Melatonin ameliorates murine fetal oocyte meiotic dysfunction in F1 and F2 offspring caused by nicotine exposure during pregnancy
Melatonin ameliorates murine fetal oocyte meiotic dysfunction in F1 and F2 offspring caused by nicotine exposure during pregnancy
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褪黑素改善妊娠期间尼古丁暴露引起的 F1 和 F2 后代小鼠胎儿卵母细胞减数分裂功能障碍
DOI：
10.1016/j.envpol.2020.114519
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发表时间：
2020-08-01
影响因子：
8.9
通讯作者：
Cheng, Shun-Feng
中科院分区：
文献类型：
--
作者：
Liu, Wen-Xiang;Tan, Shao-Jing;Cheng, Shun-Feng
虽然有大量证据表明母亲在怀孕期间吸烟会损害后代的健康，但孕妇使用尼古丁对女性后代卵子发生和卵泡发生的影响尚未得到广泛的研究。在这里，我们专注于尼古丁对胎儿卵母细胞减数分裂进程的影响。数据表明，在用尼古丁处理的怀孕小鼠中，胎儿卵巢内卵泡中的细胞内ROS增加。过量的细胞内过氧化氢（H2 O2）和超氧阴离子（O-2（中心点-））降低线粒体膜电位，诱导线粒体功能障碍，触发自噬级联反应并抑制抗自噬蛋白。尼古丁处理的孕鼠F1代胚胎卵母细胞减数分裂前期I延迟，尤其是从粗线期延迟到双线期。在青春期的F1后代中，我们观察到卵泡数量减少;在F2后代中也观察到同样的减少。值得注意的是，我们发现褪黑激素改善尼古丁诱导的卵母细胞损伤，并增加MnSOD的表达，从而减少尼古丁诱导的细胞内ROS的产生。此外，褪黑激素还维持正常的H3 K4和H3 K9的二甲基化和三甲基化在F1和F2卵巢。总之，目前的证据表明，在小鼠中，褪黑激素可以防止尼古丁损害的胎儿卵子发生和后代卵泡发生。(c)2020爱思唯尔有限公司版权所有。
Although there is abundant evidence to demonstrate that maternal smoking during pregnancy will harm the health of future generations, the impact of nicotine use by pregnant woman upon the oogenesis and folliculogenesis of female offspring has not been as widely scrutinized. Here we focus on the effects of nicotine on the meiotic progression of fetal oocytes. The data indicated that in pregnant mice treated with nicotine, intracellular ROS increased in follicles within the fetal ovary. Excessive intracellular hydrogen peroxide (H2O2) and superoxide anion (O-2(center dot-)) decreased mitochondrial membrane potential, inducing mitochondrial dysfunction, triggering an autophagic cascade and inhibiting anti-autophagic proteins. Fetal oocytes in F1 offspring of pregnant mice treated with nicotine exhibited a delay in meiotic prophase I, especially from the stage of pachytene to diplotene. In pubertal F1 offspring we observed a reduced number of follicles; the same reduction was also observed in F2 offspring. Of note, we found that melatonin ameliorated nicotine-induced oocyte damage and increased the expression of MnSOD, which decreased the production of nicotine-induced intracellular ROS. In addition, melatonin also maintained normal H3K4 and H3K9 di- and tri-methylation in F1 and F2 ovaries. Taken together, the current evidence suggests that, in the mouse, melatonin could prevent nicotine-impaired fetal oogenesis and folliculogenesis in offspring. (c) 2020 Elsevier Ltd. All rights reserved.