The incorporation of a
subcutaneous injection of [14C]
riboflavin (2.5 muCi/100 g body wt) into
flavin mononucleotide (
FMN),
flavin adenine dinucleotide (
FAD), and
flavins bound covalently to
proteins was determined at 1, 6, and 18 h in liver, cerebrum, and cerebellum from progeny of normal and maternally
riboflavin-deficient Holtzman rats. Radioactivity remaining as
riboflavin was also determined under these circumstances. Experiments were initiated within 24 h of birth. In both groups of newborn rats, the incorporation of radioactive
riboflavin into covalently bound
flavins in liver and brain proceeded more slowly than into the other
flavin fractions. In addition, radioactivity incorporated into covalently bound
flavins comprised a relatively smaller proportion of the total amount incorporated in brain than in liver. In progeny of
riboflavin-deficient dams, an increased rate of incorporation of
riboflavin into all three
flavin derivatives, particularly
FAD, was observed in liver and brain, compared to results in normal progeny. These data provide evidence that maternal
riboflavin deficiency enhances the incorporation of
riboflavin into tissue
flavins in liver, cerebrum, and cerebellum from newborn rats.