Cellular and molecular oxidative stress-related effects in uterine myometrial and trophoblast-decidual tissues after perigestational alcohol intake up to early mouse organogenesis
Cellular and molecular oxidative stress-related effects in uterine myometrial and trophoblast-decidual tissues after perigestational alcohol intake up to early mouse organogenesis
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DOI：
10.1007/s11010-017-3158-y
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发表时间：
2018-03-01
影响因子：
4.3
通讯作者：
Cebral, Elisa
中科院分区：
文献类型：
--
作者：
Anahi Coll, Tamara;Chaufan, Gabriela;Cebral, Elisa
胎盘在母亲饮酒后的胚胎-胎儿缺陷和胎儿宫内发育迟缓中起主要作用。我们的目的是确定氧化状态和细胞和分子氧化应激对子宫肌层和滋养层-蜕膜组织的影响后，在早期器官形成围产期酒精摄入。CF-1雌性小鼠在妊娠前17天至妊娠第10天饮用含10%酒精的饮用水。对照组雌性动物接受无乙醇水。与对照组相比，经处理的小鼠具有较小的着床部位（p < 0.05），母体血管腔缩小，蜕膜血管内皮不规则/不连续。滋养层巨细胞层结构紊乱，核频率异常增加。给药组雌性子宫肌层亚硝酸盐含量降低，超氧化物歧化酶活性升高，还原型谷胱甘肽（GSH）含量升高（p < 0.05）。然而，与对照组相比，给药组雌性的滋养层-蜕膜组织亚硝酸盐含量增加（p < 0.05），GSH水平增加（p <0.001），硫代巴比妥酸反应物质浓度增加（p < 0.001），3-硝基酪氨酸免疫反应增加，凋亡指数增加（p < 0.05）。总之，在CF-1小鼠中，器官发生时摄入围产期酒精可诱导子宫肌层和滋养层-蜕膜组织的氧化应激，主要影响早期器官发生周围的滋养层和蜕膜组织的细胞和大分子，并表明氧化诱导的早期胎盘形成异常可能导致早产和足月胎儿生长障碍的风险。
The placenta plays a major role in embryo-fetal defects and intrauterine growth retardation after maternal alcohol consumption. Our aims were to determine the oxidative status and cellular and molecular oxidative stress effects on uterine myometrium and trophoblast-decidual tissue following perigestational alcohol intake at early organogenesis. CF-1 female mice were administered with 10% alcohol in drinking water for 17 days prior to and up to day 10 of gestation. Control females received ethanol-free water. Treated mice had smaller implantation sites compared to controls (p < 0.05), diminished maternal vascular lumen, and irregular/discontinuous endothelium of decidual vessels. The trophoblast giant cell layer was disorganized and presented increased abnormal nuclear frequency. The myometrium of treated females had reduced nitrite content, increased superoxide dismutase activity, and reduced glutathione (GSH) content (p < 0.05). However, the trophoblast-decidual tissue of treated females had increased nitrite content (p < 0.05), increased GSH level (p < 0.001), increased thiobarbituric acid-reactive substance concentration (p < 0.001), higher 3-nitrotyrosine immunoreaction, and increased apoptotic index (p < 0.05) compared to controls. In summary, perigestational alcohol ingestion at organogenesis induced oxidative stress in the myometrium and trophoblast-decidual tissue, mainly affecting cells and macromolecules of trophoblast and decidual tissues around early organogenesis, in CF-1 mouse, and suggests that oxidative-induced abnormal early placental formation probably leads to risk of prematurity and fetal growth impairment at term.