1. Folate deficiency is commonly found in alcoholic subjects although the causative mechanism is uncertain. It has been suggested that microsomal enzyme induction resulting from chronic alcohol ingestion might accelerate the rate of folate catabolism thus causing deficiency. 2. By using an experimental animal model to determine the rate of catabolism of [ 3 H]pteroylglutamate (folic acid) by the quantitative estimation of the two urinary catabolites p -[ 3 H]aminobenzoylglutamate and [ 3 H]acetamidobenzoylglumate, we have measured both the rate of folate catabolism and the extent of microsomal-enzyme induction in mice after acute and chronic alcohol ingestion. 3. Despite significant evidence of enzyme induction in the chronic alcohol group, there was no difference in the rate of folate catabolism after acute or chronic alcohol ingestion when compared with that of the controls.
1. The recent suggestions that folate polyglutamate biosynthesis demonstrated in vivo with [3′5′9( n )- 3 H]folic acid is due to exchange and cannot be achieved with [2- 14 C]folic acid has been demonstrated to be untrue. 2. The compounds formed with both types of radioactive tracer have been shown to be folate polyglutamates from their elution position from precalibrated ion-exchange columns and their susceptibility to hydrolysis by a γ-carboxypeptidase (conjugase) from human sera. 3. By the use of the methods involving [2- 14 C]folic acid, reported by others to give only folate monoglutamates, we have been able to demonstrate clearly the presence of folate polyglutamates.