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Carcinogenesis Advance Access published online on January 16, 2006
Carcinogenesis, doi:10.1093/carcin/bgi342
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© The Author 2006. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received July 18, 2005
Revised November 29, 2005
Accepted January 3, 2006

CANCER BIOLOGY

{beta}-carotene breakdown products enhance genotoxic effects of oxidative stress in primary rat hepatocytes

A. J. Alija 1, N. Bresgen 1, O. Sommerburg 2, C. D. Langhans 3, W. Siems 4, and P. M. Eckl 1 *

1 Department of Cell Biology, University of Salzburg, Hellbrunnerstr.34, A-5020 Salzburg, Austria
2 Children's Hospital, University of Ulm, Germany
3 Children's Hospital, University of Heidelberg, Germany
4 Herzog-Julius Hospital for Rheumatology and Orthopedics, Kurhausstrasse 13-17, D-38667 Bad Harzburg, Germany

* To whom correspondence should be addressed.
P. M. Eckl, E-mail: peter.eckl{at}sbg.ac.at


  Abstract

Since it has to be expected that individuals exposed to oxidative stress who take supplements of beta carotene are simultaneously exposed to both beta carotene cleavage products (CP) and oxidative stress, and both exposures have been demonstrated to cause genotoxic effects in primary rat hepatocytes, cyto- and genotoxic effects on primary rat hepatocytes after supplementation of the medium with increasing concentrations of a CP mixture during exposure to oxidative stress either by treatment with DMNQ (2,3-dimethoxy-1,4-naphthoquinone) or hypoxia/reoxygenation was investigated. The cytological endpoints analysed were: the mitotic indices, the percentages of apoptotic and necrotic cells, the percentages of micronucleated cells (MN), and the number of chromosomal aberrations (CA) and sister chromatid exchanges (SCE). The results obtained clearly demonstrate that the CP mixture enhances the genotoxic effects of oxidative stress exposure while it had no effect at all on the endpoints of cytotoxicity studied. These results further support the hypothesis that CP might be responsible for the reported carcinogenic response in The CARET and ATBC chemoprevention trials.

Keywords: {beta}-carotene; {beta}-carotene breakdown products; DMNQ; hypoxia/reoxygenation; genotoxicity; hepatocytes.
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