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Oxidative stress and inflammatory responses induced by 1.2-Naphthoquinone.

Toxicological studies have found associations between inflammation and exposure to diesel exhaust constituents, such as the organic electrophile 1,2-naphthoquinone (1,2-NQ). Cheng et al. (p. 267) investigated the mechanism of action of this association by examining the role of oxidant stress in, 2-NQ-induced expression of inflammatory and adaptive genes in a human airway epithelial cell line. Cytosolic redox status and hydrogen peroxide ([H.sub.2][O.sub.2]) were measured in living cells using genetically encoded GFP-based fluorescent indicators, and expression of interleukin-8 (IL-8), cyclooxygenase-2 (COX-2), and heme oxygenase-1 (HO-1) mRNA was measured in BEAS-2B cells exposed to 1,2-NQ. Catalase overexpression and metabolic inhibitors were used to determine the role of redox changes and [H.sub.2][O.sub.2] in 1,2-NQ-induced gene expression. Results indicate that exposure to 1,2-NQ induced mitochondrial production of [H.sub.2][O.sub.2] that mediated the expression of inflammatory genes but not the concurrent loss of reducing redox potential. 1,2-NQ exposure also caused marked expression of HO-1 that appeared to be enhanced by suppression of [H.sub.2][O.sub.2]. These findings shed light on the oxidant-dependent events that underlie cellular responses to environmental electrophiles found in diesel exhaust.
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Title Annotation:Research
Publication:Environmental Health Perspectives
Article Type:Brief article
Geographic Code:1USA
Date:Feb 1, 2012
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