ABSTRACT
An experimental ischemia (EI)-induced mouse model was used to analyze pathological and biochemical alterations in testes. Initial morphological changes were observed in Sertoli cells of EI testes at the light microscopic level. Examination of the ultrastructure using transmission electron microscopy confirmed that Sertoli cells were partially detached from the basement membrane of the seminiferous epithelium and that the cell membranes of adjacent Sertoli cells were not joined. The functional integrity of the blood-testis barrier (BTB) was assessed using the lanthanum tracer technique. Lanthanum had penetrated into the spaces between adjacent Sertoli cells in the adluminal compartment up to the lumen of the seminiferous epithelium in EI testes. Proteome analysis showed that the expression of heat shock protein (HSP) 70 was significantly upregulated in EI testes. Western blot analysis confirmed that the expression of HSP70 increased in a time-dependent manner after the EI procedure. HSP70 immunostaining was observed in spermatocytes and in round and elongated spermatids in EI testes. Our results suggest that a change in the junctions between adjacent Sertoli cells on the basal compartment is involved in the BTB disruption in EI testes. Therefore, male infertility caused by the BTB disruption could be associated with heat stress induced by ischemia.
Subject(s)
Blood-Testis Barrier/pathology , Disease Models, Animal , Intercellular Junctions/pathology , Ischemia/pathology , Oligospermia/etiology , Sertoli Cells/pathology , Testis/blood supply , Animals , Blood-Testis Barrier/metabolism , Blood-Testis Barrier/ultrastructure , Extracellular Space/metabolism , HSP70 Heat-Shock Proteins/chemistry , HSP70 Heat-Shock Proteins/metabolism , HSP72 Heat-Shock Proteins/chemistry , HSP72 Heat-Shock Proteins/metabolism , Immunohistochemistry , Intercellular Junctions/metabolism , Intercellular Junctions/ultrastructure , Ischemia/metabolism , Ischemia/physiopathology , Male , Mice, Inbred ICR , Microscopy, Electron, Transmission , Peptide Mapping , Proteomics/methods , Seminiferous Epithelium/blood supply , Seminiferous Epithelium/metabolism , Seminiferous Epithelium/pathology , Seminiferous Epithelium/ultrastructure , Sertoli Cells/metabolism , Sertoli Cells/ultrastructure , Spermatocytes/metabolism , Spermatocytes/pathology , Spermatocytes/ultrastructure , Spermatogenesis , Testis/metabolism , Testis/pathology , Testis/ultrastructureABSTRACT
La disminución del aporte de O2 a los tejidos provoca daños de éstos, incluido el epitelio seminífero. Últimamente, se ha incrementado la población que trabaja a gran altura, interesando así el estudio de la hipoxia hipobárica sobre la espermatogénesis. Para este estudio se utilizaron dos grupos de ratones machos sexualmente maduros: Control (540 metros sobre el nivel del mar (msnm)) y grupo con hipoxia hipobárica simulada crónica (HHSC) (4.600 msnm) expuestos por 8, 16, 24 ó 33 días. Fueron evaluados hematocrito, reticulocitosis, peso de testículos, epidídimos y vesícula seminal; altura del epitelio seminífero, diámetro tubular, recuento y morfología espermática y lipoperoxidación de membranas de espermatozoides y parénquima testicular. El peso de testículos, epidídimos y vesícula seminal se redujo para empezar a recuperarse a los 33 días. El diámetro tubular y la altura del epitelio se redujeron y luego tendieron a aumentar sin normalizarse. El recuento y la morfología espermáticos fluctaron en el tiempo. Se puede concluir que la exposición a HHSC induce daño del epitelio seminífero, disminución de la lipoperoxidación en espermatozoides y tejido testicular, y altera la morfología testicular y espermática.
Reduction of O2 delivery to tissues damage them, including the seminiferous epithelium. Recently, population working in high altitude has increased, so that the study of hypobaric hypoxia on spermatogenesis becomes of interest. In this study we used two groups of male, sexually mature mice Control (C) (540 meters above sea level (masl)) and chronic simulated hypobaric hypoxia (CSHH) (4,600 masl) exposed during 8, 16, 24 or 33 days. Hematocrit; reticulocytosis; testicular, epididymal and seminal vesicle weight; seminiferous epithelium height, tubular diameter, sperm count and morphology and testicular parenchyme and spermatozoa membranes lipoperoxidation were measured. Weight of testis, epididymis and seminal vesicle were reduced but they recuperate at 33 days. Tubular diameter and epithelial height are reduced, subsequently they tend to increase without returning to normal values. The count and sperm morphology fluctuate along the exposure time. Lipoperoxidation levels of spermatozoa and testicular parenchyme are reduced. Therefore, we can conclude that exposure to CSHH induce damage in the seminiferous epithelium, decrease of lipoperoxidation in spermatozoa and testicular tissue, and damages the testicular and sperm morphology.
Subject(s)
Animals , Male , Adult , Mice , Seminiferous Epithelium/anatomy & histology , Seminiferous Epithelium/growth & development , Seminiferous Epithelium/blood supply , Seminiferous Epithelium/ultrastructure , Cell Hypoxia/physiology , Spermatogenesis/physiology , MiceABSTRACT
The reactions of the germinative testicular epithelium after definite ischemia periods were studied in rats. Using heparin the testicular ischemia tolerance has already been prolonged; this can be distinctly improved by adding alphareceptor blockers. The consequences of a 30 min and 2 h period of testicular ischemia are nearly eliminated by the described medicamentous combination. The experimental results show that at present the use of heparin and alpha-receptor blockers seems to be the best way, to extend the ischemia tolerance during autotransplantation of testicles.
