Congenital eye defects in rats following maternal folic-acid deficiency during pregnancy

Development ◽  
1966 ◽  
Vol 16 (3) ◽  
pp. 531-542
Author(s):  
R. Christy Armstrong ◽  
I. W. Monie
Keyword(s):  
Folic Acid ◽  
Pantothenic Acid ◽  
Folic Acid Deficiency ◽  
Teratogenic Effects ◽  
Maternal Vitamin ◽  
Vitamin Deficiencies ◽  
Fetal Rat ◽  
Acid Deficiency ◽  
Pteroylglutamic Acid ◽  
Developing Rat

Malformations of fetal rat eyes result from a variety of maternal vitamin deficiencies employed either transiently or continuously during pregnancy. Thus, eye defects have been produced in rat fetuses as a result of maternal deficiencies of vitamin A (Wilson, Jordan & Brent, 1953), pantothenic acid (Lefebvres-Boisselot, 1951; Nelson, Asling & Evans, 1957), niacin (Chamberlain & Nelson, 1963) and pteroylglutamic acid (PGA or folic acid) (Evans, Nelson & Asling, 1951; Nelson, Asling & Evans, 1952; Giroud & Boisselot, 1951; Giroud, Lefebvres & Dupuis, 1952; Giroud, Delmas, Lefebvres &Prost, 1954). Previous studies on the teratogenic effects of PGA-deficiency on the developing rat eye, although informative, have been concerned mainly with stages after the 15th day of pregnancy (the day of finding sperm in the vagina is considered to be day zero).

scholarly journals Folates: Key Nutrients to Remember

2017 ◽  
Vol 9 (2) ◽  
pp. 75
Author(s):  
Gourchala Freha ◽  
Mihoub Fatma ◽  
Henchiri Cherifa
Keyword(s):  
Folic Acid ◽  
Macrocytic Anemia ◽  
Folic Acid Supplementation ◽  
Intestinal Lumen ◽  
Folic Acid Deficiency ◽  
Hydrogen Atoms ◽  
Rapid Multiplication ◽  
Vitamin B9 ◽  
Acid Deficiency ◽  
Pteroylglutamic Acid

Folic acid or vitamin B9 or pteroylglutamic acid, is a relatively simple molecule with two characteristics; firstly, it must be reduced by 2 or 4 hydrogen atoms to be metabolically active which makes it sensitive to oxidation and must be protected by ascorbic acid, secondly it may include in addition to the constituent residues of the molecule, 1-7 glutamate residue at one of its ends. These polyglutamate forms that make up the largest share of food folate, must be deconjugated by a specific enzyme present in the intestinal lumen before being absorbed in the jejunum. It is in the methylated form after passing through the enterocyte it is transported in the blood, excreted in bile and reabsorbed. It must be demethylated to integrate folic cell cycle and methyl transfer, that allows the synthesis of methionine (only possible in the presence of vitamin B12), purine, serine and especially thymidylic acid, constitutive DNA. As a methyl donor that plays a fundamental role in cerebral and nervous metabolism. Folates are involved in cell division thus; any folic acid deficiency causes a slowdown in rapid multiplication systems which may lead to red blood cell disorders (macrocytic anemia), immunity, and neural tube defects, in addition to physiological disorders (cardiovascular, cancer ...). Folic acid supplementation appears to allow the correction of these disorders.

scholarly journals Teratogenic effects of folic acid deficiency induced by methotrexate in heart development in a rat model

2007 ◽  
Vol 306 (1) ◽  
pp. 417-418
Author(s):  
Mara Torres-Martínez ◽  
Manuel Arteaga ◽  
Isabel García ◽  
Oswaldo Aguirre
Keyword(s):  
Folic Acid ◽  
Rat Model ◽  
Heart Development ◽  
Folic Acid Deficiency ◽  
Teratogenic Effects ◽  
Acid Deficiency

FOLIC-ACID DEFICIENCY IN PREGNANCY

The Lancet ◽  
1959 ◽  
Vol 274 (7110) ◽  
pp. 1033-1034 ◽  
Author(s):  
H.H. Francis ◽  
J.S. Scott
Keyword(s):  
Folic Acid ◽  
Folic Acid Deficiency ◽  
Acid Deficiency ◽  
In Pregnancy
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