Induction of Heme Oxygenase-1 Expression in Macrophages by Diesel Exhaust Particle Chemicals and Quinones via the Antioxidant-Responsive Element

摘要: Diesel exhaust particles (DEP) contain organic chemicals that contribute to the adverse health effects of inhaled particulate matter. Because DEP induce oxidative stress in lung and macrophages, effective antioxidant defenses are required. One type defense is through expression enzyme, heme oxygenase I (HO-1). HO-1 as well phase II detoxifying enzymes induced via response elements (ARE) their promoters gene. We show a crude total extract, aromatic polar fractions, benzo(a)pyrene quinone, phenolic RAW264.7 cells an ARE-dependent manner. N-acetyl cysteine flavonoid, luteolin, inhibited protein expression. also demonstrate same stimuli mRNA parallel with activation SX2 enhancer Mutation ARE core, but not overlapping AP-1 binding sequence, disrupted activation. Finally, we biological agents, such oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine, could mechanism. Prior induction expression, using cobalt-protoporphyrin, protected against DEP-induced toxicity. Taken together, these data plays important role cytoprotection redox-active chemicals, including quinones.