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![Anatomy of healthy adult seminiferous tubules [26] and spermatogenesis in healthy and heat-stress exposed mice [27]. (a) Spermatogenesis takes place in the seminiferous tubules of adult testes. The magnification of a seminiferous tubule wedge highlights various cell types created in the differentiation of primordial germ cells to mature sperm. (b) Testicular structure in controlled male mice. (c) Complete spermatogenesis occurs in the seminiferous tubules. (d) Testicular structure in heat-stress exposed male mice. (e) Spermatogenesis arrest occurs in the seminiferous tubules from heat-stress exposed mice; Le: Leydig cells, Se: Sertoli cells, Sg: spermatogonia, Sc: spermatocytes, rs: round spermatids, es: elongating spermatids, S: spermatozoa.](publication/355507783/figure/fig1/AS:1082895758299136@1635193876138/Anatomy-of-healthy-adult-seminiferous-tubules-26-and-spermatogenesis-in-healthy-and.png)
Anatomy of healthy adult seminiferous tubules [26] and spermatogenesis in healthy and heat-stress exposed mice [27]. (a) Spermatogenesis takes place in the seminiferous tubules of adult testes. The magnification of a seminiferous tubule wedge highlights various cell types created in the differentiation of primordial germ cells to mature sperm. (b) Testicular structure in controlled male mice. (c) Complete spermatogenesis occurs in the seminiferous tubules. (d) Testicular structure in heat-stress exposed male mice. (e) Spermatogenesis arrest occurs in the seminiferous tubules from heat-stress exposed mice; Le: Leydig cells, Se: Sertoli cells, Sg: spermatogonia, Sc: spermatocytes, rs: round spermatids, es: elongating spermatids, S: spermatozoa.
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![Figure 1. Anatomy of healthy adult seminiferous tubules [26] and...](publication/355507783/figure/fig1/AS:1082895758299136@1635193876138/Anatomy-of-healthy-adult-seminiferous-tubules-26-and-spermatogenesis-in-healthy-and_Q320.jpg)
Chronic heat stress-induced testicular damage and function therefore adversely affect their reproduction. Some research shows that heat stress has a negative effect on histopathological features of testicular tissue structure and spermatogenesis. An animal model was used to evaluate the effect of heat stress on testicular histology changes and sper...
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Purpose
Rapid and easy detection of spermatogonial stem/progenitor cells (SSPCs) is crucial for clinicians dealing with male infertility caused by prepubertal testicular damage. Deep learning (DL) methods may offer visual tools for tracking SSPCs on testicular strips of prepubertal animal models. The purpose of this study is to detect and count the...
Citations
... After fixation, samples were prepared using the standard paraffin embedding method, then sectioned into 4 µm thick sections and finally stained with Hematoxylin and eosin (H&E) [20]. Semiquantitative scoring of the degree of testicular damage and spermatogenesis efficiency were assessed using Cosentino's scoring system [21] and the mean Johnsen testicular biopsy score (MJTBS) [22], respectively. The testis is divided into 4 categories in Cosentino's grading system. ...
One of the most significant chemotherapeutic side effects of cisplatin (Cis) that limits its use and efficacy is testicular toxicity. Thus, the objective of the present study was to investigate the possible ameliorative effect of Fenofibrate (Fen), Diosmetin (D), and their combination against cis-mediated testicular damage. Fifty-four adult male albino rats were randomly allocated into nine groups (6 rats each): Control group, Fen (100 mg/kg), D20 (20 mg/kg), D40 (40 mg/kg), Cis group (7 mg/kg), Cis +Fen group (7 mg/kg+100 mg/kg), Cis+D20 group (7 mg/kg+20 mg/kg), Cis+D40 group (7 mg/kg+40 mg/kg), Cis+Fen+D40 treated group (7 mg/kg+100 mg/kg+40 mg/kg). Relative testicular weight, epididymal sperm count and viability, serum testosterone level, testicular oxidative stress indices, mRNA expression of peroxisome proliferator-activated receptor alpha (PPAR-α), nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1), histopathological, and immunohistochemical alterations were assessed. Our results revealed that cis administration induced testicular oxidative and inflammatory damage as indicated by a substantial reduction in relative testicular weight, sperm parameters, serum testosterone levels, the antioxidant enzyme activity of catalase, and Johnson's histopathological score, PPAR-α/NRF-2/HO-1 and proliferating cell nuclear antigen (PCNA) immunoexpression with marked increment in malondialdehyde (MDA), Cosentino's score, nuclear factor kappa B (NF-κβ p65), interleukin (IL)- 1β and caspase 3 in testicular tissue. Interestingly, Fen and D diminished the harmful effects of cis on testes via upregulation of the antioxidant activities and downregulation of lipid peroxidation, apoptosis, and inflammation. Moreover, the combination therapy Fen/D40 also exhibited a more pronounced enhancement of previous markers than either treatment alone. In conclusion, because of their antioxidant, anti-inflammatory, and anti-apoptotic properties, cotreatment with Fen or D or their combination could be beneficial in reducing the harmful impacts of cis on testicular tissue, particularly in patients that receive cis chemotherapy.
... The testicular structure of a heat-stressed male mice model had a disorganized germinal epithelium, with marked sloughing or obliteration of the lumen and the absence of many types of sperm cells [76]. A reduced number or loss of germ cells, such as spermatocytes and spermatids, has been reported to be due to the high sensitivity to heat in rams and adult male mice [71,77]. ...
