Effect of pyridoxine deficiency and prednisolone on .BETA.-alanine-oxoglutarate aminotransferase and D-3-aminoisobutyrate aminotransferase in rat liver and kidney.

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Abstract
β-Alanine-oxoglutarate aminotransferase (β-Ala-T I) was found to be distributed mainly in liver, brain, kidney, and testis (decreas-ing order of enzyme activity in the rat). D-3-Aminoisobutyrate aminotrans-ferase (β-Ala-T II) was distributed in kidney and liver. Both β-AIa-TI and β-Ala-T II were localized in the mitochondrial fraction in rat kidney. β-Ala-TI in the liver of rats fed on pyridoxine-deficient or control diets was induced by injecting with prednisolone, while β-Ala-T II in the liver of these rats was unaffected by prednisolone injection. The activities of β-Ala-TI and β-AIa-T II in the liver of rats fed on pyridoxine deficient diet did not change. However, in kidney, pyridoxine deficiency suppressed both enzyme activities, while treatment with prednisolone did not induce either enzyme. The ratios of the apo- to holo-enzyme for β-AIa-TI and β-Ala-T II in control rat kidney were 1.04 and 0.11, respectively. The values increased to 2.69 and 1.53, respectively, in pyridoxine-deficient rat kidney. These experiments indicate that pyridoxine deficiency and prednisolone affect the activities of β-alanine degrading enzymes, but that the degree is different between liver and kidney.