Heat stress is associated with increased production of reactive oxygen species (ROS) and disruption of bovine oocyte function. Here, we examined whether the antioxidant melatonin can alleviate the deleterious effects of heat stress on oocyte developmental competence. Cumulus-oocyte complexes were matured for 22 h at 38.5 °C (control) or for 22 h at 41.5 °C (heat shock) with or without 1.0 × 10-7 M melatonin. At the end of maturation, a subgroup of oocytes was examined for nuclear and cytoplasmic maturation, ROS level and mitochondrial membrane potential. A second subgroup of oocytes underwent fertilization (18 h), and putative zygotes were cultured in an incubator equipped with a time-lapse system for ∼190 h. Cleavage rate and the proportion of blastocysts, as well as embryo kinetics were recorded. Expanded blastocysts were collected and their transcript abundance was evaluated. Heat shock increased ROS and reduced the proportion of oocytes that resumed meiosis and reached the metaphase-II stage. Exposing oocytes to heat shock with melatonin alleviated these effects to some extent, expressed by a marginal reduction in ROS level and increased proportion of metaphase-II stage oocytes. Neither the distribution of oocyte cortical granules nor polarization of the mitochondrial membrane differed between control and heat-shocked oocytes cultured with or without melatonin. Heat shock reduced the proportion of embryos that cleaved and developed to blastocysts, characterized by alterations in kinetics of the developed embryos expressed by a delay in the first cleavage, second cleavage and blastocyst formation for heat-shock vs. control groups. Melatonin did not restore the competence or kinetics of embryos developed from heat-shocked oocytes. However, expanded blastocysts developed from heat-shocked oocytes treated with melatonin expressed a higher transcript abundance of genes associated with mitochondrial function, relative to the control and heat-shock group. In summary, melatonin improved the oxidative status of heat-shocked oocytes to some extent and had a beneficial effect on maternal mitochondrial transcripts in the developed blastocysts.

中文翻译：

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褪黑激素略微减轻热休克对牛卵母细胞和由此产生的囊胚的影响

热应激与活性氧 (ROS) 的产生增加和牛卵母细胞功能的破坏有关。在这里，我们检查了抗氧化剂褪黑激素是否可以减轻热应激对卵母细胞发育能力的有害影响。卵丘-卵母细胞复合物在 38.5 °C（对照）下成熟 22 小时或在 41.5 °C（热休克）下成熟 22 小时，有或没有 1.0 × 10-7 M 褪黑激素。在成熟结束时，检查一组卵母细胞的核和细胞质成熟、ROS 水平和线粒体膜电位。第二组卵母细胞进行受精（18 小时），并将推定的受精卵在配备有延时系统的培养箱中培养约 190 小时。记录卵裂率和囊胚比例，以及胚胎动力学。收集扩大的囊胚并评估它们的转录本丰度。热休克增加 ROS 并降低恢复减数分裂并达到中期 II 期的卵母细胞比例。将卵母细胞暴露于褪黑激素的热休克在一定程度上减轻了这些影响，表现为 ROS 水平的略微降低和中期 II 期卵母细胞的比例增加。对照和热休克卵母细胞在有或没有褪黑激素的情况下培养的卵母细胞皮质颗粒的分布和线粒体膜的极化都没有差异。热休克降低了胚胎分裂并发育成囊胚的比例，其特征是已发育胚胎动力学的改变，表现为热休克组与对照组的第一次卵裂、第二次卵裂和囊胚形成延迟。褪黑激素不能恢复从热休克卵母细胞发育的胚胎的能力或动力学。然而，相对于对照组和热休克组，用褪黑激素处理的热休克卵母细胞发育出的膨胀囊胚表达了更高的转录丰度与线粒体功能相关的基因。总之，褪黑激素在一定程度上改善了热休克卵母细胞的氧化状态，并对发育的囊胚中的母体线粒体转录物产生了有益的影响。