Diesel exhaust particle extracts and associated polycyclic aromatic hydrocarbons inhibit Cox-2-dependent prostaglandin synthesis in murine macrophages and fibroblasts.
Diesel exhaust particles (DEP) and their organic constituents modulate the immune system and exacerbate allergic airway inflammation. We investigated the role of DEP extract and associated polycyclic aromatic hydrocarbons (PAHs) on prostaglandin synthesis in endotoxin-activated murine macrophages and in mitogen-stimulated fibroblasts. In both macrophages and fibroblasts, DEP extract, phenanthrene, anthracene, phenanthrenequinone, and beta-napthoflavone inhibit prostaglandin production from endogenous arachidonic acid in response to ligand stimulation. However, DEP extract and PAHs do not block ligand induction of cyclooxygenase-2 ( COX-2) protein, either in mitogen-stimulated fibroblasts or endotoxin-treated macrophages. Release of total arachidonic acid and total lipid products is not reduced by DEP or PAHs following ligand stimulation of macrophages or fibroblasts. DEP extract and the PAHs inhibit the activity of purified COX-2 enzyme in vitro but do not inhibit COX-1 activity. Thus, DEP and PAHs do not affect ligand-induced COX-2 gene expression, phospholipase activation, or arachidonic acid release in macrophages and fibroblasts but exert their inhibitory effect on prostaglandin production by preferentially blocking COX-2 enzyme activity.[1]References
- Diesel exhaust particle extracts and associated polycyclic aromatic hydrocarbons inhibit Cox-2-dependent prostaglandin synthesis in murine macrophages and fibroblasts. Rudra-Ganguly, N., Reddy, S.T., Korge, P., Herschman, H.R. J. Biol. Chem. (2002) [Pubmed]
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