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.