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Transfer of mouse blastocysts exposed to ambient oxygen levels can lead to impaired lung development and redox balance.
Molecular Human Reproduction ( IF 3.6 ) Pub Date : 2019-11-30 , DOI: 10.1093/molehr/gaz052
Nedim Karagenç 1 , Göksel Doğan 2 , Kerem Esmen 3 , Bengi Çınar Kul 4 , Hasan Yeşilkaya 5 , Mehmet Nurullah Orman 6 , Mustafa Sandıkçı 2 , Hümeyra Ünsal 7 , Levent Karagenç 2
Affiliation  

In vitro culture under atmospheric oxygen puts embryos under oxidative stress and impairs preimplantation development. However, to what extent this process alters the redox balance in the perinatal period remains largely unknown. The aim of the present study was to examine if the redox balance is altered in the lung tissue of fetuses generated through transfer of mouse embryos exposed to atmospheric oxygen at different stages of development and to determine if this has any effect on lung morphogenesis and gene expression. Two experimental groups (EGs) were generated by transferring in vitro- and in vivo-derived blastocysts to pseudo-pregnant females. In vivo-developed fetuses served as control. Enzymatic/nonenzymatic antioxidants, malondialdehyde (MDA) levels, total antioxidant capacity, stage of lung development and gene expression were evaluated on day 18 of pregnancy. Weight of fetuses was significantly less in both experimental cohorts (ANOVA, P < 0.001 versus control), associated with delayed lung development, higher amounts of MDA (ANOVA, P < 0.001 versus control) and altered expression of several genes in oxidative stress/damage pathways. Evidence gathered in the present study indicates that pre-implantation stress caused by culture under atmospheric oxygen, even for a short period of time, leads to fetal growth restriction, impaired lung development and redox balance along with dysregulation of several genes in oxidative stress response. Absence of an EG in which in vitro embryo culture was performed at 5% oxygen and the use of genetically heterogeneous F2 fetuses are the limitations of the study. In any case, the long-term impact of such dramatic changes in the developmental programming of resulting fetuses warrants further investigations.

中文翻译:

暴露于环境氧气水平下的小鼠胚泡转移可能导致肺发育受损和氧化还原平衡。

在大气氧气下进行体外培养会使胚胎处于氧化应激状态,并损害植入前的发育。然而,这个过程在围产期改变氧化还原平衡的程度尚不清楚。本研究的目的是研究在不同发育阶段暴露于大气氧的小鼠胚胎的转移所产生的胎儿肺组织中氧化还原平衡是否发生改变,并确定这是否对肺形态和基因表达有影响。通过将体外和体内囊胚转移到假孕雌性动物中,产生了两个实验组(EGs)。体内发育的胎儿作为对照。酶/非酶抗氧化剂,丙二醛(MDA)含量,总抗氧化剂容量,在怀孕的第18天评估肺发育的阶段和基因表达。在两个实验组中,胎儿的重量均显着减少(ANOVA,与对照相比,P <0.001),与肺发育迟缓,MDA含量较高(ANOVA,与对照相比,P <0.001)以及氧化应激/损伤中几个基因表达的改变有关途径。在本研究中收集到的证据表明,即使在很短的时间内,在大气氧下培养引起的植入前应激也会导致胎儿生长受限,肺发育和氧化还原平衡受损,以及氧化应激反应中的几个基因失调。该研究的局限性在于缺乏在5%氧气下进行体外胚胎培养的EG和遗传异质F2胎儿的使用。任何状况之下,
更新日期:2019-11-01
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