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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
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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