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

Results from recent intervention trials indicated that supplemental beta -c arotene enhances lung cancer incidence and mortality among smokers. It was hypothesized that beta -carotene was exerting its deleterious effects throu gh a prooxidant effect in the smoke-exposed lung. To test this hypothesis w e examined the interactions of beta -carotene and cigarette smoke in transf ormed human bronchial epithelial cells. We studied the effects of beta -car otene supplementation on rates of gas phase smoke-induced lipid peroxidatio n, membrane damage and depletion of endogenous antioxidants in BEAS-2B cell s. Gas phase cigarette smoke caused cellular beta -carotene levels to decre ase over time. The oxidation of beta -carotene by smoke generated various o xidation products, including 4-nitro-beta -carotene, beta -apo-carotenals a nd beta -carotene epoxides. Peroxidation of membrane lipids by gas phase sm oke progressed at a slower rate than did oxidation of beta -carotene and in corporation of beta -carotene into the cells did not enhance the overall ra te of lipid peroxidation. Additionally, lactate dehydrogenase release durin g smoke exposure was also unaffected by the presence or absence of beta -ca rotene in cells. beta -Carotene incorporation in cells was not found to acc elerate the rates of alpha -tocopherol and glutathione depletion by cigaret te smoke. Our results indicate that beta -carotene is more sensitive than l ipids to cigarette smoke oxidation, but that this preferential oxidation of beta -carotene does not lead to a prooxidant effect in human bronchial epi thelial cells.