VITAMIN-E, PULMONARY FUNCTIONS, AND PHAGOCYTE-MEDIATED OXIDATIVE STRESS IN SMOKERS AND NONSMOKERS

Relationships among the plasma levels of vitamin E (VE), the numbers a nd prooxidative activities of circulating phagocytes, serum alpha-1-pr otease inhibitor (API), and pulmonary functions were investigated in 8 3 asymptomatic male cigarette smokers and 65 nonsmoking controls. Plas ma levels of VE, of cholesterol, and of API were measured using high p erformance liquid chromatography, spectrophotometry, and nephelometry, respectively, whereas reactive oxidant (ROS) generation by activated blood phagocytes was measured using a whole blood luciginen-enhanced c hemiluminescence method. Smoking was associated with significantly inc reased circulating neutrophil counts (p 0.0001), serum API (p 0.0001) and phagocyte-derived ROS-generation (p 0.0001), and decreased spirome tric values (FEV(1): p 0.0138 and FEF25-75: p 0.0654). Plasma VE and c holesterol levels were not significantly different between smokers and nonsmokers. However, in smokers both plasma VE and cholesterol correl ated significantly and positively with serum API (r 0.24, p 0.03 and r 0.30, p 0.005, respectively), neutrophil counts (r 0.24, p 0.03 and r 0.25, p 0.03, respectively), and phagocyte-derived ROS-generation (r 0.32, p 0.003 and r 0.32, p 0.003, respectively), and significantly an d inversely with FEV(1) (r -0.23, p 0.03 and r -0.22, p 0.04, respecti vely) and FEF25-75 (r -0.32, p 0.003 and r -0.26, p 0.02, respectively ). In nonsmokers plasma VE, but not cholesterol, was positively correl ated with FEV(1) (r 0.34, p 0.007) and FEF25-75 (r 0.40, p 0.001). The results suggest that VE protects the lungs of both smokers and nonsmo kers and may act as a mobilizable antioxidant in response to smoking-i nduced oxidative stress.