Studies in biochemical adaptation. The origin of urinary ammonia as indicated by the effect of chronic acidosis and alkalosis on some renal enzymes in the rat

Abstract

Changes in ammonia excretion were produced,in rats by the induction of chronic acidosis and chronic alkalosis. After 3-8 mos. kidney slices from these animals were used to determine ammonia production from L-glutamine, glycine, L-leucine, L-as-partic acid and L-alanine. These substrates would permit investigation of the possible adaptation of L-glutaminase, glycine oxidase, L-amino-acid oxidase and the transaminase system, all of which might be concerned in ammonia production. Chronic acidosis produced an appreciable increase, and chronic alkalosis an appreciable decrease in ammonia production from L-glutamine, glycine and L-leucine, but no significant change in ammonia production from L-aspartic acid and L-alanine. These results support the possibility that urinary ammonia may be produced, at least in part, by deamination of glutamine, deamination of glycine by glycine oxidase, or deamination of other monoamino monocarboxylic acids by L-amino-acid oxidase. Reasons are given for supposing that the deamination of L-alanine was effected chiefly, if not entirely, by the transaminase system which also acts upon L-aspartic acid. Either this system plays no part in the normal mechanism of urinary ammonia formation, or one or more of its component enzymes is not adaptive. The adaptive changes found indicate that acidosis and alkalosis cause a change in ammonia formation, not merely in ammonia elimination.