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

• Published in: Carcinogenesis (New York) 2001-08, Vol.22 (8), p.1173
• Main Authors: Arora, Arti, Willhite, Celeste A, Liebler, Daniel C
• Format: Article
• Language: English
• ISSN: 0143-3334; 1460-2180

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.