Severe acute respiratory syndrome coronavirus 2 (SARS- CoV-2) that causes COVID-19 infections penetrates body cells by binding to angiotensin-converting enzyme-2 (ACE2) receptors. Evidence shows that SARS-CoV-2 can also affect the urogenital tract. Hence, it should be given serious attention when treating COVID-19-infected male patients of reproductive age group. Other viruses like HIV, mumps, papilloma and Epstein–Barr can induce viral orchitis, germ cell apoptosis, inflammation and germ cell destruction with attending infertility and tumors. The blood-testis barrier (BTB) and blood-epididymis barrier (BEB) are essential physical barricades in the male reproductive tract located between the blood vessel and seminiferous tubules in the testes. Despite the significant role of these barriers in male reproductive function, studies have shown that a wide range of viruses can still penetrate the barriers and induce testicular dysfunctions. Therefore, this mini-review highlights the role of ACE2 receptors in promoting SARS-CoV-2-induced blood-testis/epididymal barrier infiltration and testicular dysfunction.

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Although selenium is known to be essential for reproductive function, studies have indicated the adverse effect with its prolonged use. The present study investigated the duration-related effect of selenium administrations on reproductive hormones and estrous cycle indices in adult female Wistar rats exposed to a model of light pollution using altered photoperiod (AP). Ninety-six cyclic female Wistar rats displaying 4–5 days' estrous cycle length (ECL) and weighing 148–152 g were randomly divided into short and long experimental cohorts consisting of six groups each and spanning for 1 and 8 weeks, respectively. Each consisted of control, high selenium dose (HSE), low selenium dose (LSE), AP, AP + HSE, and AP + LSE. The rats were orally administered high dose (150 μg/kg) and low dose (100 μg/kg) of sodium selenite once per day. The estrous cycle indices were monitored. Plasma levels of follicle-stimulating hormone, luteinizing hormone (LH), estradiol (E), progesterone (P), prolactin, E/P ratio, and histology of ovary and uterine horn were evaluated. The statistical analysis was performed using Statistical Package for the Social Sciences. In AP rats, HSE and LSE caused no significant effect on LH, E, P, and E/P ratio, ECL, estrus interval (EI), and estrous cycle ratio (ECR). The effect of HSE and LSE on LH, E, P, E/P ratio, and ECL showed no duration-dependent increase, but there was a duration-dependent increase in EI and ECR at low dose. The study indicated that administration of HSE of selenium improved reproductive function in photo-pollution-exposed rats irrespective of the duration of treatment.

BackgroundIt is estimated that about 5–10% of women suffer from polycystic ovarian syndrome (PCOS) which is a major cause of female reproductive dysfunction. This study examined the role of quercetin on dehydroepiandrosterone (DHEA)-induced PCO in Wistar rats.MethodsTwenty-eight pre-pubertal female Wistar rats that are 21 days old weighing 16–21 g were sorted into four groups (n = 7). Group I served as control and was given distilled water only, Group II were injected with 6 mg/100 g BW of DHEA in 0.2 mL of corn oil subcutaneously, Group III received 100 mg/kg BW of quercetin orally and Group IV received 6 mg/100 g BW of DHEA in 0.2 mL of corn oil subcutaneously and 100 mg/kg BW of quercetin orally. Rats were sacrificed after 15 days by cervical dislocation method. Blood samples and ovaries were collected for hormonal, biochemical, and histopathological analysis and expressions of mRNA androgen receptor gene were determined using RT–qPCR. All data were analysed using one-way ANOVA.ResultsA significant decrease (p < 0.05) in the antioxidant and metabolic enzyme activity in the DHEA treated group was observed when compared with control. DHEA co-administration with quercetin showed a significant decrease in malondialdehyde and cytokines when compared with DHEA treated group. Also a significant increase in progesterone, metabolic and antioxidant enzyme activity was observed. The histopathology demonstrates a reduction in cystic and atretic cells, improved expression of BCl2, E-Cadherin and a decrease in Bax.ConclusionsQuercetin alleviated DHEA-induced PCO. These effects could be attributed to its antioxidant property.

Objectives: Polycystic ovary syndrome (PCOS) represents 75% of the cases of anovulatory infertility. The aim of this study was to investigate the role of aspirin on dehydroepiandrosterone (DHEA)-induced polycystic ovary syndrome in Wistar rats. Methods: Twenty eight (28) pre-pubertal female Wistar rats of 21 days old weighing 16-21 g were divided into 4 groups (7 rats/group) and treated as follows; group I received distilled water and served as Control; Group II received 6 mg/100 g body weight DHEA in 0.2 ml of oil subcutaneously to induce PCOS. Group III received 7.5 mg/ kg of aspirin orally; Group IV received 6 mg/100kg of body weight of DHEA in 0.2ml of oil subcutaneously and 7.5 mg/ kg of aspirin orally. After 15 days of administration, the rats were slaughtered by cervical dislocation. Blood samples and ovaries were collected for reproductive hormonal analysis, biochemical and histopathological analysis. The expressions of mRNA androgen receptor (AR) gene in the ovary were determined by real time reverse transcriptase polymerase chain reaction (qPCR). All the data was analyzed using one way ANOVA with the Graph pad prism software version 6. A p<0.05 was considered significant. Results: The results obtained showed that dehydroepiandrosterone treatment caused significant decrease (p<0.05) in total protein, superoxide Dismutase (SOD), glutathione-s-transferase (GST), Ca 2+ ATPase, and significant increase (p<0.05) in malondialdehyde, vascular endothelial growth factor, tumor necrosis factor and estrogen as compared to Controls. The group co-administered with DHEA and aspirin showed significant increases in SOD, GST, CAT, GSH, Progesterone, Ca 2+ ATPase, Na + ATPase, H + ATPase and significant reduction (p<0.05) in malondialdehyde, VEGF, TNF-α and estrogen as compared with the DHEA group. The histopathological analysis showed reductions in cystic fibrosis, atretic ovaries, increased expression of Bcl-2 and E-Cadherin and reduced Bax expression in the group that received Aspirin and DHEA. Conclusion: This study clearly demonstrates that Aspirin has ameliorating effects against polycystic ovary syndrome via anti-inflammatory and hormonal modulatory pathways.