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Micro-organisms are tightly integrated into host-microbiota ecosystem. Microbiota of human semen has been studied so far mostly in case of infertility or prostatitis. We aimed to reveal possible impact of sexual debut on seminal microbiota in healthy young men. The study group included 68 young healthy men, of them 12 men without sexual experience, 11 men with single lifetime sexual partner and 45 men with multiple lifetime sexual partners. Basic semen parameters were similar for all subgroups, and no correlation between sexual experience and WBC counts in semen was found. A man could harbour one to nine different bacteria in his semen; the total concentration of bacteria ranged from 2.3 to 7.3 log10 CFU/mL of semen. Lower total bacterial concentration and lower bacterial diversity was observed in men without sexual experience than in sexually experienced men (p < 0.05), with significant positive correlation between these two parameters (r = 0.54; p < 0.0001). In conclusion, the sexual debut is associated with the enrichment of seminal microbiota but not with the influx of WBC or changes in basic seminal parameters.

We investigated the prevalence of oxidative stress in male partners of infertile couples displaying different inflammation patterns in their genital tract and/or oligospermia. The levels of acknowledged oxidative stress markers (8-isoprostanes [8-EPI], diene conjugates, reactive oxygen species-total antioxidant capacity [ROS-TAC] score) were elevated in both leukocytospermic men and subjects whose inflammation was limited only to expressed prostatic secretion and/or post-massage urine. Oligospermic men with severe inflammation were different from oligospermic men who had no inflammation at all - the former had elevated 8-EPI, diene conjugates and ROS-TAC score when compared to the latter indicating that inflammation has substantially more significant impact on oxidative stress markers than oligospermia status. At the same time nitric oxide (NO) and hydrogen peroxide (H2 O2 ) levels were significantly increased not only in the men with severe inflammation but also in men with borderline inflammation in their genital tact and in men having non-inflammatory oligospermia. NO, H2 O2 and 8-EPI were negatively correlated with per cent of normal sperms, and NO and H2 O2 showed negative correlation also with sperm count. We can conclude that in men presenting with couple infertility the acknowledged oxidative stress markers are substantially associated with markers of inflammation in genital tract while NO and H2 O2 display high levels also in patients with mild inflammation and non-inflammatory oligospermia.

The purpose of the current study was to evaluate the importance of androgen receptor (AR) gene haplotypes and polymorphic CAG/GGN microsatellites in the aetiology of male infertility. We genotyped six haplotype-tagging single nucleotide polymorphisms and CAG/GGN microsatellites of the AR gene in 112 infertile and 212 control Estonian men. A total of 13 AR haplotypes (HAP1-13) were identified, among which HAP4 was found to confer increased risk for male infertility (OR = 5.15, 95% CI = 1.75-15.15, p = 0.003). However, infertile patients and controls had similar lengths and distributions of both AR CAG (mean +/- SD number of repeats 21.1 +/- 2.5 vs. 21.2 +/- 2.3, respectively) and GGN (mean +/- SD number of repeats 22.5 +/- 1.5 vs. 22.4 +/- 1.9, respectively) repeats. In addition, HAP2 was associated with more CAG repeats (r = 1.17, p = 0.033) and HAP3 with fewer CAG repeats (r = -2.93, p < 0.001) than the major haplotype HAP1. HAP3 and HAP4 were associated with more GGN repeats (r = 1.35, p = 0.001 and r = 1.36, p = 0.002, respectively) than HAP1. In conclusion, our results implicated the AR-HAP4 gene haplotype in increased risk for male infertility, while no association was found between AR CAG/GGN microsatellites and impaired spermatogenesis.