In the vast majority of instances, the causes of male infertility are unknown, although scientists have lately attempted to correlate epigenetics to infertility mechanisms. DNA methylation is an important biological modification that gives phenotypic diversity and adaptability. The aim of this study was whether the methylation status of the methylenetetrahydrofolate reductase (MTHFR) gene promoter in Iraqi men’s spermatozoa is correlated with male infertility. Semen samples were collected from 100 infertile and healthy fertile men. Divided into 4 groups included 25 subjects of healthy fertile men as a control group(C) and infertile groups, which divided into (3) subgroups: Asthenozoospermia (A) (n=25), Oligoasthenozoospermia (OA) (n = 25) and severe Oligoasthenoteratozoospermia (SOA) (n =25). Sperm DNAs and RNAs from all samples were isolated; followed by sperm-specific methylation detection using the EpiJET DNA Methylation Analysis Kit, which is simple digestion was performed with two restriction enzymes (MspI/HpaII). The methylation percentage (mean ± SD) of the MTHFR gene promoter was quantified in each studied group as follow:[ (C) ( 1.76±0.46) (A) (3.59±0.89), (OA) (26.10±4.14) and (SOA)( 29.13±4.88)]. The percentage of MTHFR promoter methylation infertile men was significantly higher than that in the healthy control group (p = 0.00). Methylation level was determined via receiver operator characteristic (ROC) analysis as the cut-off values of each infertile subgroup were as follows: [(A) (2.43%), (OA) (7.59%) and (SOA) (10.96%)]. According to WHO guidelines, sperm concentration, progressive motility and morphologically normal sperm were determining (WHO, 2010). The qRT-PCR was used to evaluate MTHFR gene expression in all sperm samples. The results revealed a substantial reduction in fold expression (2–∆∆Ct) in all infertile groups when compared to the control g roup, with a P-value (0.002). In this research findings suggest that epigenetic impairment (hypermethylation) of the MTHFR promoter region in sperm DNA from OA and SOA patients may increase male infertility risk.
Introduction and Aim: Idiopathic infertility accounts for at least 30% of all cases of infertility, and oxidative stress has been identified as a novel developing factor in idiopathic male infertility. Oxidative stress occurs when antioxidant defense mechanisms are outmatched by the creation of reactive oxygen species (ROS). The purpose of this research was to examine the impact of enzymatic antioxidants (catalase and superoxide dismutase; CAT and SOD) on sperm DNA fragmentation and associated sperm alteration in Iraqi males with idiopathic infertility. Materials and Methods: One hundred infertile guys (50 oligozoospermia and 50 asthenozoospermia) and 50 normospermia) had their superoxide dismutase, catalase, and malondialdehyde levels tested. Results: Our study showed that the sperm DNA fragmentation index (DFI) of patients who suffered from oligozoospermia and asthenozoospermia was higher than that of individuals who suffered from normozoospermia. Seminal plasma SOD and MDA levels were higher in infertile participants compared to controls (P < 0.001) .The concentration of CAT in the seminal plasma of oligozoospermic and asthenozoospermic men was not significantly different from that of normospermic men. DFI correlated negatively with seminal antioxidant status (SOD, CAT) and MDA, while CAT correlated positively with SOD and MDA. Conclusion: The impacts of oxidative stress include the breakage of DNA in sperm, with lipid peroxidation being the primary cause of idiopathic male infertility. This is associated with less successful fertility outcomes in couples. According to the findings that we obtained, the sperm DNA fragmentation index as well as malondialdehyde are substantially associated with the quality of the sperm.
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