The oxidation of glycine and formate to CO2 by rat liver homogenates.

Literature on the subject of glycine metabolism has been reviewed by Weinhouse (1) and by Arnstein (2). The three catabolic pathways for which there has been most support are: (a) the deamination of glycine to glyoxylate, and decarboxylation of the latter to CO2 and formate; in a liver homogenate the formate is oxidized to CO2 and water by catalase and the hydrogen peroxide produced by the action of xanthine oxidase on xanthine or hypoxanthine; (b) the conversion of glycine to serine and subsequent oxidation of the serine; and (c) the succinate-glycine cycle proposed by Shemin (3). In the present studies, measurements were made of the rates of COZ formation from glycine-l-C14, glycine-2-CY4, and formateCl4 by liver homogenates from rats which were fed diets deficient in either vitamin Bs, molybdenum, or folic acid. Studies with vitamin Be-deficient livers were of interest, because it was found previously that blood from vitamin Bs-deficient ducklings incorporated glycine-2-C? into heme poorly (4) and oxidized glytine-2-C14 to CO, at a reduced rate (5). Molybdenum deficiency was studied in order to eliminate xanthine oxidase from the livers (6). Weinhouse and coworkers (7, 8) reported lower rates of formate and CO2 production from the a-carbon of glycine in uiuo in folic acid-deficient rats, and an impaired formate oxidation in uivo and by homogenates of folic acid-deficient livers. Decreased rates of COZ formation from both glycine carbons and from formate were found with livers from vitamin Bs-deficient rats. The formation of CO2 from the glycine carbons, but not from formate was stimulated by the addition of pyridoxal5’-phosphate. The impaired formate oxidation could be related to the observed decrease of xanthine oxidase in vitamin BE-deficient livers. Liver homogenates depleted of xanthine oxidase in molybdenum deficiency gave essentially normal rates of COZ evolution from both glycine carbons, but the oxidation of formate toCO2 was diminished. Omission of folic acid from the diet decreased the production of CO2 from the a-carbon of glycine by about 75 per cent, and from the carboxyl carbon of glycine by about 25 per cent.