Vitamin B12 suppresses GADD153, prevents apoptosis and regulates the testicular function in methotrexate treated rat testis

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dc.authoridAKIN, Ali Tugrul/0000-0002-1408-8571
dc.authoridKAYMAK, EMIN/0000-0002-3818-2693
dc.contributor.authorKarabulut, Derya
dc.contributor.authorOzturk, Emel
dc.contributor.authorKaymak, Emin
dc.contributor.authorKuloglu, Nurhan
dc.contributor.authorAkin, Ali Tugrul
dc.contributor.authorYakan, Birkan
dc.date.accessioned2024-11-07T13:34:52Z
dc.date.available2024-11-07T13:34:52Z
dc.date.issued2022
dc.departmentNiğde Ömer Halisdemir Üniversitesi
dc.description.abstractMethotrexate (MTX) is an anti-neoplastic drug that also causes testicular damage. Vitamin B12 (Vit B12) is a water soluble vitamin that is required for normal metabolism. We investigated Vit B12 as a possible protective agent against testicular damage caused by MTX treatment. We divided rats into four groups: control group, Vit B12 group treated with Vit B12 daily for 15 days, MTX group treated with MTX on day 8, MTX + Vit B12 group treated with MTX on day 8 + Vit B12 for 15 days. Serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone were measured. We also measured proliferating cell nuclear antigen (PCNA), connexin43 (Cx43) and the growth arrest- and DNA damage-inducible gene, 153 (GADD153), using immunohistochemical staining. Apoptosis was assessed using TUNEL staining. The MTX group exhibited degeneration of seminiferous tubules; decreased serum testosterone, LH and FSH levels; fewer PCNA positive cells; increased Cx43 expression; and increased GADD153 and TUNEL stained cells compared to the control group. These pathologic findings were substantially reversed In the MTX + Vit B12 group. MTX caused increased endoplasmic reticulum stress and apoptosis via GADD153. Consequently, Vit B12 potentially is a protective agent against damage caused by MTX.
dc.description.sponsorshipErciyes University Scientific Research Projects Unit [TSA-2019-8673]
dc.description.sponsorshipThis work was supported by Erciyes University Scientific Research Projects Unit, TSA-2019-8673 project code.
dc.identifier.doi10.1080/10520295.2021.1962976
dc.identifier.endpage297
dc.identifier.issn1052-0295
dc.identifier.issn1473-7760
dc.identifier.issue4
dc.identifier.pmid34365888
dc.identifier.scopus2-s2.0-85112088530
dc.identifier.scopusqualityQ2
dc.identifier.startpage290
dc.identifier.urihttps://doi.org/10.1080/10520295.2021.1962976
dc.identifier.urihttps://hdl.handle.net/11480/16221
dc.identifier.volume97
dc.identifier.wosWOS:000683212200001
dc.identifier.wosqualityQ4
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherTaylor & Francis Ltd
dc.relation.ispartofBiotechnic & Histochemistry
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241106
dc.subjectApoptosis
dc.subjectCx43
dc.subjectGADD153
dc.subjectmethotrexate
dc.subjectPCNA
dc.subjectrat
dc.subjecttestis
dc.subjectvitamin B12
dc.titleVitamin B12 suppresses GADD153, prevents apoptosis and regulates the testicular function in methotrexate treated rat testis
dc.typeArticle

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