Kosenko E, Felipo V, Miñana M D, Grau E, Grisolía S
Instituto de Investigaciones Citógicas, Centro Asociado del CSIC, Valencia, Spain.
Arch Biochem Biophys. 1991 Nov 1;290(2):484-8. doi: 10.1016/0003-9861(91)90570-9.
Ingestion of an ammonium containing diet produces hyperammonemia and protects rats against acute ammonium intoxication. Acute ammonium toxicity has been attributed to the depletion of energy metabolite intermediates. We show here that hyperammonemia affords considerable protection against depletion of hepatic energy metabolites evoked by ammonium acetate injection. In control rats there were marked decreases in the content of acetoacetate, beta-hydroxybutyrate, ATP, 2-oxoglutarate, lactate, and pyruvate while phosphoenolpyruvate increased markedly. In hyperammonemic rats beta-hydroxybutyrate, ATP, 2-oxoglutarate, and lactate were not significantly affected while pyruvate increased markedly and phosphoenolpyruvate slightly. These results suggest that in controls the activity of pyruvate kinase is inhibited after ammonium injection while in hyperammonemic rats it is not inhibited. The content of alanine (an inhibitor of pyruvate kinase) reached 2.8 mumol/g in controls and 1.6 mumol/g in hyperammonemic rats, 15 min after ammonium injection. This could explain the different effects of ammonium injection on control and hyperammonemic rats.
摄入含铵饮食会导致高氨血症，并保护大鼠免受急性铵中毒。急性铵毒性被认为是由于能量代谢中间产物的消耗所致。我们在此表明，高氨血症对乙酸铵注射引起的肝脏能量代谢物消耗具有显著的保护作用。在对照大鼠中，乙酰乙酸、β-羟基丁酸、ATP、2-氧代戊二酸、乳酸和丙酮酸的含量显著降低，而磷酸烯醇式丙酮酸显著增加。在高氨血症大鼠中，β-羟基丁酸、ATP、2-氧代戊二酸和乳酸没有受到显著影响，而丙酮酸显著增加，磷酸烯醇式丙酮酸略有增加。这些结果表明，在对照大鼠中，注射铵后丙酮酸激酶的活性受到抑制，而在高氨血症大鼠中则未受到抑制。注射铵15分钟后，丙氨酸（丙酮酸激酶的抑制剂）的含量在对照大鼠中达到2.8 μmol/g，在高氨血症大鼠中达到1.6 μmol/g。这可以解释注射铵对对照大鼠和高氨血症大鼠的不同影响。
