Kisspeptin-10 improves testicular redox status but does not alter the unfolded protein response (UPR) that is downregulated by hypothyroidism in a rat model

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dc.creatorLuciano Cardoso Santos
dc.creatorJeane Martinha dos Anjos Cordeiro
dc.creatorMaria Clara da Silva Galrão Cunha
dc.creatorBianca Reis Santos
dc.creatorLuciana Santos de Oliveira
dc.creatorAdriana Lopes da Silva
dc.creatorErikles Macêdo Barbosa
dc.creatorRaquel Vieira Niella
dc.creatorGustavo José Cota de Freitas
dc.creatorDaniel de Assis Santos
dc.creatorRogéria Serakides
dc.creatorNatália de Melo Ocarino
dc.creatorStephanie Carvalho Borges
dc.creatorMário Sérgio Lima de Lavor
dc.creatorJuneo Freitas Silva
dc.date.accessioned2026-01-06T21:13:34Z
dc.date.issued2024-01-24
dc.identifier.doihttps://doi.org/10.3390/ijms25031514
dc.identifier.issn1422-0067
dc.identifier.urihttps://hdl.handle.net/1843/1302
dc.languageeng
dc.publisherUniversidade Federal de Minas Gerais
dc.relation.ispartofInternational journal of molecular sciences
dc.rightsAcesso aberto
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internationalen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectHipotireoidismo
dc.subjectMicrobiologia
dc.subject.otherThyroid
dc.subject.otherMale
dc.subject.otherOxidative stress
dc.subject.otherReticular stress
dc.subject.otherRat
dc.titleKisspeptin-10 improves testicular redox status but does not alter the unfolded protein response (UPR) that is downregulated by hypothyroidism in a rat model
dc.typeArtigo de periódico
local.citation.epage13
local.citation.issue3
local.citation.spage1
local.citation.volume25
local.description.resumoHypothyroidism compromises the testicular redox status and is associated with reduced sperm quality and infertility in men. In this regard, studies have demonstrated the antioxidant potential of kisspeptin in reproductive and metabolic diseases. In this study, we evaluate the effects of kisspeptin-10 (Kp10) on the testicular redox, as well as mediators of the unfolded protein response (UPR) in adult rats with hypothyroidism. Adult male Wistar rats were randomly separated into the Control (n = 15), Hypo (n = 13) and Hypo + Kp10 (n = 14) groups, and hypothyroidism was induced with 6-propyl-2-thiouracil (PTU) for three months. In the last month, half of the hypothyroid animals received Kp10. Testis samples were collected for enzymatic, immunohistochemical and/or gene evaluation of mediators of oxidative stress (TBARs, lipid hydroperoxides (LOOH), ROS, peroxynitrite, SOD, CAT and GPX), endoplasmic reticulum stress (GRP78, ATF6, PERK, CHOP, HO-1 and sXBP1) and antiapoptocytes (BCL-2). Hypothyroidism increased apoptosis index, TBARS and LOOH concentrations, and reduced testicular gene expression of Sod1, Sod2 and Gpx1, as well as the expression of Grp78, Atf6, Ho1 and Chop. Treatment with Kp10, in turn, reduced testicular apoptosis and the production of peroxynitrite, while increased SOD1 and GPX ½ expression, and enzymatic activity of CAT, but did not affect the lower expression of UPR mediators caused by hypothyroidism. This study demonstrated that hypothyroidism causes oxidative stress and dysregulated the UPR pathway in rat testes and that, although Kp10 does not influence the low expression of UPR mediators, it improves the testicular redox status, configuring it as an important antioxidant factor in situations of thyroid dysfunction.
local.identifier.orcidhttps://orcid.org/0000-0001-7679-1353
local.identifier.orcidhttps://orcid.org/0000-0002-7209-6043
local.identifier.orcidhttps://orcid.org/0009-0008-9713-3315
local.identifier.orcidhttps://orcid.org/0000-0001-7587-6662
local.identifier.orcidhttps://orcid.org/0009-0007-8242-3267
local.identifier.orcidhttps://orcid.org/0000-0002-3639-9223
local.identifier.orcidhttps://orcid.org/0000-0003-3544-1757
local.identifier.orcidhttps://orcid.org/0000-0002-1108-5666
local.identifier.orcidhttps://orcid.org/0000-0001-5374-6242
local.identifier.orcidhttps://orcid.org/0000-0002-9542-4759
local.identifier.orcidhttps://orcid.org/0000-0002-2534-143X
local.identifier.orcidhttps://orcid.org/0000-0003-0795-5320
local.identifier.orcidhttps://orcid.org/0000-0002-9881-1236
local.publisher.countryBrasil
local.publisher.departmentICB - DEPARTAMENTO DE MICROBIOLOGIA
local.publisher.initialsUFMG
local.subject.cnpqCIENCIAS BIOLOGICAS::MICROBIOLOGIA
local.url.externahttps://www.mdpi.com/1422-0067/25/3/1514

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