Open AccessFollicle-stimulating hormone (FSH) receptor gene polymorphisms in Iraqi patients with non-obstructive azoospermia
Author(s) -
Abdul-Rahim A. Ali,
Omar F. AbdulRasheed,
Ula Al-Kawaz
Publication year - 2021
Publication title -
baghdad journal of biochemistry and applied biological sciences/baghdad journal of biochemistry and applied biological sciences
Language(s) - English
Resource type - Journals
eISSN - 2706-9915
pISSN - 2706-9907
DOI - 10.47419/bjbabs.v2i04.76
Subject(s) - azoospermia , genotype , single nucleotide polymorphism , infertility , follicle stimulating hormone receptor , follicle stimulating hormone , male infertility , allele frequency , medicine , genotype frequency , genotyping , snp , allele , biology , hormone receptor , endocrinology , luteinizing hormone , andrology , hormone , gene , genetics , pregnancy , cancer , breast cancer
Background: Follicle-stimulating hormone (FSH) is a pivotal hormone for male fertility, and its action on gonads is exerted by FSH receptors (FSHRs).Objectives: To examine whether the presence of FSHR gene single nucleotide polymorphisms (SNPs), G919A and A2039G, involved in non-obstructive azoospermia (NOA) in Iraqi infertile men.Methods: Two common SNPs, A919G and A2039G, in the FSHR gene were analyzed in 104 subjects (70 infertile patients with NOO: 33 NOA patients were not receiving treatment and 37 were on infertility treatment, and 34 normozoospermic fertile men as controls).Results: The results revealed that the homozygous wild genotype (AA) of rs6165 FSHR gene SNP was more abundant than (AG) and (GG) genotypes in both groups of infertile NOA patients with a frequency of 49% in those who untreated, 81% in patients undergoing treatment and in the control group 41%. Whereas, the highest percentage of heterozygous genotype (AG) in the fertile control group was 41% when compared to NOApatients with a genotype frequency of 24% (for those who untreated) and 11% (for patients on treatment), respectively; with (A) allele frequency of 86% and the observed frequency of (G) allele was only 14% in the patients’ group as compared to that of controls that were (65 %) and (35 %), respectively. The rs6166 genotyping revealed that the homozygous wild genotype (GG) of FSHR gene was more abundant than (AG) and (AA) genotypes in NOA patients receiving infertility treatment with a frequency of (68%), in NOA patients who didn’t receive treatment 49%, while the lowest frequency was detected in the healthy fertile control group (47%).Conclusions: These results support the evidence that rs6165 and rs6166, FSHR SNPs, might be involved in the pathogenesis and protection against NOA, respectively.