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Hum. Reprod. Advance Access published online on December 16, 2005

Human Reproduction, doi:10.1093/humrep/dei429
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© The Author 2005. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received April 11, 2005
Revised November 9, 2005
Accepted November 16, 2005

Article

Increased sperm DNA damage in patients with varicocele: relationship with seminal oxidative stress

R. Smith 1 *, H. Kaune 1, D. Parodi 1, M. Madariaga 1, R. Rios 2, I. Morales 3, and A. Castro 1

1 Institute of Maternal and Child Research, School of Medicine, University of Chile and San Borja-Arriarán Clinical Hospital
2 Department of Endocrinology, San Borja-Arriarán Clinical Hospital, National Health Service
3 Department of Urology, Barros-Luco Trudeau Hospital, National Health Service, Santiago, Chile

* To whom correspondence should be addressed.
R. Smith, E-mail: rsmith{at}med.uchile.cl


   Abstract

BACKGROUND: The pathophysiology of the testicular damage in varicocele has not been completely understood. Oxidative stress and related sperm DNA damage have been identified as significant causes of male infertility. The current study was designed to determine the extent of sperm nuclear DNA damage in patients with varicocele and to examine its relationship with oxidative stress. METHODS: Semen samples from 55 patients with clinical varicocele and 25 normozoospermic donors were examined. Varicocele sperm samples were classified as normal or abnormal according to World Health Organization guidelines. Sperm DNA damage was evaluated by the sperm chromatin structure assay/flow cytometry and by the terminal deoxyribonucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL) assay. Levels of reactive oxygen species (ROS) and total antioxidant capacity were assessed by a chemiluminescence assay. RESULTS: DNA fragmentation index (DFI) (percentage of sperm with denatured DNA) values and the percentage of TUNEL-positive cells were significantly greater in patients with varicocele, either with normal (DFI, 20.7 ± 4.0; TUNEL positive, 26.1 ± 3.2) or with abnormal (DFI, 35.5 ± 9.0; TUNEL positive, 32.2 ± 4.1) semen profile, compared with controls (DFI, 7.1 ± 0.9; TUNEL positive, 14.2 ± 1.2). Similarly, ROS levels were significantly higher (P < 0.01) in both groups of patients with varicocele. CONCLUSIONS: The presence of a varicocele is associated with high levels of DNA-damage spermatozoa even in the presence of normal semen profile. The results also indicate that oxidative damage is associated with sperm DNA damage in these patients.

Keywords: apoptosis/DNA damage/oxidative stress/spermatozoa/varicocele.
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