Sarcosine oxidase activity of rat liver tissue: effect of folic acid deficiency and induced hyperthyroidism.

Experimental evidence linking the vitamins, folic acid and B12, to methyl group metabolism has been <obtained in bacterial, mammalian, and avian species (1, 2). The role of the folic acid group of vitamins in the metabolism of l-carbon intermediates has been placed on a definitive basis through isotopic studies involving formate transfer (3-6), whereas the participation of vitamin B,z in the same metabolic area has remained more obscure (2). In regard to the actual enzymes with which these two vitamins can be presumed to be associated, present knowledge is extremely limited. Oginsky (7) found that liver tissue from Blz-deficient rats was relatively incapable of carrying out the enzymic transfer of methyl groups from choline or betaine to homocystine. Buchanan (8), studying the exchange of formate carbon with inosinate as catalyzed by a cell-free pigeon liver homogenate, found an increase in rate of transfer on addition of citrovorum factor, a metabolic analog of folic acid. Sarcosine, a metabolite of betaine in the rat (9), has been shown by Mackenzie (10) and by Handler and co-workers (11) to be oxidatively demethylated to formaldehyde and glycine in rat liver homogenates. Since this enzymic reaction occurs in the metabolic area where folic acid and vitamin Blz are believed to function, and since the enzyme involved, sarcosine oxidase, can be quantitated, it was decided in this present study to measure the sarcosine ox&se activity in the hepatic tissue of rats maintained on diets producing deficiencies of these vitamins. It has been found that under the experimental conditions employed, liver tissue from AminopterinJ or Sulfasuxidine-treated rats has