Details
| Original language | English |
|---|---|
| Pages (from-to) | 336-346 |
| Number of pages | 11 |
| Journal | Archives of Biochemistry and Biophysics |
| Volume | 465 |
| Issue number | 2 |
| Early online date | 18 Jul 2007 |
| Publication status | Published - 15 Sept 2007 |
| Externally published | Yes |
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/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. 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.
Keywords
- β-Carotene, Cigarette smoke exposure, Lung cancer, Retinoic acid
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
- Biophysics
- Biochemistry, Genetics and Molecular Biology(all)
- Biochemistry
- Biochemistry, Genetics and Molecular Biology(all)
- Molecular Biology
Sustainable Development Goals
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In: Archives of Biochemistry and Biophysics, Vol. 465, No. 2, 15.09.2007, p. 336-346.
Research output: Contribution to journal › Article › Research › peer review
}
TY - JOUR
T1 - Transcriptomics does not show adverse effects of β-carotene in A/J mice exposed to smoke for 2 weeks
AU - Kuntz, Emmanuelle
AU - Borlak, Jürgen
AU - Riss, Georges
AU - Aebischer, Claude Pierre
AU - Bachmann, Heinrich
AU - Seifert, Nicole
AU - Hunziker, Petra Buchwald
AU - Sölle, Dörte
AU - Hunziker, Willi
AU - Goralczyk, Regina
AU - Wertz, Karin
PY - 2007/9/15
Y1 - 2007/9/15
N2 - 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/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. 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.
AB - 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/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. 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.
KW - β-Carotene
KW - Cigarette smoke exposure
KW - Lung cancer
KW - Retinoic acid
UR - http://www.scopus.com/inward/record.url?scp=34548494191&partnerID=8YFLogxK
U2 - 10.1016/j.abb.2007.06.034
DO - 10.1016/j.abb.2007.06.034
M3 - Article
C2 - 17707332
AN - SCOPUS:34548494191
VL - 465
SP - 336
EP - 346
JO - Archives of Biochemistry and Biophysics
JF - Archives of Biochemistry and Biophysics
SN - 0003-9861
IS - 2
ER -