MECHANISM OF PATHOPHYSIOLOGICAL EFFECTS OF DIESEL EXHAUST PARTICLES ON ENDOTHELIAL-CELLS

Citation
M. Ikeda et al., MECHANISM OF PATHOPHYSIOLOGICAL EFFECTS OF DIESEL EXHAUST PARTICLES ON ENDOTHELIAL-CELLS, Environmental toxicology and pharmacology, 6(2), 1998, pp. 117-123
Citations number
49
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Pharmacology & Pharmacy",Toxicology,"Environmental Sciences
ISSN journal
1382-6689
Volume
6
Issue
2
Year of publication
1998
Pages
117 - 123
Database
ISI
SICI code
1382-6689(1998)6:2<117:MOPEOD>2.0.ZU;2-J
Abstract
The suspension of diesel exhaust particles (DEP) inhibited endothelium -dependent relaxation (EDR). The mechanism of the impairment of EDR by DEP was investigated with cultured porcine endothelial cells (PEC) an d NO synthase (NOS) cell free system. Incubation of PEC with DEP (50-1 50 mu g/ml) for 10-30 min did not induce cell damage. Bradykinin-induc ed endothelium-dependent relaxing factor (EDRF) release from PEC was b ioassayed by cyclic GMP formation in RFL-6 cells. A 10-min preincubati on of PEC with DEP (0.1-100 mu g/ml) inhibited EDRF release. NOS activ ity from rat cerebellum cytosol was measured either by the conversion of 3H-L-arginine to H-3-L-citrulline or the NO2- formation. A 10-min p reincubation of NOS with DEP (0.1-100 mu g/ml) did not affect the form ation of H-3-L-citrulline. In contrast, it inhibited NO2- formation. T hese results suggest that DEP neither induced cell damage nor inhibite d EDRF release from PEC, but DEP scavenged NO to block its physiologic al action. (C) 1998 Elsevier Science B.V. All rights reserved.