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Lack of embryotoxicity of homocysteine thiolactone in mouse embryos in vitro.

机译:高半胱氨酸硫代内酯在小鼠胚胎体外缺乏胚胎毒性。

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Recent work from humans and chick embryos has suggested that homocysteine may play a role in producing neural tube defects (NTDs). In an effort to determine if homocysteine is able to produce NTDs in mammalian embryos, mouse embryos were explanted on GD 8 and cultured for 44 h. When either homocysteine or homocysteine thiolactone was added to the culture medium, treated embryos developed as well as controls and had closed neural tubes. Homocysteine thiolactone was also microinjected into the amniotic sac of mouse embryos. Again, development proceeded normally with no significant increase in the number of embryos with open neural tubes at the end of the culture period. HPLC analysis of embryonic thiols 24 h after microinjection revealed a significant increase in embryonic cystathionine levels. These data suggest that homocysteine does not produce NTDs in mouse embryos cultured in vitro and that early organogenesis-stage embryos are able to metabolize homocysteine.
机译:人类和鸡胚的最新研究表明,同型半胱氨酸可能在产生神经管缺陷(NTD)中起作用。为了确定同型半胱氨酸是否能够在哺乳动物胚胎中产生NTD,将小鼠胚胎移植到GD 8上并培养44 h。当将同型半胱氨酸或同型半胱氨酸硫代内酯添加到培养基中时,处理过的胚胎与对照一样发育,并且具有封闭的神经管。同型半胱氨酸硫内酯也被显微注射到小鼠胚胎的羊膜囊中。同样,发育正常进行,在培养期末,带有开放式神经管的胚胎数量没有明显增加。显微注射后24小时,对胚胎硫醇的HPLC分析表明,胚胎胱硫醚水平显着增加。这些数据表明,同型半胱氨酸在体外培养的小鼠胚胎中不产生NTD,并且早期器官形成阶段的胚胎能够代谢同型半胱氨酸。

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