Linus Pauling Institute, College of Public Health and Human Sciences, Oregon State University, Corvallis, OR, USA.
Proc Nutr Soc. 2021 Aug;80(3):319-326. doi: 10.1017/S0029665121000914. Epub 2021 Apr 26.
Vitamin E, discovered in 1922, is essential for pregnant rats to carry their babies to term. However, 100 years later, the molecular mechanisms for the vitamin E requirement during embryogenesis remain unknown. Vitamin E's role during pregnancy has been difficult to study and thus, a vitamin E-deficient (E-) zebrafish embryo model was developed. Vitamin E deficiency in zebrafish embryos initiates lipid peroxidation, depletes a specific phospholipid (DHA-phosphatidyl choline), causes secondary deficiencies of choline, betaine and critical thiols (such as glutathione), and dysregulates energy metabolism. Vitamin E deficiency not only distorts the carefully programmed development of the nervous system, but it leads to defects in several developing organs. Both the α-tocopherol transfer protein and vitamin E are necessary for embryonic development, neurogenesis and cognition in this model and likely in human embryos. Elucidation of the control mechanisms for the cellular and metabolic pathways involved in the molecular dysregulation caused by vitamin E deficiency will lead to important insights into abnormal neurogenesis and embryonic malformations.
维生素 E 于 1922 年被发现，对于怀孕的老鼠将其胎儿孕育至足月是必不可少的。然而，100 年后，维生素 E 在胚胎发生过程中的分子机制仍不清楚。维生素 E 在怀孕期间的作用难以研究，因此开发了一种维生素 E 缺乏（E-）斑马鱼胚胎模型。斑马鱼胚胎中的维生素 E 缺乏会引发脂质过氧化，消耗特定的磷脂（DHA-磷脂酰胆碱），导致胆碱、甜菜碱和关键硫醇（如谷胱甘肽）的继发性缺乏，并扰乱能量代谢。维生素 E 缺乏不仅会扭曲神经系统的精心编程发育，还会导致几个正在发育的器官缺陷。在该模型以及可能在人类胚胎中，α-生育酚转移蛋白和维生素 E 对于胚胎发育、神经发生和认知都是必需的。阐明涉及维生素 E 缺乏引起的分子失调的细胞和代谢途径的控制机制，将为异常神经发生和胚胎畸形提供重要的见解。
