Acid-labile (amide) nitrogen metabolism of brain proteins.

Abstract

Abstract—When the TCA‐insoluble fraction of samples of rat brain was extracted with organic (lipid) solvents, a soluble protein fraction was obtained which was metabolically active in the release and uptake of ammonia. The total nitrogen content of this fraction increased during aerobic incubation of slices of cerebral cortex and in brain samples after electrical stimulation of the rats, but under these conditions the content of protein‐bound, acid‐labile (amide) nitrogen decreased. Treatment of rats with intraperitoneally injected camphor caused a decrease in the content of acid‐labile nitrogen both in the proteins extracted into lipid solvents from the TCA precipitate of brain tissue samples and in the residual, washed TCA precipitate. By contrast, after treatment of rats with pentobarbitone, the content of proteinbound, acid‐labile nitrogen increased in the lipid solvent extract but decreased in the residual, washed TCA precipitate. After electrical stimulation of rats, the content of acid‐labile nitrogen in proteins of subcellular particles isolated from homogenates of brain exhibited dissimilar changes from control level: a pronounced decrease in the crude nuclear fraction but no change or a slight increase in the crude mitochondrial and in the combined microsomal and supernatant fractions. When slices of rat brain were incubated aerobically in the presence of glucose, ammonia was transferred from free amino acids to the acid‐labile (amide) nitrogen of protein. Evidence was obtained indicating the participation of aspartate and purine nucleotides in this transfer.