Embryo vitamin deficiency

It is recommended that women of childbearing age take 400 pg/d synthetic folic acid as a supplement in order to reduce the risk of neural tube defects of the embryo when they later become pregnant (periconcep-tional folic acid supplementation) [2]. When supplementing folic acid, it should be considered that this vitamin can mask the simultaneous presence of vitamin B12 deficiency. The typical symptom of vitamin B12 deficiency, megaloblastic (= macrocytic) anemia, will be reduced by high doses of folic acid, yet the nervous system will - in the long run - be irreversibly damaged (= funicular myelitis) when vitamin B12 is not provided as well. 

Maden, M., Gale, E., Kostetskii, I., Zile, M. 1996. Vitamin a-deficient quail embryos have half a hindbrain... 

White, J.C., Highland, M., Kaiser, M., Clagett-Dame, M. 2000. Vitamin A-deficiency in the rat embryo results in anteriorization of the posterior hindbrain which is prevented by maternal consumption of retinoic acid or retinol. Dev. Biol. 220, 263-284. 

Embryos, fetuses, and neonates to age 2-3 months Crigler-Najjar syndrome Gilbert s syndrome Vitamin A deficiency... 

Vitamin A, an essential vitamin, has an embryo or fetal toxicity for humans in higher amounts. Although a deficiency of this essential vitamin will lead to severe health effects, so also will an excess. Obviously two thresholds exist a lower threshold below which deficiency symptoms occur and an upper threshold above which there can be developmental defects. The concentration of vitamin A in food, including specific vitamin drinks, is usually well below any risk level. However, some medicines with high concentrations of vitamin A can activate embryo or fetal toxic effects. Therefore the instructions on the package have to be studied carefully ... 

In non-ruminants, deficiencies of the B vitamins riboflavin and folic acid have been shown to reduce embryo survival. 

Quadro, L., L. Hamberger, M. E. Gottesman, et al. 2005. Pathways of Vitamin A Delivery to the Embryo Insights from a New Tunable Model of Embryonic Vitamin A Deficiency. Endocrinology 146, no 10 4479-90. 

White, J. C., M. Highland, M. Kaiser, and M. Clagett-Dame. 2000. Vitamin A Deficiency Results in the Dose-Dependent Acquisition of Anterior Character and Shortening of the Caudal Hindbrain of the Rat Embryo. Dev Biol 220, no 2 263-84. 

The hepatic 31 kDa a-TTP is a cytosolic protein that has been purified and found to exist as two charge isoforms (Kuhlenkamp et al, 1993). The primary structures of a-TTP from rat liver (Sato et al, 1993) and human liver (Arita et al, 1995) have been determined and found to have a structural homology with retinaldehyde-binding protein (Sato et al, 1993). It is now known that a defect in a-TTP is the cause of ataxia (a nervous disorder characterized by the inability to coordinate muscular movement) associated with familial isolated vitamin E deficiency (Traber etal, 1990c Schuelke etal, 1999). Recent work also indicates that a-TTP is very important for the normal development of placental labyrinthine trophoblasts the placenta of female mice deficient in a-TTP was found to be extremely impaired and the embryos died at mid-gestation (Jishage et al, 2001). 

The developing eye is not only highly vulnerable to vitamin A deficiency, but also an excess of exogenous RA is known to cause severe eye malformations [1, 2, 13, 25]. We analyzed the mechanism of retinoid-related ocular teratology and its normal correlate in early zebrafish and mouse embryos, and we conclude that for the proper formation of the ventro-dorsal retina dimension, the eye anlage has to contain both a RA-rich and a RA-poor region. 

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