Mechanism of pathophysiological effects of diesel exhaust particles on endothelial cells

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) and NO synthase (NOS) cell free system. Incubation of PEC with DEP (50-150 mu g/ml) for 10-30 min did not induce cell damage. Bradykinin-induced endothelium-dependent relaxing factor (EDRF) release from PEC was bioassayed by cyclic GMP formation in RFL-6 cells. A 10-min preincubation of PEC with DEP (0.1-100 mu g/ml) inhibited EDRF release. NOS activity 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 preincubation of NOS with DEP (0.1-100 mu g/ml) did not affect the formation of H-3-L-citrulline. In contrast, it inhibited NO2- formation. These results suggest that DEP neither induced cell damage nor inhibited EDRF release from PEC, but DEP scavenged NO to block its physiological action. (C) 1998 Elsevier Science B.V. All rights reserved.