Melatonin, a major hormone of the pineal gland, exerts many beneficial effects on mitochondria. Several studies have shown that melatonin can protect against toxin-induced oocyte quality impairment during maturation. However, there is little information regarding the beneficial effects of melatonin on toxin-exposed early embryos, and the mechanisms underlying such effects have not been determined. Rotenone, a chemical widely used in agriculture, induces mitochondrial toxicity, therefore, damaging the reproductive system, impairing oocyte maturation, ovulation, and fertilization. We investigated whether melatonin attenuated rotenone exposure-induced impairment of embryo development by its mitochondrial protection effect. Activated oocytes were randomly assigned to four groups: the control, melatonin treatment, rotenone-exposed, and "rotenone + melatonin" groups. Treatment with melatonin abrogated rotenone-induced impairment of embryo development, mitochondrial dysfunction, and ATP deficiency, and significantly decreased oxidative stress and apoptosis. Melatonin also increased SIRT1 and PGC-1α expression, which promoted mitochondrial biogenesis. SIRT1 knockdown or pharmacological inhibition abolished melatonin's ability to revert rotenone-induced impairment. Thus, melatonin rescued rotenone-induced impairment of embryo development by reducing ROS production and promoting mitochondrial biogenesis. This study shows that melatonin rescues toxin-induced impairment of early porcine embryo development by promoting mitochondrial biogenesis.

中文翻译：

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褪黑素增强线粒体的生物发生，并防止鱼藤酮诱导的早期猪胚胎线粒体缺乏。

褪黑激素是松果体的一种主要激素，对线粒体具有许多有益的作用。几项研究表明，褪黑素可以防止毒素在成熟过程中引起卵母细胞质量受损。但是，关于褪黑素对毒素暴露的早期胚胎的有益作用的信息很少，并且尚未确定引起这种作用的机制。鱼藤酮是一种广泛用于农业的化学物质，会诱发线粒体毒性，因此会损害生殖系统，损害卵母细胞的成熟，排卵和受精。我们调查了褪黑素是否通过其线粒体保护作用来减轻鱼藤酮暴露诱导的胚胎发育损伤。激活的卵母细胞随机分为四组：对照组，褪黑激素治疗，鱼藤酮暴露组和“ 和ATP缺乏症，并显着降低氧化应激和细胞凋亡。褪黑素还增加了SIRT1和PGC-1α的表达，从而促进了线粒体的生物发生。SIRT1抑制或药理抑制作用消除了褪黑激素恢复鱼藤酮诱导的损伤的能力。因此，褪黑素通过减少ROS的产生并促进线粒体的生物发生来挽救鱼藤酮诱导的胚胎发育损伤。这项研究表明，褪黑素可通过促进线粒体生物发生来挽救毒素诱导的早期猪胚胎发育损伤。和ATP缺乏症，并显着降低氧化应激和细胞凋亡。褪黑素还增加了SIRT1和PGC-1α的表达，从而促进了线粒体的生物发生。SIRT1抑制或药理抑制作用消除了褪黑激素恢复鱼藤酮诱导的损伤的能力。因此，褪黑素通过减少ROS的产生并促进线粒体的生物发生来挽救鱼藤酮诱导的胚胎发育损伤。这项研究表明，褪黑素可通过促进线粒体生物发生来挽救毒素诱导的早期猪胚胎发育损伤。恢复鱼藤酮引起的损伤的能力。因此，褪黑素通过减少ROS的产生并促进线粒体的生物发生来挽救鱼藤酮诱导的胚胎发育损伤。这项研究表明，褪黑素可通过促进线粒体生物发生来挽救毒素诱导的早期猪胚胎发育损伤。恢复鱼藤酮引起的损伤的能力。因此，褪黑素通过减少ROS的产生并促进线粒体的生物发生来挽救鱼藤酮诱导的胚胎发育损伤。这项研究表明，褪黑素可通过促进线粒体生物发生来挽救毒素诱导的早期猪胚胎发育损伤。