Multiple Congenital Abnormalities in the Rat Resulting from Riboflavin Deficiency Induced by the Antimetabolite Galactoflavin

Abstract

Little effect on fetal development was observed when stock female rats of the Long-Evans strain were given riboflavin-deficient diets for the period of gestation. However, when the vitamin deficiency was accentuated by the addition of the antimetabolite, galactoflavin, to the deficient diet for the entire gestation period or for only 4 to 6 days early in gestation, a high incidence of fetal death or congenital abnormalities resulted. The abnormalities observed included those of the skeleton, the cardiovascular and urogenital systems, the cerebrum and the eyes; herniations of the diaphragm and body walls were also observed. Skeletal defects predominated when the antimetabolite was given throughout gestation. Both skeletal and cardiovascular anomalies were prevalent when the antimetabolite was given from days 7 to 13 followed by vitamin supplementation for the remainder of gestation. Cardiovascular defects were the only anomalies resulting from the transitory deficiency induced by galactoflavin ingestion from days 7 to 11. When diets containing the highest level of the antimetabolite were supplemented with riboflavin throughout gestation, fetal development was normal.