[Clinical evaluation and application of lipid peroxidation produced by tobacco smoke in the tracheal mucosa].

The oxidative stress level produced by tobacco smoke on the respiratory system was evaluated by studying lipid peroxidation in the tracheal mucosa of samples obtained by tracheostomy from nonsmokers. Conjugated dienes, derived from fatty acids present in tissue, were measured in the sample. The absence of polymorphonuclear leukocytes and macrophages in the tracheal mucosa make it a more suitable model than lung parenchyma because it excludes the peroxidation produced by inflammatory cells. The tracheal mucosa was exposed to different numbers of smoke puffs, then submitted to recovery with humidified air for different time periods. The effect of diene production on several antioxidants--superoxide dismutase, catalase, deferroxamine--was studied. Exposure to four puffs of tobacco smoke from a cigarette was enough to produce lipid oxidation in samples. This activity was evident 15 minutes after exposure to smoke. When antioxidants were placed on sample surfaces, lipid peroxidation was abolished. We conclude that tobacco smoke has a peroxidant activity independent of that produced by inflammatory cells, but probably mediated by free radicals. Therefore, the tracheal model seems suitable for the evaluation of respiratory epithelial oxidation in response to tobacco smoke.