A determination of the main regulators of necroptosis in testicular tissue under different heat stresses

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dc.authoridTATAR, Musa/0000-0002-5707-8832
dc.authoridTufekci, Kiymet Kubra/0000-0002-4722-3813
dc.contributor.authorTatar, Musa
dc.contributor.authorTufekci, Kiymet Kubra
dc.contributor.authorUslu, Sema
dc.date.accessioned2025-05-04T16:47:25Z
dc.date.available2025-05-04T16:47:25Z
dc.date.issued2025
dc.departmentSivas Cumhuriyet Üniversitesi
dc.description.abstractAlthough minimal increases in testicular temperature can compromise spermatogenesis and lead to fertility-related problems, the basic mechanism involved in germ cell destruction as a response to heat stress is still unclear. However, necroptosis is known to regulate a number of physiological and pathological events. This study investigated the role of RIPK1/RIPK3 and MLKL, the main regulators of necroptosis, against different heat stresses in testis tissue. Forty-two Wistar albino rats were divided into seven groups: six experimental exposed to heat stress and one control. Heat stress was induced by causing the rats to swim for 30 min daily for 60 days in a water bath at temperatures of 39 degrees C and 43 degrees C. Testis tissues were collected while the animals were under anesthesia on the 1st, 7th, and 14th days after 60 days of heat application. The tissues were first fixed in Bouin's solution. After routine histological procedures, immunohistochemical staining was performed on one-half of the tissues using RIPK1/RIPK3 and MLKL primary antibodies on serially collected 5 mu m-thick sections. Immunoblotting analysis was performed on the other half. Analyses revealed an increase in the expression of RIPK1/RIPK3 and MLKL proteins, regulators of necroptosis, in both the 39 degrees C and 43 degrees C groups, although this was greater in the tissue exposed to 43 degrees C heat stress. These molecules were also especially affected by round and elongated spermatids, and reactivity was observed in Leydig cells. In conclusion, exposure to increased temperature may cause RIPK1/RIPK3 and MLKL-mediated cellular changes in the testis.
dc.description.sponsorshipScientific Research Foundation of Kastamonu University [KUBAP-01/2022-37]
dc.description.sponsorshipThis study was supported by the Scientific Research Foundation of Kastamonu University KUBAP-01/2022-37.
dc.identifier.doi10.1007/s10735-024-10350-x
dc.identifier.issn1567-2379
dc.identifier.issn1567-2387
dc.identifier.issue1
dc.identifier.pmid39856359
dc.identifier.scopus2-s2.0-85216998895
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1007/s10735-024-10350-x
dc.identifier.urihttps://hdl.handle.net/20.500.12418/35615
dc.identifier.volume56
dc.identifier.wosWOS:001405395800001
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofJournal of Molecular Histology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WOS_20250504
dc.subjectHeat stress
dc.subjectTestis
dc.subjectNecroptosis
dc.subjectInfertility
dc.titleA determination of the main regulators of necroptosis in testicular tissue under different heat stresses
dc.typeArticle

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