Effects of β-Carotene and Its Cleavage Products in Primary Pneumocyte Type II Cells
β-Carotene has been shown to increase the risk of developing lung cancer in smokers and asbestos workers in two large scale trails, the Beta-Carotene and Retinol Efficacy Trial (CARET) and the Alpha-Tocopherol Beta-carotene Cancer Prevention Trial (ATBC). Based on this observation, it was proposed t...
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Published in | Antioxidants Vol. 6; no. 2; p. 37 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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Abstract | β-Carotene has been shown to increase the risk of developing lung cancer in smokers and asbestos workers in two large scale trails, the Beta-Carotene and Retinol Efficacy Trial (CARET) and the Alpha-Tocopherol Beta-carotene Cancer Prevention Trial (ATBC). Based on this observation, it was proposed that genotoxic oxidative breakdown products may cause this effect. In support of this assumption, increased levels of sister chromatid exchanges, micronuclei, and chromosomal aberrations were found in primary hepatocyte cultures treated with a mixture of cleavage products (CPs) and the major product apo-8'carotenal. However, because these findings cannot directly be transferred to the lung due to the exceptional biotransformation capacity of the liver, potential genotoxic and cytotoxic effects of β-carotene under oxidative stress and its CPs were investigated in primary pneumocyte type II cells. The results indicate that increased concentrations of β-carotene in the presence of the redox cycling quinone dimethoxynaphthoquinone (DMNQ) exhibit a cytotoxic potential, as evidenced by an increase of apoptotic cells and loss of cell density at concentrations > 10 µM. On the other hand, the analysis of micronucleated cells gave no clear picture due to the cytotoxicity related reduction of mitotic cells. Last, although CPs induced significant levels of DNA strand breaks even at concentrations ≥ 1 µM and 5 µM, respectively, β-carotene in the presence of DMNQ did not cause DNA damage. Instead, β-carotene appeared to act as an antioxidant. These findings are in contrast with what was demonstrated for primary hepatocytes and may reflect different sensitivities to and different metabolism of β-carotene in the two cell types. |
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AbstractList | β-Carotene has been shown to increase the risk of developing lung cancer in smokers and asbestos workers in two large scale trails, the Beta-Carotene and Retinol Efficacy Trial (CARET) and the Alpha-Tocopherol Beta-carotene Cancer Prevention Trial (ATBC). Based on this observation, it was proposed that genotoxic oxidative breakdown products may cause this effect. In support of this assumption, increased levels of sister chromatid exchanges, micronuclei, and chromosomal aberrations were found in primary hepatocyte cultures treated with a mixture of cleavage products (CPs) and the major product apo-8′carotenal. However, because these findings cannot directly be transferred to the lung due to the exceptional biotransformation capacity of the liver, potential genotoxic and cytotoxic effects of β-carotene under oxidative stress and its CPs were investigated in primary pneumocyte type II cells. The results indicate that increased concentrations of β-carotene in the presence of the redox cycling quinone dimethoxynaphthoquinone (DMNQ) exhibit a cytotoxic potential, as evidenced by an increase of apoptotic cells and loss of cell density at concentrations > 10 µM. On the other hand, the analysis of micronucleated cells gave no clear picture due to the cytotoxicity related reduction of mitotic cells. Last, although CPs induced significant levels of DNA strand breaks even at concentrations ≥ 1 µM and 5 µM, respectively, β-carotene in the presence of DMNQ did not cause DNA damage. Instead, β-carotene appeared to act as an antioxidant. These findings are in contrast with what was demonstrated for primary hepatocytes and may reflect different sensitivities to and different metabolism of β-carotene in the two cell types. |
Author | Knasmüller, Siegfried Stutz, Hanno Bojaxhi, Ekramije Ferk, Franziska Bresgen, Nikolaus Alija, Avdulla Eckl, Peter M Haider, Cornelia Martano, Giuseppe |
