alexa Oxidative Damage to Sperm DNA: Clinical Implications
ISSN: 2167-0250

Andrology-Open Access
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Research Article

Oxidative Damage to Sperm DNA: Clinical Implications

Swetasmita Mishra1, Kranthi V1, Rajeev Kumar2, Neena Malhotra3, Kuldeep Mohanty4, Vinay Pathak1 and Rima Dada1*
1Laboratory for Molecular Reproduction and Genetics, Dept. of Anatomy, All India Institute of Medical Sciences, New Delhi, India
2Deptartment of Urology, All India Institute of Medical Sciences, New Delhi, India
3Deptartment of Obstetrics and Gynaecology, All India Institute of Medical Sciences, New Delhi, India
4Dept. of Ophthalmology, All India Institute of Medical Sciences, New Delhi, India
*Corresponding Author : Rima Dada
Laboratory of Molecular Reproduction and Genetics
Department of Anatomy, All India Institute of Medical Sciences (AIIMS)
New Delhi-110029, India
Tel: 26588500 ext-3517,26593517
Fax: 91-11-26588663
E-mail: [email protected]
Received April 17, 2014; Accepted May 15, 2014; Published May 27, 2014
Citation: Mishra S, Kranthi V, Kumar R, Malhotra N, Mohanty K (2014) Oxidative Damage to Sperm DNA: Clinical Implications. Andrology 3:116. doi:10.4172/2167-0250.1000116
Copyright: © 2014 Dada R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 

Abstract

Background: Sperm DNA is susceptible to oxidative damage due to intrinsic and extrinsic factors which cause oxidative stress and due to limited DNA damage detection and repair mechanism. Reactive oxygen species (ROS) are the chief cause of sperm DNA damage. So, this study was planned to assess oxidative stress levels and correlate with sperm DNA damage.

Material and Method: The study included 35 men who had fathered a child in the last one year and 54 male partners of couple experiencing primary infertility. Semen analysis was done according to World Health Organization (1999) criteria. ROS measurement was done by direct chemiluminescence method using luminol as a probe. DNA damage was assessed by sperm chromatin structure assay (SCSA) and expressed as percentage DFI. 8- Hydroxy-2’-deoxyguanosine (8-OHdG) estimation was carried out by competitive ELISA.

Results: The seminal ROS level (RLU/sec/million sperm) was significantly higher (40.52 ± 18.32) in infertile men as compared to fertile controls (14.04 ± 6.67) (p<0.0001). The mean values of 8-OHdG levels (pg/ml) were also significantly higher in patients (30.92 ± 3.27) as compared to fertile controls (14.29 ± 2.24) (p<0.0001) and mean DFI (%) of infertile men was found to be 35.48 ± 12.95, which was higher as compared to controls (24.18 ± 8.76). There was a strong positive correlation between these parameters.

Conclusion: Majority of the sperm DNA damage in infertile men is caused by oxidative damage to the genomic DNA. In presence of limited DNA damage detection and repair mechanism in sperm, prevention of oxidative stress by simple lifestyle interventions may actually be therapeutic.

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