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Mol. Cells 2007; 23(2): 198-206

Published online January 1, 1970

© The Korean Society for Molecular and Cellular Biology

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

Ji Yeon Lee, Joo Young Kim, Yong Gyu Lee, Won Cheol Shin, Taehoon Chun, Man Hee Rhee, Jae Youl Cho

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)-?, 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.

Keywords Akt; Cell-Cell Adhesion;, Cytokines; Cytotoxic Molecules;, Heme Oxygenase-1; Hydroquinone;, Macrophages

Article

Research Article

Mol. Cells 2007; 23(2): 198-206

Published online April 30, 2007

Copyright © The Korean Society for Molecular and Cellular Biology.

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

Ji Yeon Lee, Joo Young Kim, Yong Gyu Lee, Won Cheol Shin, Taehoon Chun, Man Hee Rhee, Jae Youl Cho

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)-?, 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.

Keywords: Akt, Cell-Cell Adhesion,, Cytokines, Cytotoxic Molecules,, Heme Oxygenase-1, Hydroquinone,, Macrophages

Mol. Cells
May 31, 2023 Vol.46 No.5, pp. 259~328
COVER PICTURE
The alpha-helices in the lamin filaments are depicted as coils, with different subdomains distinguished by various colors. Coil 1a is represented by magenta, coil 1b by yellow, L2 by green, coil 2a by white, coil 2b by brown, stutter by cyan, coil 2c by dark blue, and the lamin Ig-like domain by grey. In the background, cells are displayed, with the cytosol depicted in green and the nucleus in blue (Ahn et al., pp. 309-318).

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