Tobacco smoke. Effects on pulmonary host defense.
Tobacco smoke affected both the metabolism and function of pulmonary alveolar macrophages (PAM). Phagocytosis of viable Staphylococcus aureus and inert starch particles was minimally but consistently depressed in PAM from rats exposed to tobacco smoke for six months. Oxygen consumption, superoxide and hydrogen peroxide release, and hexose monophosphate shunt activity were elevated in cells from smokers. Oxidation of glucose, labelled in the carbon-six position, remained unchanged. All observed effects of tobacco smoke on oxygen metabolism occurred during phagocytosis and did not affect the basal metabolism of the nonstimulated cell.
D000818:Animals; D006600:Hexosephosphates / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism*; D008297:Male; D010101:Oxygen Consumption; D010587:Phagocytosis; D011650:Pulmonary Alveoli / Q000276:immunology*; D051381:Rats; D012906:Smoke; D012907:Smoking / Q000503:physiopathology*; D013203:Staphylococcal Infections / Q000276:immunology; D013481:Superoxides / Q000378:metabolism; D013997:Time Factors
D006600:Hexosephosphates; D012906:Smoke; D013481:Superoxides; D006861:Hydrogen Peroxide