Journal Article Epublish 4 citations
PubMed: 38338793 DOI: 10.3390/ijms25031514
Kisspeptin-10 Improves Testicular Redox Status but Does Not Alter the Unfolded Protein Response (UPR) That Is Downregulated by Hypothyroidism in a Rat Model.
Int J Mol Sci 25(3)
Authors: Luciano Cardoso Santos, Jeane Martinha Dos Anjos Cordeiro, Maria Clara da Silva Galrão Cunha, Bianca Reis Santos, Luciana Santos de Oliveira, Adriana Lopes da Silva, Erikles Macêdo Barbosa, Raquel Vieira Niella, Gustavo José Cota de Freitas, Daniel de Assis Santos, Rogéria Serakides, Natália de Melo Ocarino, Stephanie Carvalho Borges, Mário Sérgio Lima de Lavor, Juneo Freitas Silva
Affiliations
- Electron Microscopy Center, Department of Biological Sciences, State University of Santa Cruz, Campus Soane Nazare de Andrade, Ilheus 45662-900, Brazil.
- Veterinary Hospital, Department of Agricultural and Environmental Sciences, State University of Santa Cruz, Campus Soane Nazare de Andrade, Ilheus 45662-900, Brazil.
- Department of Microbiology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte 31270-901, Brazil.
- 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 ( = 15), Hypo ( = 13) and Hypo + Kp10 ( = 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 , and , as well as the expression of , , and . 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.
MeSH
Genes, Stress, Physiological, Thyroid Gland, Oxidative Stress, Kisspeptins, Thiouracil, Antioxidants, Hypothyroidism, Apoptosis, Unfolded Protein Response, Testis