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.

To evaluate the incidence of apoptosis within the testes of patients who died from severe acute respiratory syndrome coronavirus 2 (COVID-19) complications, testis tissue was collected from autopsies of COVID-19 positive (n = 6) and negative men (n = 6). They were then taken for histopathological experiments, and RNA extraction, to examine the expression of angiotensin-converting enzyme 2 (ACE2), transmembrane protease, serine 2 (TMPRSS2), BAX, BCL2 and Caspase3 genes. Reactive oxygen species (ROS) production and glutathione disulfide (GSH) activity were also thoroughly examined. Autopsied testicular specimens of COVID-19 showed that COVID-19 infection significantly decreased the seminiferous tubule length, interstitial tissue and seminiferous tubule volume, as well as the number of testicular cells. An analysis of the results showed that the Johnsen expressed a reduction in the COVID-19 group when compared to the control group. Our data showed that the expression of ACE2, BAX and Caspase3 were remarkably increased as well as a decrease in the expression of BCL2 in COVID-19 cases. Although, no significant difference was found for TMPRSS2. Furthermore, the results signified an increase in the formation of ROS and suppression of the GSH activity as oxidative stress biomarkers. The results of immunohistochemistry and TUNEL assay showed that the expression of ACE2 and the number of apoptotic cells significantly increased in the COVID-19 group. Overall, this study suggests that COVID-19 infection causes spermatogenesis disruption, probably through the oxidative stress pathway and subsequently induces apoptosis.

Background The aim of this study is to investigate the effects of pravastatin (PS) against doxorubicin (DOX)-induced testicular toxicity. Methods A total of 24 healthy male Sprague-Dawley rats were equally divided into four groups. Group I received normal saline, Group II received PS (20 mg/kg b.w.) by gavage, Group III was treated with DOX alone (15 mg/kg b.w., i.p.) and Group IV received the combination of DOX and PS. Results After 8 weeks, the results displayed that DOX caused a decrease in testicular volume and index, epididymal sperm count, seminiferous tubule diameter and germinal epithelium. DOX also reduced the number of spermatogonia, spermatoctyes and Sertoli cells as well as increased the lumen diameter of seminiferous tubules (p<0.05) and the incidence of histopathological changes of the testis. Moreover, elevated malondialdehyde (MDA) levels and declined glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities were observed (p<0.05). On the contrary, PS treatment significantly ameliorated nearly all of these abnormalities (p<0.05). Conclusions PS protects against DOX-induced testicular toxicity in rats, which is likely via the inhibition of oxidative stress and the increase of antioxidant enzyme activity.

There are two types of cell death, one is accidental cell death (ACD) and the other is regulated cell death (RCD). ACD is a biologically uncontrollable process caused by disease, while RCD includes welltuned and structured signalling cascades defined as effective molecular mechanisms (Tang et al., 2019). The scientific observation in RCD research started when researchers introduced and defined the terms apoptosis, autophagy, necroptosis, ferroptosis and pyroptosis. Cell death may occur in response to oxidative stress, which activates signalling pathways in multiple forms and can therefore contribute to human diseases such as cancer, tissue damage, autoimmune and inflammatory diseases (Tang et al., 2019). Apoptosis can activate caspase nucleus oligo DNA fragmentation eventually

Background: Rutin (quercetin-3-rhamnosyl-glucoside), a flavonoid, is derived from plants and has antioxidant properties. Objectives: This study aimed to evaluate the effect of different concentrations of rutin on mouse ovary heterotopic allotransplantation. Methods: The present animal experimental study was conducted on 40 female adult Balb/c mice weighing 30 ± 5 g at the Jundisha