Volume 16, Issue 8 (August 2018)                   IJRM 2018, 16(8): 491-496 | Back to browse issues page


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Ebrahim Abadi Z, Khademi Bami M, Golzadeh M, Kalantar S M, Sheikhha M H. The frequency of TP53 R72P and MDM2 309T>G polymorphisms in Iranian infertile men with spermatogenetic failure: A case-control study. IJRM 2018; 16 (8) :491-496
URL: http://ijrm.ir/article-1-1175-en.html
1- Department of Medical Genetics, Medical Faculty, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
2- Medical Biotechnology Research Center, Ashkezar Branch, Islamic Azad University, Ashkezar, Yazd, Iran
3- Abortion Research Center, Yazd Reproductive Sciences Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
4- Research and Clinical Center for Infertility, Yazd Reproductive Sciences Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
5- Research and Clinical Center for Infertility, Yazd Reproductive Sciences Institute, Shahid Sadoughi University of Medical Sciences, Yazd, Iran , sheikhha@yahoo.com
Abstract:   (3201 Views)
Background: Tumor protein p53 (TP53) is a tumor suppressor transcriptional regulator protein which plays a critical role in the spermatogenesis. One of the most important regulators of p53 is Murine double minute 2 (MDM2), which acts as a negative regulator of the p53 pathway. Based on the key role of p53 and MDM2 in germ cell apoptosis, polymorphisms that cause a change in their function might affect germ cell apoptosis and the risk of male infertility. Objective: This study was designed to examine associations of TP53 72 Arg>Pro (rs1042522), and MDM2 309 T>G (rs937283) polymorphisms with spermatogenetic failure in an Iranian population.
Materials and Methods: A case-control study was conducted with 150 nonobstructive azoospermia or severe oligozoospermia and 150 fertile controls. The two polymorphisms, 72 Arg>Pro in TP53 and 309 T>G in MDM2, were genotyped using PCR-RFLP and ARMS-PCR respectively.
Results: Our analyses revealed that the allele and genotype frequencies of the TP53 R72P polymorphism were not significantly different between the cases and controls (p=0.41, p=0.40 respectively). Also, no significant differences were found in the allelic (p=0.46) and genotypic (p=0.78) distribution of MDM2 309 T>G polymorphism between patients and controls.
Conclusion: The results of this study indicate that polymorphisms of TP53 and MDM2 genes are unlikely to contribute to the pathogenesis of male infertility with spermatogenetic failure.
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Type of Study: Original Article |

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