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Antioxidants 2017, 6(2), 37; doi:10.3390/antiox6020037

Effects of β-Carotene and Its Cleavage Products in Primary Pneumocyte Type II Cells

1
Department of Cell Biology and Physiology, University of Salzburg, Hellbrunnerstr. 34, Salzburg A-A-5020, Austria
2
Institute of Cancer Research, Department of Internal Medicine 1, Medical University of Borschkegasse 8a, Vienna A-1090, Austria
3
Department of Molecular Biology, University of Salzburg, Hellbrunnerstr. 34, Salzburg 5020, Austria
4
Department of Biology, University of Prishtina, Xhorxh Bush, n.n., Prishtina 10000, Kosova
*
Author to whom correspondence should be addressed.
Academic Editors: Andrew J. Young and Gordon M. Lowe
Received: 3 March 2017 / Revised: 8 May 2017 / Accepted: 16 May 2017 / Published: 21 May 2017
(This article belongs to the Special Issue Carotenoids—Antioxidant Properties)
View Full-Text   |   Download PDF [1975 KB, uploaded 21 May 2017]   |  

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. View Full-Text
Keywords: β-carotene; β-carotene cleavage products; apo-8′carotenal; dimethoxy-naphthoquinone; pneumocytes; Comet assay; micronuclei; apoptosis β-carotene; β-carotene cleavage products; apo-8′carotenal; dimethoxy-naphthoquinone; pneumocytes; Comet assay; micronuclei; apoptosis
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Haider, C.; Ferk, F.; Bojaxhi, E.; Martano, G.; Stutz, H.; Bresgen, N.; Knasmüller, S.; Alija, A.; Eckl, P.M. Effects of β-Carotene and Its Cleavage Products in Primary Pneumocyte Type II Cells. Antioxidants 2017, 6, 37.

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