139
Views
54
CrossRef citations to date
0
Altmetric
ORIGINAL ARTICLE

DNA damage, DNA susceptibility to oxidation and glutathione level in women with polycystic ovary syndrome

, , , &
Pages 721-728 | Received 11 May 2005, Accepted 15 Sep 2005, Published online: 08 Jul 2009
 

Abstract

Recent studies have addressed the possibility of an association between polycystic ovaries and ovarian cancer. DNA damage is the first step of the carcinogenesis, and susceptibility to cancer, in general, is characterized by high DNA damage. Free radical‐mediated DNA damage and impaired antioxidant defence have been implicated as contributory factors for the development of cancer. This study evaluates DNA damage (strand breakage, base oxidation, formamidopyrimidine DNA glycosylase (Fpg) sensitive sites), H2O2‐induced DNA damage, a marker of DNA susceptibility to oxidation and glutathione (GSH) level, a powerful antioxidant, in women with polycystic ovary syndrome (PCOS). Women with PCOS showed a significant decrease in GSH level, a significant increase in DNA strand breakage and H2O2‐induced DNA damage. Although Fpg‐sensitive sites were higher in the PCOS group compared to the control group, the difference did not reach a statistically significant level. Significant correlations were found between free testosterone and DNA strand breakage (r = 0.46, p<0.01) and free testosterone and H2O2‐induced DNA damage (r = 0.41, p<0.05). The data indicate that DNA damage and susceptibility of DNA to oxidative stress are increased in women with PCOS and may explain the association between PCOS and ovarian cancer.

Acknowledgements

We thank Dr. Michael H. L. Green and Dr. Andrew Collins for skilful instructions in establishing the comet assay and Dr. Deborah Barnes and Graham Dally for their kind gift of Fpg protein. The work was supported by the Research Fund of İstanbul University (project numbers: BYP‐138/20122002 and UDP‐400/07102004).

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.