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 (12)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Dobrzynska, M. M.
Right arrow Articles by Anderson, D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dobrzynska, M. M.
Right arrow Articles by Anderson, D.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Mutagenesis vol. 19 no. 4 pp. 325-330, July 2004
© 2004 UK Environmental Mutagen Society/Oxford University Press

Antioxidants modulate thyroid hormone- and noradrenaline-induced DNA damage in human sperm

Malgorzata M. Dobrzynska1,2, Adolf Baumgartner1 and Diana Anderson1

1Department of Biomedical Sciences, University of Bradford, Bradford, UK and 2Department of Radiation Protection and Radiobiology, National Institute of Hygiene, Warsaw, Poland

The genotoxic effects of steroidal oestrogens are probably brought about by metabolic changes in their phenolic groups accompanied by the generation of quinones and reactive oxygen species. Although non-steroidal oestrogens and related compounds have not been thoroughly investigated for genotoxicity, some of them also contain phenolic groups that could be involved in redox cycling. Therefore, the aim of the present study was to evaluate the possible DNA-damaging effects of the thyroid hormones triiodothyronine (T3) and L-thyroxine sodium salt (T4) and the neurotransmitter noradrenaline (NA) in human sperm using the Comet assay. They were compared with diethylstilboestrol (DES), a steroidal oestrogen, as a positive control. After dose–response studies, doses of 80 µM T3, 80 µM T4, 300 µM NA and 175 µM DES, which produced DNA damage but retained good cell viability, were chosen for further experiments with the antioxidant catalase and the flavonoids kaempferol and quercetin. Since the scavenging enzyme catalase reduced the DNA-damaging effects of T3, T4 and NA, it can be surmised that these compounds under these conditions induced DNA damage mainly via the production of reactive oxygen species. This was further confirmed by the inhibitory responses produced by the flavonoids, which are known to have antioxidant effects. Therefore, the mechanism of mutagenic action of both steroidal and non-steroidal compounds imply the creation of oxidative stress and subsequent DNA damage due to reactive oxygen species and possibly due to reactive hormone derivatives created during their redox cycling.

3To whom correspondence should be addressed at: Department of Biomedical Sciences, University of Bradford, Bradford BD7 1DP, UK. Email: d.anderson1{at}bradford.ac.uk

Received on March 22, 2004; revised on May 17, 2004; accepted on May 24, 2004


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
 Toxicol SciHome page
E. Cordelli, A. M. Fresegna, A. D'Alessio, P. Eleuteri, M. Spano, F. Pacchierotti, and P. Villani
ReProComet: A New In Vitro Method to Assess DNA Damage in Mammalian Sperm
Toxicol. Sci., October 1, 2007; 99(2): 545 - 552.
[Abstract] [Full Text] [PDF]

Home page
 J AndrolHome page
E. Greco, M. Iacobelli, L. Rienzi, F. Ubaldi, S. Ferrero, and J. Tesarik
Reduction of the Incidence of Sperm DNA Fragmentation by Oral Antioxidant Treatment
J Androl, May 1, 2005; 26(3): 349 - 353.
[Abstract] [Full Text] [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.