Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (18)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Lautraite, S.
Right arrow Articles by Chipman, J.K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lautraite, S.
Right arrow Articles by Chipman, J.K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Mutagenesis, Vol. 17, No. 1, 45-53, January 2002
© 2002 UK Environmental Mutagen Society/Oxford University Press

Flavonoids inhibit genetic toxicity produced by carcinogens in cells expressing CYP1A2 and CYP1A1

S. Lautraite, A.C. Musonda, J. Doehmer1, G.O. Edwards and J.K. Chipman,2

School of Biosciences, University of Birmingham, Birmingham B15 2TT, UK and 1 GenPharmTox Biotech AG, Fraunhoferstrasse 9, D-82152 Martinsreid/Planegg, Germany

The effects of the flavonoids quercetin, apigenin and chrysin (10 µM) on the genetic toxicity of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) and benzo[a]pyrene (BaP) was investigated at sub-cytotoxic concentrations in Chinese hamster V79 cells expressing human or rat cytochromes P450. In V79 r1A2-NH and V79 h1A1-MZ cells, none of the flavonoids increased DNA strand breaks (SB) (measured by the Comet assay) or produced detectable DNA adducts (measured by 32P-post-labelling). Neither IQ nor BaP produced DNA damage in the absence of expressed CYP1A2 or CYP1A1, respectively. DNA damage measured as SB and DNA adducts was detectable in V79 r1A2-NH cells expressing rat CYP1A2 when treated with IQ (2.5–50 µM) and this was inhibited by quercetin. Likewise, DNA damage (SB and DNA adducts) was elevated in V79 h1A1-MZ cells expressing human CYP1A1 when treated with BaP (0.1–0.5 µM) and this was inhibited by chrysin and apigenin, but not by quercetin. The specificity of CYP1A1 inhibition by chrysin and apigenin and CYP1A2 inhibition by quercetin was confirmed by ethylresorufin O-deethylase assay.

2 To whom correspondence should be addressed. Email: j.k.chipman{at}bham.ac.uk


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 CarcinogenesisHome page
L. C. Wilms, A. W. Boots, V. C.J. de Boer, L. M. Maas, D. M.F.A. Pachen, R. W.H. Gottschalk, H. B. Ketelslegers, R. W.L. Godschalk, G. R.M.M. Haenen, F. J. van Schooten, et al.
Impact of multiple genetic polymorphisms on effects of a 4-week blueberry juice intervention on ex vivo induced lymphocytic DNA damage in human volunteers
Carcinogenesis, August 1, 2007; 28(8): 1800 - 1806.
[Abstract] [Full Text] [PDF]

Home page
 Food Science and Technology InternationalHome page
A. I. Haza, A. Zabala, N. Arranz, and P. Morales
Protective Effect of a Lactobacillus salivarius Strain of Human Origin
Food Science and Technology International, August 1, 2005; 11(4): 251 - 259.
[Abstract] [PDF]

Home page
 Food Science and Technology InternationalHome page
R. M. Lamuela-Raventos, A. I. Romero-Perez, C. Andres-Lacueva, and A. Tornero
Review: Health Effects of Cocoa Flavonoids
Food Science and Technology International, June 1, 2005; 11(3): 159 - 176.
[Abstract] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.