AuthorAffiliation | 3 Department of Molecular Biology, University of Salzburg, Hellbrunnerstr. 34, Salzburg 5020, Austria; giuseppe.martano@hotmail.it (G.M.); hanno.stutz@sbg.ac.at (H.S.) 1 Department of Cell Biology and Physiology, University of Salzburg, Hellbrunnerstr. 34, Salzburg A-A-5020, Austria; haider.cornelia@gmail.com (C.H.); ekramije.bojaxhi@stud.sbg.ac.at (E.B.); nikolaus.bresgen@sbg.ac.at (N.B.) 2 Institute of Cancer Research, Department of Internal Medicine 1, Medical University of Borschkegasse 8a, Vienna A-1090, Austria; franziska.ferk@meduniwien.ac.at (F.F.); siegfried.knasmueller@meduniwien.ac.at (S.K.) 4 Department of Biology, University of Prishtina, Xhorxh Bush, n.n., Prishtina 10000, Kosova; avdulla.alija@uni-pr.edu |
AuthorAffiliation_xml | – name: 1 Department of Cell Biology and Physiology, University of Salzburg, Hellbrunnerstr. 34, Salzburg A-A-5020, Austria; haider.cornelia@gmail.com (C.H.); ekramije.bojaxhi@stud.sbg.ac.at (E.B.); nikolaus.bresgen@sbg.ac.at (N.B.) – name: 3 Department of Molecular Biology, University of Salzburg, Hellbrunnerstr. 34, Salzburg 5020, Austria; giuseppe.martano@hotmail.it (G.M.); hanno.stutz@sbg.ac.at (H.S.) – name: 4 Department of Biology, University of Prishtina, Xhorxh Bush, n.n., Prishtina 10000, Kosova; avdulla.alija@uni-pr.edu – name: 2 Institute of Cancer Research, Department of Internal Medicine 1, Medical University of Borschkegasse 8a, Vienna A-1090, Austria; franziska.ferk@meduniwien.ac.at (F.F.); siegfried.knasmueller@meduniwien.ac.at (S.K.) |
Author_xml | – sequence: 1 givenname: Cornelia surname: Haider fullname: Haider, Cornelia email: haider.cornelia@gmail.com organization: Department of Cell Biology and Physiology, University of Salzburg, Hellbrunnerstr. 34, Salzburg A-A-5020, Austria. haider.cornelia@gmail.com – sequence: 2 givenname: Franziska surname: Ferk fullname: Ferk, Franziska email: franziska.ferk@meduniwien.ac.at organization: Institute of Cancer Research, Department of Internal Medicine 1, Medical University of Borschkegasse 8a, Vienna A-1090, Austria. franziska.ferk@meduniwien.ac.at – sequence: 3 givenname: Ekramije surname: Bojaxhi fullname: Bojaxhi, Ekramije email: ekramije.bojaxhi@stud.sbg.ac.at organization: Department of Cell Biology and Physiology, University of Salzburg, Hellbrunnerstr. 34, Salzburg A-A-5020, Austria. ekramije.bojaxhi@stud.sbg.ac.at – sequence: 4 givenname: Giuseppe surname: Martano fullname: Martano, Giuseppe email: giuseppe.martano@hotmail.it organization: Department of Molecular Biology, University of Salzburg, Hellbrunnerstr. 34, Salzburg 5020, Austria. giuseppe.martano@hotmail.it – sequence: 5 givenname: Hanno surname: Stutz fullname: Stutz, Hanno email: hanno.stutz@sbg.ac.at organization: Department of Molecular Biology, University of Salzburg, Hellbrunnerstr. 34, Salzburg 5020, Austria. hanno.stutz@sbg.ac.at – sequence: 6 givenname: Nikolaus surname: Bresgen fullname: Bresgen, Nikolaus email: nikolaus.bresgen@sbg.ac.at organization: Department of Cell Biology and Physiology, University of Salzburg, Hellbrunnerstr. 34, Salzburg A-A-5020, Austria. nikolaus.bresgen@sbg.ac.at – sequence: 7 givenname: Siegfried surname: Knasmüller fullname: Knasmüller, Siegfried email: siegfried.knasmueller@meduniwien.ac.at organization: Institute of Cancer Research, Department of Internal Medicine 1, Medical University of Borschkegasse 8a, Vienna A-1090, Austria. siegfried.knasmueller@meduniwien.ac.at – sequence: 8 givenname: Avdulla surname: Alija fullname: Alija, Avdulla email: avdulla.alija@uni-pr.edu organization: Department of Biology, University of Prishtina, Xhorxh Bush, n.n., Prishtina 10000, Kosova. avdulla.alija@uni-pr.edu – sequence: 9 givenname: Peter M surname: Eckl fullname: Eckl, Peter M email: peter.eckl@sbg.ac.at organization: Department of Cell Biology and Physiology, University of Salzburg, Hellbrunnerstr. 34, Salzburg A-A-5020, Austria. peter.eckl@sbg.ac.at |
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Keywords | dimethoxy-naphthoquinone apo-8′carotenal apoptosis β-carotene micronuclei β-carotene cleavage products Comet assay pneumocytes |
Language | English |
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SubjectTerms | Antioxidants apo-8′carotenal Apoptosis Asbestos Biotransformation Cell density Chromosome aberrations Cleavage Comet assay Cytotoxicity dimethoxy-naphthoquinone DNA damage Genotoxicity Hepatocytes Liver Lung cancer Micronuclei Oxidative stress pneumocytes Quinones Redox properties Vitamin A Workers β-Carotene β-carotene cleavage products |
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Title | Effects of β-Carotene and Its Cleavage Products in Primary Pneumocyte Type II Cells |
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