Shahat A M, Rizzoto G, Kastelic J P
Department of Production Animal Health, Faculty of Veterinary Medicine, University of Calgary, Calgary, AB, Canada; Department of Theriogenology, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt.
Department of Production Animal Health, Faculty of Veterinary Medicine, University of Calgary, Calgary, AB, Canada.
Theriogenology. 2020 Dec;158:84-96. doi: 10.1016/j.theriogenology.2020.08.034. Epub 2020 Sep 8.
Heat stress (HS) occurs when temperatures exceed a physiological range, overwhelming compensatory mechanisms. Most mammalian testes are ∼4-5 °C cooler than core body temperature. Systemic HS or localized warming of the testes affects all types of testicular cells, although germ cells are more sensitive than either Sertoli or Leydig cells. Increased testicular temperature has deleterious effects on sperm motility, morphology and fertility, with effects related to extent and duration of the increase. The major consequence of HS on testis is destruction of germ cells by apoptosis, with pachytene spermatocytes, spermatids and epididymal sperm being the most susceptible. In addition to the involvement of various transcription factors, HS triggers production of reactive oxygen species (ROS), which cause apoptosis of germ cells and DNA damage. Effects of HS on testes can be placed in three categories: testicular cells, sperm quality, and ability of sperm to fertilize oocytes and support development. Various substances have been given to animals, or added to semen, in attempts to ameliorate heat stress-induced damage to testes and sperm. They have been divided into various groups according to their composition or activity, as follows: amino acids, antibiotics, antioxidant cocktails, enzyme inhibitors, hormones, minerals, naturally produced substances, phenolic compounds, traditional herbal medicines, and vitamins. Herein, we summarized those substances according to their actions to mitigate HS' three main mechanisms: oxidative stress, germ cell apoptosis, and sperm quality deterioration and testicular damage. The most promising approaches are to use substances that overcome these mechanisms, namely reducing testicular oxidative stress, reducing or preventing apoptosis and promoting recovery of testicular tissue and restoring sperm quality. Although some of these products have considerable promise, further studies are needed to clarify their ability to preserve or restore fertility following HS; these may include more advanced sperm analysis techniques, e.g. sperm epigenome or proteome, or direct assessment of fertilization and development, including in vitro fertilization or breeding data (either natural service or artificial insemination).
当温度超过生理范围，压倒代偿机制时，就会发生热应激（HS）。大多数哺乳动物的睾丸比核心体温低约4-5摄氏度。全身性热应激或睾丸局部升温会影响所有类型的睾丸细胞，不过生殖细胞比支持细胞或间质细胞更敏感。睾丸温度升高对精子活力、形态和生育能力具有有害影响，其影响与温度升高的程度和持续时间有关。热应激对睾丸的主要后果是通过凋亡破坏生殖细胞，其中粗线期精母细胞、精子细胞和附睾精子最为敏感。除了各种转录因子的参与外，热应激还会触发活性氧（ROS）的产生，ROS会导致生殖细胞凋亡和DNA损伤。热应激对睾丸的影响可分为三类：睾丸细胞、精子质量以及精子使卵母细胞受精并支持发育的能力。人们已将各种物质给予动物或添加到精液中，试图改善热应激对睾丸和精子造成的损伤。根据其成分或活性，它们被分为以下不同类别：氨基酸、抗生素、抗氧化剂混合物、酶抑制剂、激素、矿物质、天然产生的物质、酚类化合物、传统草药和维生素。在此，我们根据这些物质减轻热应激的三种主要机制的作用进行了总结：氧化应激、生殖细胞凋亡以及精子质量恶化和睾丸损伤。最有前景的方法是使用能够克服这些机制的物质，可以减少睾丸氧化应激、减少或预防凋亡以及促进睾丸组织恢复并恢复精子质量。尽管其中一些产品前景可观，但仍需要进一步研究来阐明它们在热应激后保持或恢复生育能力的能力；这些研究可能包括更先进的精子分析技术，例如精子表观基因组或蛋白质组，或直接评估受精和发育情况，包括体外受精或繁殖数据（自然交配或人工授精）。
