Gómez-Zúñiga Andrea, Landero-Huerta Daniel Adrián, Rojas-Castañeda Julio César, Sánchez-Huerta Karla, Contreras-García Itzel Jatziri, Reynoso-Robles Rafael, Arteaga-Silva Marcela, Vigueras-Villaseñor Rosa María
Posgrado en Biología Experimental, Universidad Autónoma Metropolitana Unidad Iztapalapa, Mexico City, Mexico.
Laboratorio de Biología de la Reproducción, Instituto Nacional de Pediatría, Mexico City, Mexico.
Front Cell Dev Biol. 2024 Nov 21;12:1493872. doi: 10.3389/fcell.2024.1493872. eCollection 2024.
Congenital hypothyroidism (CH) is a pathology that affects various organs, including the testicles. The mechanisms by which this condition alters fertility is unknown. This study aimed at determining if experimental CH affects gonocyte differentiation and arrests meiosis; and the possible role of the Sertoli cell (SC) in this condition.
Two groups of rats consisting of Control group and Methimazole (MMI) induced CH rats were formed. The induction of CH was achieved by the administration of MMI starting on day 16 postcoitum and continued until euthanized. Euthanasia was performed at 5, 8, 10, 16 and 64 days of age. Following this, the testicular tissue of each animal was extracted and processed for histopathological and ultrastructural analysis. In addition, the tissue was used for the determination of proteins and their transcriptions, events which are characteristics of gonocyte differentiation. The SC functionality proteins was determined immunohistochemically, while sperm parameters of the cauda epididymis were verified.
CH caused a delay in the gonocyte differentiation, and arrested meiosis and spermiogenesis. These events had long-term repercussions on the quality of the seminiferous epithelium. The results show that CH induces alterations in the functional state of SCs that may have led to the deficiency in the synthesis and/or in the release of molecules necessary for gonocyte differentiation; as well as disorders in the process of meiosis that resulted in sperm absence.
These results suggest that CH affects gonocyte differentiation and arrests meiosis, possibly through altering the functional status of SCs.
先天性甲状腺功能减退症(CH)是一种会影响包括睾丸在内的多个器官的病理状况。这种病症改变生育能力的机制尚不清楚。本研究旨在确定实验性CH是否会影响生殖母细胞分化并使减数分裂停滞;以及支持细胞(SC)在这种情况下可能发挥的作用。
将大鼠分为两组,即对照组和甲巯咪唑(MMI)诱导的CH大鼠组。通过在受孕后第16天开始给予MMI来诱导CH,并持续给药直至安乐死。在5、8、10、16和64日龄时实施安乐死。此后,提取每只动物的睾丸组织并进行组织病理学和超微结构分析。此外,该组织用于蛋白质及其转录的测定,这些是生殖母细胞分化的特征性事件。通过免疫组织化学法测定支持细胞功能蛋白,同时检测附睾尾的精子参数。
CH导致生殖母细胞分化延迟,减数分裂和精子发生停滞。这些事件对生精上皮的质量产生了长期影响。结果表明,CH诱导支持细胞功能状态的改变,这可能导致生殖母细胞分化所需分子的合成和/或释放不足;以及减数分裂过程紊乱,导致无精子产生。
这些结果表明,CH可能通过改变支持细胞的功能状态来影响生殖母细胞分化并使减数分裂停滞。