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International Journal of Reproductive BioMedicine
Research and Clinical Center for Infertility, Shahid Sadoughi University of Medical Sciences of Yazd
ISSN: 1680-6433
EISSN: 2008-2177
Vol. 16, No. 8, 2018, pp. 491-496
Bioline Code: rm18058
Full paper language: English
Document type: Research Article
Document available free of charge

International Journal of Reproductive BioMedicine, Vol. 16, No. 8, 2018, pp. 491-496

 en The frequency of TP53 R72P and MDM2 309T>G polymorphisms in Iranian infertile men with spermatogenetic failure: A case-control study
Abadi, Zeinab Ebrahim; Bami, Maryam Khademi; Golzadeh, Maryam; Kalantar, Seyed Mehdi & Sheikhha, Mohammad Hasan


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 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.

Apoptosis; Male infertility; MDM2; TP53; Polymorphisms.

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