Nascimento Danisvânia Ripardo, Azevedo Venância Antonia Nunes, Ribeiro Regislane Pinto, Ximenes Gabrielle de Oliveira, Silva Andreza de Aguiar, Barbalho Efigênia Cordeiro, Barrozo Laryssa Gondim, Chaves Sueline Cavalcante, Castro Maria Samires Martins, Marcelino Erica Costa, Vaz da Silva Leopoldo Rugieri Carvalho, Batista André Mariano, Silva José Roberto Viana
Laboratory of Biotechnology and Physiology of Reproduction, Federal University of Ceara, Sobral 62041-040, CE, Brazil.
Laboratory of Biotechniques Applied to Reproduction, Department of Veterinary Medicine, Federal Rural University of Pernambuco, Recife 52171-900, PE, Brazil.
Animals (Basel). 2025 Aug 6;15(15):2296. doi: 10.3390/ani15152296.
This review aims to discuss how heat stress affects ovarian follicles and oocytes, steroidogenesis, and embryo development in ruminants. The literature shows that quiescent primordial follicles appear to be less susceptible to heat stress, but from the primary follicle stage onwards, they begin to suffer the consequences of heat stress. These adverse effects are exacerbated when the follicles are cultured in vitro. In antral follicles, heat stress reduces granulosa cell viability and proliferation in both in vivo and in vitro models. Oocyte maturation, both nuclear and cytoplasmic, is also compromised, and embryo quality declines under elevated thermal conditions. These effects are linked to intracellular disturbances, including oxidative imbalance, mitochondrial dysfunction, and altered hormonal signaling. The differences between in vivo and in vitro responses reflect the complexity of the biological impact of heat stress and emphasize the protective role of the physiological microenvironment. A better understanding of how heat stress alters the function of ovarian follicles, oocytes, and embryos is crucial. This knowledge is critical to devise effective strategies that mitigate damage, support fertility, and improve outcomes in assisted reproduction for livestock exposed to high environmental temperatures.
本综述旨在探讨热应激如何影响反刍动物的卵巢卵泡和卵母细胞、类固醇生成以及胚胎发育。文献表明，静止的原始卵泡似乎对热应激不太敏感，但从初级卵泡阶段开始，它们就开始受到热应激的影响。当卵泡在体外培养时，这些不利影响会加剧。在有腔卵泡中，热应激在体内和体外模型中均会降低颗粒细胞的活力和增殖。卵母细胞的核成熟和胞质成熟也会受到损害，并且在高温条件下胚胎质量会下降。这些影响与细胞内紊乱有关，包括氧化失衡、线粒体功能障碍和激素信号改变。体内和体外反应的差异反映了热应激生物学影响的复杂性，并强调了生理微环境的保护作用。更好地理解热应激如何改变卵巢卵泡、卵母细胞和胚胎的功能至关重要。这一知识对于制定有效的策略以减轻损害、支持生育能力并改善暴露于高温环境下的家畜辅助生殖结局至关重要。
