Metabolism of glutamic acid-1- 14C and aspartic acid-4- 14C in rat brain and kidney homogenates

Abstract

Whole rat kidney and rat brain homogenates utilize the l-form of aspartic acid or glutamic acid only. If the supernatant is incubated, the same conclusion holds, except in the case of brain tissue supernatant where the d-form might be utilized somewhat. Whole rabbit kidney homogenate dissimilates d-aspartic acid. Both AMP and ATP inhibit the oxidation of aspartic acid by kidney homogenate. But AMP stimulates this reaction in brain. Addition of DPN, TPN, pyruvate or a-ketoglutarate enhances dissimilation of this amino acid by either whole kidney or brain homogenates. In the case of the kidney (but not the brain) the enzymes responsible for the oxidation are present in the supernatant obtained by centrifuging. ATP, AMP, DPN, TPN, oxalacetate have a stimulatory effect on the catabolismof glutamic acid by rat kidney or brain homogenates. The responsible enzymes can be extracted into the supernatant, at least to some degree. The oxidation of aspartic acid and glutamic acid by various tissues decreases in the following order: liver, kidney, brain, spleen and blood. Activity in the blood is nil. The rate of oxidation of the two amino acids is low in fetal liver, livers of Walker tumor bearing hosts, and in the tumor tissue itself.