Interactions of β-carotene and cigarette smoke in human bronchial epithelial cells

Results from recent intervention trials indicated that supplemental beta -carotene enhances lung cancer incidence and mortality among smokers. It was hypothesized that beta -carotene was exerting its deleterious effects through a prooxidant effect in the smoke-exposed lung. To test this hypothesis we examined the interactions of beta -carotene and cigarette smoke in transformed human bronchial epithelial cells. We studied the effects of beta -carotene supplementation on rates of gas phase smoke-induced lipid peroxidation, membrane damage and depletion of endogenous antioxidants in BEAS-2B cells. Gas phase cigarette smoke caused cellular beta -carotene levels to decrease over time. The oxidation of beta -carotene by smoke generated various oxidation products, including 4-nitro-beta -carotene, beta -apo-carotenals and beta -carotene epoxides. Peroxidation of membrane lipids by gas phase smoke progressed at a slower rate than did oxidation of beta -carotene and incorporation of beta -carotene into the cells did not enhance the overall rate of lipid peroxidation. Additionally, lactate dehydrogenase release during smoke exposure was also unaffected by the presence or absence of beta -carotene in cells. beta -Carotene incorporation in cells was not found to accelerate the rates of alpha -tocopherol and glutathione depletion by cigarette smoke. Our results indicate that beta -carotene is more sensitive than lipids to cigarette smoke oxidation, but that this preferential oxidation of beta -carotene does not lead to a prooxidant effect in human bronchial epithelial cells.