Objective Junctional proteins are the most important component of the blood-testis barrier and maintaining the integrity of this barrier is essential for spermatogenesis and male fertility. The present study elucidated the effect of SARS-CoV-2 infection on the blood–testis barrier (BTB) in patients who died from severe acute respiratory syndrome coronavirus 2 (COVID-19) complications. Methods In this study, lung and testis tissue was collected from autopsies of COVID-19 positive ( n = 10) and negative men ( n = 10) and was taken for stereology, immunocytochemistry, and RNA extraction. Results Evaluation of the lung tissue showed that the SARS-CoV-2 infection caused extensive damage to the lung tissue and also increases inflammation in testicular tissue and destruction of the testicular blood barrier. Autopsied testicular specimens of COVID-19 showed that COVID-19 infection significantly changes the spatial arrangement of testicular cells and notably decreased the number of Sertoli cells. Moreover, the immunohistochemistry results showed a significant reduction in the protein expression of occluding, claudin-11, and connexin-43 in the COVID-19 group. In addition, we also observed a remarkable enhancement in protein expression of CD68 in the testes of the COVID-19 group in comparison with the control group. Furthermore, the result showed that the expression of TNF-α, IL1β, and IL6 was significantly increased in COVID-19 cases as well as the expression of occludin, claudin-11, and connexin-43 was decreased in COVID-19 cases. Conclusions Overall, the present study demonstrated that SARS-CoV-2 could induce the up-regulation of the pro-inflammatory cytokine and down-regulation of junctional proteins of the BTB, which can disrupt BTB and ultimately impair spermatogenesis.

The current study was conducted to assess the relationship between testicular cells in spermatogenesis, through which the production of healthy and mature sperm is essential. However, it seems necessary to obtain more information about the three‐dimensional pattern of the testis cells arrangement, which is directly related to the function of the testis after induction of diabetes. Twelve adult mice (28‐30 g) were assigned into two experimental groups: (1) control and (2) diabetic (40 mg/kg STZ). The epididymal sperm collected from the tail of the epididymis and testes samples were taken for stereology, immunocytochemistry and RNA extraction. Our data showed that diabetes could notably decrease the number of testicular cells, together with a reduction of total sperm count. In addition, the results from the second‐order stereology indicated the significant changes in the spatial arrangement of Sertoli cells and spermatogonial cells in the diabetic groups, in comparison with the control (P < .05). Moreover, the immunohistochemistry results showed a significant reduction in Sex‐determining Region Y (SRY) box 9 gene (SOX9), vimentin, occludin, and connexin‐43 positive cells in the diabetic groups compared with the control (P < .05). Furthermore, our data showed that the expression of steroidogenic acute regulatory protein steroidogenic acute regulatory protein (StAR) and peripheral benzodiazepine receptor peripheral benzodiazepine receptor (PBR) was significantly reduced in the diabetic groups, in comparison with the control (P < .05). These findings suggest that structural and functional changes of testis cells after induction of diabetes cause the alterations in the spatial arrangement of Sertoli and spermatogonial cells, ultimately influencing the normal spermatogenesis in mice.

Animal models of azoospermia are very applicable when evaluating new treatment methods for research purposes. The present study aimed to compare azoospermia induction in mice using busulfan or hyperthermia. To do this, about 36 adult male mice (28–30 g) were included into three experimental groups randomly (n = 12): control, busulfan (injected by a single dose of 40 mg/kg busulfan intraperitoneally) and hyperthermia (exposure to a temperature of 43°C every other day for 5 weeks). Animals were preserved for 35 and 70 days following interventions and then were sacrificed for further evaluations. After 35 days, busulfan and hyperthermia groups revealed a significant decrease in the sperm count and weight of testis compared to the control group (p < .0001). In addition, after 70 days, sperm count and weight of testis in group busulfan showed a significant increase compared to group hyperthermia (p < .01). No significant difference was observed regarding the mortality of mice between busulfan and hyperthermia groups. In group busulfan, degenerative changes in the germinal epithelium were detected in some tubules, although in group hyperthermia, degenerative changes and complete depletion of all tubules were observed. Continuous hyperthermia is a more effective method in the induction of as animal model of azoospermia compared to the busulfan.

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Insulin-like peptide 3 (INSL3) belongs to the large family of peptide hormones called 'insulin relaxin' (Shabanpoor et al., 2011). INSL3 is secreted by testicular Leydig cells as a marker for the complete differentiation of adult Leydig cells in men and all mammalians that mediates the descent of the testicle during the embryonic period and, as a paracrine factor, mediates gonadotropin activity in adults (Anand-Ivell et al., 2006; Muda et al., 2005). This hormone binds to the RXPF2 receptor and plays an important role in regulating spermatogenesis in adolescents. INSL3 is a peptide hormone that is known as a significant marker for the function and amount of Leydig cells and steroid capacity, and despite testicular steroids, it is free of the HPG axis effects (Anand-Ivell, Heng, Hafen, Setchell, & Ivell, 2009). Analysis of different sections of the semen fluid shows a high concentration of INSL3 in the interstitial cells. It passes through the blood-testis barrier to enter the seminiferous, testis and epididymis, and if its concentration is sufficient, RXFP2 as its specific receptor can be discovered on the post-mitotic cells and also in the epididymis. This hormone is a G protein of class C that binds to the RXFP2 receptor and generates Gs-dependent signals to produce cAMP. The cAMP activates protein kinase A (PKA), which in turn can inhibit Bid (BH3 interacting domain death agonist), a proapoptotic protein. Therefore, this hormone has an

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