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
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.