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

Abstract β-Carotene (βC) 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 βC/cigarette smoke (CS) interactions potentially influencing lung cancer risk in smokers. A/J mice received a diet containing 120 or 600 ppm βC for six weeks, and exposed to mainstream CS (140 mg total suspended particulates/m 3 ) during the last two weeks. Lung transcriptomics analysis revealed that CS induced drug metabolism, oxidative stress, extracellular matrix (ECM) degradation, inflammation markers, and apoptosis. βC reduced CS-induced inflammation markers and ECM degradation. βC modulated the CS effect on apoptosis without a clear pro- or anti-apoptotic trend. βC alone induced only minor changes of gene expression. In conclusion, βC/CS interactions caused gene regulations in lungs. CS was the main effector. The gene regulations overall did not indicate that βC exacerbated CS effects. Dose-dependency of βC effects was minor and not detectable by genome-wide data mining.