... Lymphoid depletion [21] Thinner thymic cortex [59] Increased heterophils, apoptosis histiocytes and cell depletion [60] Reduced lobule and lymphoid follicle [61] Severe necrosis, mononuclear inflammatory cell infiltration [41] Testes Cattle Thickened lining, enlarged lumen, impaired cellular elements, cavities in tubules with narrow spermatogenous epithelium and less sperms [72] Buffalo No significant changes [74] Necrotic desquamated seminiferous tubular lumen cells [73] In epididymis-epithelial cell vacuolisation, desquamated and necrotic with pyknosis, presence of spermatozoa and cytoplasmic hyper eosinophilia [73] Sheep Germ line cell degeneration [67] Vacuolation, intertubular multinucleate giant cells, thickened basement membrane with interstitial fibrosis and increased peri-tubular connective tissue [68] Goat Epithelial desquamation, fatty degeneration, necrosis and apoptosis, syncytial giant cells and macrophages, sertoli cell vacuolization and thickening of basement membrane [70] Pig Reduced seminiferous tubular epithelium height with vacuoles, decreased primary spermatocytes and round spermatids [75] Chicken Abnormal distribution of spermatogenic cell layers and absence of spermatids [63] Mice Disorganized epithelium and sloughing of lumen with absence of sperm cells [76] Thin germinal epthelium, hemorrhage, decreased sperm count, tubular necrosis, degeneration of seminiferous tubule lumen [69] Ovary Cattle Reduced follicle size [89] Buffalo Degenerated oocytes [84] Goat Abnormal antral follicle, oocyte degeneration and disorganized cumulus cells [79] Pig ...
Heat stress causes functional and metabolic alterations in different cells and tissues. There are several pathomorphological changes and biomarkers associated with head load in adaptive and productive organs of livestock. Heat stress-induced histopathological alterations in livestock were categorized as degenerative changes (fatty degeneration, steatosis, hydropic degeneration), necrosis (pyknosis, fibrosis), circulatory disturbances (hyperemia, edema, hemorrhage, congestion, thrombosis, ischemia), growth disturbances (hyperplasia, atrophy) and focal/diffuse inflammation (vascular changes, exudation). Upon immunohistochemical analysis, the biomarkers identified in growth-related organs were HSP70, HSP60, GABA, GABAAR, GABABR, HSP90, GnRH, LH, FSH, m6A, Nrf2, and C/EBPβ. The biomarkers in the reproductive organs were HSP70, Bax, Bcl-2, GABA, GABAAR, GABABR, Caspase-3, HSP90, HSPB9, HSPB10, HSF1, HSP40, T, E2, Cyt-C, CAT, BCL2L1, and VEGF. The identified biomarkers in the immune organs were CD3+ T cells, CD4+ T cells, CD8+ T cells, HSP70, and Bcl-2. All these biomarkers could serve as reliable variables in heat stress assessment in livestock. Further, HSP70, HSP90, HSP60, NPY, HSP27, Bcl-2, NF-κB, AQP2, Insulin, CD3+ T cells, CD4+ T cells, CD172a, EGF, AQP1, AQP3, AQP4, AQP5, CRYAB, GHR, 5-HT, CCK, and GLP-1 are heat stress-related biomarkers in adaptive organs that help in assessing the climate resilience of a livestock species and improving understanding about adaptive mechanisms. Among these biomarkers, HSP70 was established to be the ideal cellular biomarker for scaling heat response in livestock. Thus, examining heat-stressed organ histopathology and identifying cellular markers by immunohistochemistry may lay the foundation for screening climate-resilient livestock breeds in the challenging climatic scenario. Further, such an approach could help in developing concepts to combat the detrimental consequences of heat stress to ensure sustainability in livestock production.
Background
The role of SARS-CoV-2 in the pathogenesis of testicular damage is uncertain.
Methods
We investigated the virological, pathological, and immunological changes in testes of hamsters challenged by SARS-CoV-2 wild-type and its variants by intranasal or direct testicular inoculation using influenza virus A(H1N1)pdm09 as control.
Results
Besides self-limiting respiratory tract infection, intranasal SARS-CoV-2 challenge caused acute decrease in sperm count, and serum testosterone and inhibin B at 4 to 7 days post-infection (dpi), and subsequently reduced testicular size and weight, and serum sex hormone level at 42 to 120 dpi. Acute histopathological damage with varying degree of testicular inflammation, haemorrhage, and necrosis, degeneration of seminiferous tubules and disruption of orderly spermatogenesis were seen with increasing virus inoculum. Degeneration and necrosis of Sertoli and Leydig cells were found. Though viral loads and SARS-CoV-2 nucleocapid (N) protein expression were markedly lower in testicular than lung tissues, direct intra-testicular injection showed N expressing interstitial cells and epididymal epithelial cells. Control intranasal or intra-testicular challenge by A(H1N1)pdm09 showed no testicular infection or damage. From 7 to 120 dpi, degeneration and apoptosis of seminiferous tubules, immune complex deposition and depletion of spermatogenic cell and spermatozoa persisted. Intranasal challenge with Omicron and Delta variants could also induce similar testicular changes. These testicular damages can be prevented by vaccination.
Conclusions
SARS-CoV-2 can cause acute testicular damage with subsequent chronic asymmetric testicular atrophy and associated hormonal changes despite a self-limiting pneumonia in hamsters. Awareness of possible hypogonadism and subfertility is important in managing convalescent COVID-19 males.
