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

Research output: Contribution to journalArticlepeer-review

40 Citations (Scopus)


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)-α, interleukin (IL)1β, 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 mechanism.

Original languageEnglish
Pages (from-to)198-206
Number of pages9
JournalMolecules and cells
Issue number2
Publication statusPublished - 2007 Apr 30


  • Akt
  • Cell-cell adhesion
  • Cytokines
  • Cytotoxic molecules
  • Heme oxygenase-1
  • Hydroquinone
  • Macrophages

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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