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

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 (LefebvresBoisselot, 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). However, since the eye begins forming between the 9th and 10th days of gestation, it was felt that a study embracing both early and late stages of ocular development in rat embryos from mothers maintained on a PGAdeficient regimen for different lengths of time during gestation would be of more value in understanding the genesis of certain ocular abnormalities. The following account concerns such an investigation and describes the abnormalities encountered in the visual system.