheol, Chun, Taehoon, Rhee, Man Hee, Cho, Jae Youl
Format: Article
Language:English
Subjects:
Androstadienes - pharmacology
Animals
Benzene - pharmacology
Cell Adhesion - drug effects
Cell Line
Chromones - pharmacology
Cytokines - metabolism
Enzyme Activation
Heme Oxygenase-1 - metabolism
Hydroquinones - pharmacology
Immunity - drug effects
Integrin beta1 - metabolism
Lipopolysaccharides - pharmacology
Macrophage Activation - drug effects
Macrophage Activation - physiology
Macrophages - physiology
Mice
Morpholines - pharmacology
Nitric Oxide - metabolism
Phosphatidylinositol 3-Kinases - metabolism
Phosphoinositide-3 Kinase Inhibitors
Phosphorylation
Proto-Oncogene Proteins c-akt - antagonists & inhibitors
Proto-Oncogene Proteins c-akt - metabolism
Protoporphyrins - pharmacology
Reactive Oxygen Species - metabolism
Signal Transduction
Wortmannin
생물학
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Summary: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)-1beta, 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 phosphorylation of Akt. Therefore, our data suggest that hydroquinone inhibits macrophage-mediated immune responses by modulating intracellular signaling and protective mechanisms.
ISSN:1016-8478
0219-1032
DOI:10.1016/S1016-8478(23)07374-0