This study aimed to assess the association of oestrogen receptor alpha (ER-α) gene polymorphisms and semen variables in infertile oligoasthenoteratozoospermic (OAT) men. In all, 141 men were grouped into fertile men (n = 60) and infertile OAT men (n = 81). They were subjected to assessment of semen analysis, acrosin activity, serum reproductive hormones and genotyping of ER-α gene. Frequencies of p and x alleles in ER-α gene PvuII and XbaI polymorphisms were more prevalent among fertile men compared with infertile OAT men. Presence of P and X alleles was associated with increased incidence of male infertility for genotypes PP, XX compared with genotypes pp and xx (OR = 2.8; 95% CI: 2.36-6.97; P = 0.001 and OR = 4.1, 95% CI: 1.49-11.39; P = 0.001, respectively). The mean of semen variables and sperm acrosin activity were significantly higher in cases associated with pp than PP and in xx than XX genotypes of ER-α gene. Mean levels of all serum reproductive hormones demonstrated nonsignificant differences in different ER-α genotypes except oestrogen that was elevated in PP and XX ER-α gene genotypes. It is concluded that as oestrogen is concerned in male gamete maturation, ER-α gene polymorphisms might play a role in the pathophysiology of male infertility.

BackgroundThis is the first study to investigate spermatozoal cell death-inducing DNA fragmentation factor-α-like effector A (CIDEA) gene expression and DNA fragmentations in the spermatozoa of men diagnosed with metabolic syndrome (MS) who have normal seminograms with unexplained infertility, and to correlate these parameters with seminal glucose concentration.MethodsThis study included 120 participants: 75 male subjects with MS (38 fertile and 37 infertile), and a control group of 45 fertile males without MS. HOMA-IR, semen analysis, and biochemical measurement of seminal plasma insulin and glucose levels were carried out. Spermatozoal insulin gene and CIDEA gene expressions were performed by the RT-PCR method. The percentage of spermatozoal DNA fragmentation was also estimated.ResultsThe spermatozoal insulin and CIDEA gene expression, as well as the DNA fragmentation, were significantly higher in the infertile MS group than in the fertile MS group, and significantly higher in both the MS groups than in the control group. Seminal glucose concentration showed significant positive correlations with seminal insulin level, spermatozoa insulin, CIDEA gene expression, and DNA fragmentation. Moreover, there was a positive correlation between spermatozoa CIDEA gene expression and DNA fragmentation.ConclusionsIt can be concluded that MS may affect male fertility at the molecular level, through its possible inducing effect of spermatozoa CIDEA and insulin gene expression, DNA fragmentation, and increased seminal glucose.

Cypermethrin, a type II synthetic pyrethroid pesticide, is widely used in pest control programmes in agriculture and public health. This study aimed to assess the potential effect of cypermethrin on human spermatozoa and the possible ameliorative effects of vitamins C and E. Semen samples of 20 healthy normozoospermic men were divided into six aliquots at room temperature. The first aliquot served as control not exposed to treatments, and the second was incubated with 20 mm vit. C and 2 mm vit. E where the third one was exposed to 10 μm cypermethrin for 6 h. The other three aliquots were incubated with vit. C, vit. E and both vitamins for 30 min before cypermethrin exposure. Semen aliquots were analysed for sperm motility, sperm viability, hypo-osmotic swelling test and modified alkaline comet assay. The results demonstrated a significant decrease in sperm motion, sperm function and increased sperm DNA damage in the cypermethrin group. Addition of vitamins C and E alone/combined led to significant improvement in sperm motion, sperm function and DNA damage, being maximal with both vitamins together. It is concluded that in vitro cypermethrin can alter sperm function and induce DNA damage in spermatozoa, which is improved after using vitamins C and E.

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Background The expression signature of deregulated long non-coding RNAs (lncRNAs) and related genetic variants is implicated in every stage of tumorigenesis, progression, and recurrence. This study aimed to explore the association of lncRNA cyclin-dependent kinase inhibitor 2B antisense RNA 1 (CDKN2B-AS1) gene expression and the rs2383207A>G intronic variant with breast cancer (BC) risk and prognosis and to verify the molecular role and networks of this lncRNA in BC by bioinformatics gene analysis. Methods Serum CDKN2B-AS1 relative expression and rs2383207 genotypes were determined in 214 unrelated women (104 primary BC and 110 controls) using real-time PCR. Sixteen BC studies from The Cancer Genome Atlas (TCGA) including 8925 patients were also retrieved for validation of results. Results CDKN2B-AS1 serum levels were upregulated in the BC patients relative to controls. A/A genotype carriers were three times more likely to develop BC under homozygous (OR = 3.27, 95% CI 1.20–8.88, P = 0.044) and recessive (OR = 3.17, 95% CI 1.20–8.34, P = 0.013) models. G/G homozygous patients had a higher expression level [median and quartile values were 3.14 (1.52–4.25)] than A/G [1.42 (0.93–2.35)] and A/A [1.62 (1.33–2.51)] cohorts (P = 0.006). The Kaplan–Meier curve also revealed a higher mean survival duration of G/G cohorts (20.6 months) compared to their counterparts (A/A: 15.8 and A/G: 17.2 months) (P < 0.001). Consistently, BC data sets revealed better survival in cohorts with high expression levels (P = 0.003). Principal component analysis (PCA) showed a deviation of patients who had shorter survival towards A/A and A/G genotypes, multiple lesions, advanced stage, lymphovascular invasion, and HER2+ receptor staining. Ingenuity Pathway Analysis (IPA) showed key genes highly enriched in BC with CDKN2B-AS1. Conclusions The findings support the putative role of CDKN2B-AS1 as an epigenetic marker in BC and open a new avenue for its potential use as a therapeutic molecular target in this type of cancer.

Prostate cancer is one of the most common cancers and the second cause of cancer-related deaths among men. Metals are recognized as chemical carcinogens where chronic exposures to such metals are implicated in the development of cancer, including prostate cancer. This in vitro study demonstrates the relative death sensitivity of prostatic (RWPE-1) cells to arsenic (As), cadmium (Cd), and chromium (Cr) as environmental pollutants through its apoptotic effects and the effect of these chemicals on prostate-specific antigen (PSA) gene expression as a marker for their carcinogecity. RWPE-1 cells were divided into three groups that were treated with As, Cd, and Cr in three replicates, at three different concentrations for each metal for 48 h. A control group consisted of untreated RWPE1 cells was used. Apoptosis was assessed using comet assay and caspase 3 gene expression; meanwhile, PSA gene expression was evaluated by semiqualitative real-time PCR (RT-PCR). One of the novel findings of this study is that arsenic and cadmium at low concentrations decreased apoptosis of RWPE-1 cells in a concentration-dependent manner while chromium induced significant concentration-dependent increase in apoptosis. Yet, at the highest concentrations, apoptosis was relatively more induced by all chemicals. Arsenic was the most chemical inhibiting apoptosis in RWPE-1 cells at low concentration. While at the moderate and highest concentrations, cadmium was the most inhibiting chemical of RWPE-1 cells' apoptosis. No distinct differences between treated and untreated cells for PSA gene expression were observed. It can be concluded that As and Cd, at low concentrations, can reduce apoptosis of prostatic cells in a concentration-dependent manner while chromium induced it; however, all metal salts used in this study did not induce PSA gene expression.

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