Yang Hui, Du Libo, Wu Guangjun, Wu Zhenyu, Keelan Jeffrey A
Immunology Department, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China.
Institute of Chemistry, Chinese Academy of Sciences, Beijing, 100190, China.
Mol Med. 2018 Dec 3;24(1):62. doi: 10.1186/s10020-018-0061-2.
Gold nanoparticles (AuNPs) have been widely studied for biomedical applications, although their safety and potential toxicity in pregnancy remains unknown. The aim of this study is to explore the effect of AuNPs maternal exposure at different gestational ages on fetal survival and development, as well as the potential mechanism of AuNPs affecting embryos and fetuses.
Thirty nm polyethylene glycol (PEG)-coated AuNPs (A30) were administered to pregnant mice via intravenous injection (5 μg Au/g body weight) over three days at either early or late pregnancy. Fetal abortion rate and morphological development in E16.5 were then detected in detail. The pregnant mice physiological states with A30 exposure were examined by biochemical, histological or imaging methods; and materno-fetal distribution of gold elements was assayed by electron microscopy and mass spectrometry. Murine embryonic stem cells derived embryoid-bodies or neuroectodermal cells were treated with A30 (0.0025 to 0.25 μg Au/mL) to examine A30 effects on expression levels of the germ differentiation marker genes. Tukey's method was used for statistical analysis.
Exposure to A30 during early (A30E) but not late (A30L) pregnancy caused a high abortion rate (53.5%), lower fetal survival rate and abnormal decidualization compared with non-exposed counterparts. The developmental damage caused by A30 followed an "all-or-nothing" pattern, as the non-aborted fetuses developed normally and pregnancies maintained normal endocrine values. A30 caused minor impairment of liver and kidney function of A30E but not A30L mice. TEM imaging of fetal tissue sections confirmed the transfer of A30 into fetal brain and live as aggregates. qPCR assays showed A30 suppressed the expression of ectodermal, but not mesodermal and endodermal differentiation markers.
These results illustrate that maternal A30 exposure in early pregnant results in A30 transfer into embryonic tissues, inhibiting ectodermal differentiation of embryonic stem cells, leading to abnormal embryonic development and abortion. While exposure to A30 during late pregnancy had little or no impact on dams and fetuses. These findings suggest the safety of biomedical applications employing AuNPs during pregnancy is strongly influenced by fetal maturity and gestational age at exposure and provide the clues for AuNPs safe application period in pregnancy.
金纳米颗粒(AuNPs)已被广泛研究用于生物医学应用,但其在孕期的安全性和潜在毒性仍不明确。本研究旨在探讨不同孕期母体暴露于AuNPs对胎儿存活和发育的影响,以及AuNPs影响胚胎和胎儿的潜在机制。
通过静脉注射(5μg金/克体重),在妊娠早期或晚期的三天内,将30纳米聚乙二醇(PEG)包覆的AuNPs(A30)给予怀孕小鼠。然后详细检测E16.5时的胎儿流产率和形态发育情况。通过生化、组织学或成像方法检查暴露于A30的怀孕小鼠的生理状态;并通过电子显微镜和质谱分析金元素的母胎分布。用A30(0.0025至0.25μg金/毫升)处理小鼠胚胎干细胞衍生的胚状体或神经外胚层细胞,以检查A30对生殖分化标记基因表达水平的影响。采用Tukey方法进行统计分析。
与未暴露的对照组相比,妊娠早期(A30E)而非晚期(A30L)暴露于A30导致高流产率(53.5%)、较低的胎儿存活率和蜕膜化异常。A30造成的发育损伤呈现“全或无”模式,因为未流产的胎儿发育正常,妊娠维持正常内分泌值。A30对A30E小鼠的肝脏和肾脏功能造成轻微损害,但对A30L小鼠无此影响。胎儿组织切片的透射电镜成像证实A30以聚集体形式转移到胎儿脑和肝脏中。定量PCR分析表明,A30抑制外胚层而非中胚层和内胚层分化标记的表达。
这些结果表明,妊娠早期母体暴露于A30会导致A30转移到胚胎组织中,抑制胚胎干细胞的外胚层分化,导致胚胎发育异常和流产。而妊娠晚期暴露于A30对母鼠和胎儿几乎没有影响。这些发现表明,孕期使用AuNPs进行生物医学应用的安全性受到胎儿成熟度和暴露时孕周的强烈影响,并为AuNPs在孕期的安全应用期提供了线索。