Cigarette smoke condensate induces vascular oxidative stress and inflammation

Although the cardiovascular morbidity and mortality induced by cigarette smoking exceeds that attributable to lung cancer, the molecular basis of smoking‐induced cardiovascular injury remains unclear. To test the hypothesis that water soluble components of the cigarette smoke condensate (CSC) elicit pro‐inflammatory phenotypic changes in blood vessels we exposed isolated carotid arteries and aortas of male Wistar rats to CSC (0 to 40 μg/mL, for 6 h). Lucigenin chemiluminescence measurements showed that CSC significantly increased vascular O2.‐ production (0, 0.4, 4, 40 μg/mL: 100±12%, 126±18%, 167±26%, 199±29%, respectively). QRT‐PCR analysis showed that mRNA expression of the pro‐inflammatory cytokines IL‐1â, IL‐6 and TNFa (4 μg/mL: by 44±18%, 43±16% and 32±11%, respectively). Inhibition of poly‐(ADP)ribose‐synthase (PARS) with 3‐aminobenzamide (10–3 mol/L) prevented the up‐regulation of inflammatory cytokines by CSC. Expression of iNOS and that of ICAM‐1 was unaffected by CSC under these experimental conditions. Thus, we propose that water soluble components of cigarette smoke, which are likely to be present in the bloodstream, can elicit oxidative stress and pro‐atherogenic vascular phenotypic changes. Our data warrant further studies on the role of PARS inhibitors in pharmacological vasculoprotection in smokers. (Grant support: American Federation for Aging Research, AHAF H2004‐024; Philip Morris USA).