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Transcriptomics does not show adverse effects of beta-carotene in A/J mice exposed to smoke for 2 weeks

: Kuntz, E.; Borlak, J.; Riss, G.; Aebischer, C.P.; Bachmann, H.; Seifert, N.; Hunziker, P.B.; Sölle, D.; Hunziker, W.; Goralczyk, R.; Wertz, K.


Archives of biochemistry and biophysics 465 (2007), Nr.2, S.336-346
ISSN: 0003-9861
Fraunhofer ITEM ()
Beta-Carotene; cigarette smoke exposure; lung cancer; retinoic acid; lung cancer

Beta-Carotene (BetaC) supplementation in smokers was unexpectedly associated with increased incidence of lung cancer versus smoking alone. We performed a study in A/J mice to explore possible BetaC/cigarette smoke (CS) interactions potentially influencing lung cancer risk in smokers. A/J mice received a diet containing 120 or 600 ppm BetaC for six weeks, and exposed to mainstream CS (140 mg total suspended particulates/m3) during the last two weeks. Lung transcriptomics analysis revealed that CS induced drug metabolism, oxidative stress, extracellular matrix (ECM) degradation, inflammation markers, and apoptosis. BetaC reduced CS-induced inflammation markers and ECM degradation. BetaC modulated the CS effect on apoptosis without a clear pro- or anti-apoptotic trend. BetaC alone induced only minor changes of gene expression. In conclusion, BetaC/CS interactions caused gene regulations in lungs. CS was the main effector. The gene regulations overall did not indicate that BetaC exacerbated CS effects. Dose-dependency of BetaC effects was minor and not detectable by genome-wide data mining.