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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