Kisspeptin-10 Improves Testicular Redox Status but Does Not Alter the Unfolded Protein Response (UPR) That Is Downregulated by Hypothyroidism in a Rat Model

Author:

Santos Luciano Cardoso1ORCID,dos Anjos Cordeiro Jeane Martinha1ORCID,Cunha Maria Clara da Silva Galrão1,Santos Bianca Reis1ORCID,Oliveira Luciana Santos de1,da Silva Adriana Lopes1ORCID,Barbosa Erikles Macêdo1,Niella Raquel Vieira2ORCID,de Freitas Gustavo José Cota3,Santos Daniel de Assis3ORCID,Serakides Rogéria4ORCID,Ocarino Natália de Melo4ORCID,Borges Stephanie Carvalho1ORCID,de Lavor Mário Sérgio Lima2ORCID,Silva Juneo Freitas1ORCID

Affiliation:

1. Electron Microscopy Center, Department of Biological Sciences, State University of Santa Cruz, Campus Soane Nazare de Andrade, Ilheus 45662-900, Brazil

2. Veterinary Hospital, Department of Agricultural and Environmental Sciences, State University of Santa Cruz, Campus Soane Nazare de Andrade, Ilheus 45662-900, Brazil

3. Department of Microbiology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte 31270-901, Brazil

4. Department of Veterinary Clinic and Surgery, Veterinary School, Federal University of Minas Gerais, Belo Horizonte 31270-901, Brazil

Abstract

Hypothyroidism 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.

Funder

Conselho Nacional de Desenvolvimento Cientifico e Tecnologico

Universidade Estadual de Santa Cruz

Publisher

MDPI AG

Reference72 articles.

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5. Kisspeptin Treatment Reverses High Prolactin Levels and Improves Gonadal Function in Hypothyroid Male Rats;Santos;Sci. Rep.,2023

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