TY - JOUR AU - N. Kadhum, Nada AU - A. Abdul Hassan, Ismail PY - 2023/05/26 Y2 - 2024/03/29 TI - The association of FSHR gene polymorphism (rs6166) with the risk of oligoasthenozoospermia incidence in Iraqi patients JF - Biomedicine JA - Biomedicine VL - 43 IS - 02 SE - Original Research Articles DO - 10.51248/.v43i02.2683 UR - https://biomedicineonline.org/index.php/home/article/view/2683 SP - 769-774 AB - <p><strong>Introduction and Aim:</strong> Male infertility is a complicated multifactorial pathological disease with widely disparate symptoms, ranging from the complete lack of spermatozoa to alterations in sperm quality. Genetic factors account for at least 15% of male infertility. An increasing number of gene polymorphisms have been proposed to alter the efficacy of spermatogenesis based on association studies.  The goal of this study is to investigate whether the genotype of the <em>FSHR</em> gene associated SNP rs6166 is associated with Iraqi men's risk for oligoasthenozoospermia.</p><p> </p><p><strong>Materials and Methods:</strong> SNP rs6166 was genotyped by Real-Time Polymerase Chain Reaction (RT-PCR).</p><p><strong> </strong></p><p><strong>Results:</strong> In accordance with<em> FSHR</em> genes rs6166 G&gt;A (Ser 680Asn) SNP, the frequency of homozygous AA in fertile men was significantly lower than in oligoasthenozoospermic patients. By contrast, there was a notable increase in the occurrence of homozygous GG genotype among fertile males when compared to those diagnosed with oligoasthenozoospermia. There were no statistically significant variations in the frequency percentage of heterozygous GA genotypes between the group of fertile male participants and the group of oligoasthenozoospermic patients.</p><p> </p><p><strong>Conclusion:</strong> The results showed a significant decrease in testosterone concentration in oligoasthenozoospermic patients. The <em>FSHR</em> rs6166 polymorphism (AA) was found to contribute to individual susceptibility to oligoasthenozoospermia in a group of Iraqi patients.</p> ER -