RESUMO
During chronic metabolic acidosis, the degradation of protein and amino acids reportedly increases. Branched-chain alpha-keto acid dehydrogenase complex (BCKDH) relates amino-acid catabolism and mitochondrial-energy metabolism. This study was designed to evaluate the effect of acidosis on the activity of liver BCKDH, the key regulatory enzyme in the catabolism of branched-chain amino acids. Experimental acidosis was induced in rats by ingestion of 0.28 M ammonium chloride solution for 10 days. We made two different liver-mitochondrial extracts to assay independently the active form of BCKDH and the total BCKDH activity. Acidosis significantly increased both active and total BCKDH specific activities (P < 0.05). The mean value for the active form of the BCKDH complex was 9.27 +/- 1.10 (S.E.M., n = 7) mU/mg of mitochondrial protein in acidotic rats and 5.18 +/- 0.84 (n = 7) for the control rats. The value of the total complex was 16.10 +/- 1.22 (n = 7) for the acidosis and 11.51 +/- 0.58 (n = 7) for the control. No significant changes were found in the activity state of the complex. Citrate synthase activity did not show significant variations between treatments. The stimulation of liver BCKDH activities by the acidosis may contribute to maintaining the level of intermediates of the tricarboxylic-acid cycle in this metabolic situation in which the net release of glutamine are produced.
