title: Diabetic rat testes: morphological and functional alterations.
abstract: Reproductive dysfunction is a consequence of diabetes, but the underlying mechanisms are poorly understood. This study investigated the histological and molecular alterations in the testes of rats injected with streptozotocin at prepuperal (SPI rats) and adult age (SAI rats) to understand whether diabetes affects testicular tissue with different severity depending on the age in which this pathological condition starts. The testes of diabetic animals showed frequent abnormal histology, and seminiferous epithelium cytoarchitecture appeared altered as well as the occludin distribution pattern. The early occurrence of diabetes increased the percentage of animals with high number of damaged tubules. The interstitial compartment of the testes was clearly hypertrophic in several portions of the organs both in SPI and SAI rats. Interestingly, fully developed Leydig cells were present in all the treated animals although abnormally distributed. Besides the above-described damages, we found a similar decrease in plasma testosterone levels both in SPI and SAI rats. Oxidative stress (OS) is involved in the pathogenesis of various diabetic complications, and in our experimental models we found that manganese superoxide dismutase was reduced in diabetic animals. We conclude that in STZ-induced diabetes, the altered spermatogenesis, more severe in SPI animals, is possibly due to the effect of OS on Leydig cell function which could cause the testosterone decrease responsible for the alterations found in the seminiferous epithelium of diabetic animals.
authors.affiliation: Department of Experimental Medicine, Histology and Embryology Laboratory, School of Medicine, Second University of Naples and National Institute of Biostructures and Biosystems Interuniversitary Consortium-Unit of Sections of Naples, Naples, Italy. giulia.ricci@unina2.it
authors.forename: G
authors.initials: G
authors.lastname: Ricci
authors.forename: A
authors.initials: A
authors.lastname: Catizone
authors.forename: R
authors.initials: R
authors.lastname: Esposito
authors.forename: F A
authors.initials: FA
authors.lastname: Pisanti
authors.forename: M T
authors.initials: MT
authors.lastname: Vietri
authors.forename: M
authors.initials: M
authors.lastname: Galdieri
mesh_terms: D000375:Aging; D000818:Animals; D001814:Blood-Testis Barrier; D003921:Diabetes Mellitus, Experimental / Q000473:pathology* / Q000503:physiopathology*; D006984:Hypertrophy; D007985:Leydig Cells / Q000473:pathology; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism; D062793:Occludin; D018384:Oxidative Stress; D051381:Rats; D012670:Seminiferous Epithelium / Q000473:pathology; D012671:Seminiferous Tubules / Q000378:metabolism / Q000473:pathology; D013091:Spermatogenesis; D013482:Superoxide Dismutase / Q000378:metabolism; D013737:Testis / Q000473:pathology* / Q000503:physiopathology*; D013739:Testosterone / Q000097:blood; D014018:Tissue Distribution
chemical_list: D008565:Membrane Proteins; D062793:Occludin; C568987:Ocln protein, rat; D013739:Testosterone; D013482:Superoxide Dismutase