Heat stress decreases testicular germ cell proliferation and increases apoptosis in short term: an immunohistochemical and ultrastructural study

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dc.authorscopusid7006356462
dc.authorscopusid24436194200
dc.authorscopusid36023238400
dc.authorwosidAktas, Cevat/D-8468-2011
dc.contributor.authorKanter, Mehmet
dc.contributor.authorAktaş, Cevat
dc.contributor.authorErboğa, Mustafa
dc.date.accessioned2022-05-11T14:41:26Z
dc.date.available2022-05-11T14:41:26Z
dc.date.issued2013
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Histoloji ve Embriyoloji Ana Bilim Dalı
dc.description.abstractScrotal hyperthermia has been known as a cause of male infertility but the exact mechanism leading to impaired spermatogenesis is unknown. This work was aimed to investigate the role of scrotal hyperthermia on cell proliferation and apoptosis in testes. The rats were randomly allotted into one of the four experimental groups: A (control), B (1 day after scrotal hyperthermia), C (14 days after scrotal hyperthermia), and D (35 days after scrotal hyperthermia); each group comprised 7 animals. Scrotal hyperthermia was carried out in a thermostatically controlled water bath at 43 degrees C for 30 min once daily for 6 consecutive days. Control rats were treated in the same way, except the testes were immersed in a water bath maintained at 22 degrees C. Hyperthermia-exposed rats were killed under 50 mg/kg ketamine anaesthesia and tissue samples were obtained for biochemical and histopathological investigations. Hyperthermia treatment significantly decreased the testicular antioxidant system, including decreases in the glutathione level, superoxide dismutase, and glutathione peroxidase activities. Moreover, exposure to hyperthermia resulted in lipid peroxidation increase in testes. Our data indicate a significant reduction in the expression of proliferating cell nuclear antigen and an enhancement in the activity of terminal deoxynucleotidyl transferase dUTP nick end labelling after scrotal hyperthermia. In scrotal hyperthermia, the mitochondrial degeneration, dilatation of smooth endoplasmic reticulum, and enlarged intercellular spaces were observed in both Sertoli and spermatid cells. Scrotal hyperthermia is one of the major factors that impair spermatogenesis in testis. This heat stress is shown to be closely associated with oxidative stress, followed by apoptosis of germ cells.
dc.identifier.doi10.1177/0748233711425082
dc.identifier.endpage113
dc.identifier.issn0748-2337
dc.identifier.issn1477-0393
dc.identifier.issue2en_US
dc.identifier.pmid22082826
dc.identifier.scopus2-s2.0-84874440517
dc.identifier.scopusqualityQ3
dc.identifier.startpage99
dc.identifier.urihttps://doi.org/10.1177/0748233711425082
dc.identifier.urihttps://hdl.handle.net/20.500.11776/9182
dc.identifier.volume29
dc.identifier.wosWOS:000315761000001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorAktaş, Cevat
dc.language.isoen
dc.publisherSage Publications Inc
dc.relation.ispartofToxicology and Industrial Health
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectPCNA
dc.subjectTUNEL
dc.subjectultrastructure
dc.subjectscrotal hyperthermia
dc.subjectrat
dc.subjectSingle Exposure
dc.subjectGnrh Agonist
dc.subjectHyperthermia
dc.subjectRats
dc.subjectSpermatogenesis
dc.subjectSuppression
dc.subjectGlutathione
dc.subjectMechanisms
dc.subjectEpithelium
dc.subjectInduction
dc.titleHeat stress decreases testicular germ cell proliferation and increases apoptosis in short term: an immunohistochemical and ultrastructural study
dc.typeArticle

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