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The action of hydrazine has been studied in anesthetized dogs and in rat liver mitochondria. In vivo, hydrazine injection resulted in hyperlactatemia with hypoglycemia. To explain these findings, t...
The action of hydrazine has been studied in anesthetized dogs and in rat liver mitochondria. In vivo, hydrazine injection resulted in hyperlactatemia with hypoglycemia. To explain these findings, the possibility that hydrazine inhibited oxygen consumption with mitochondrial substrates was entertained. Significant inhibition only occurred with keto acids as substrates and only with very high levels of hydrazine. Evidence is presented that keto acid hydrazone formation was responsible for this inhibition in oxygen consumption. Phosphoryation was not affected. Mitochondrial glutamic-oxaloacetic transaminase was found to be strongly and non-competitively inhibited with hydrazine. The inhibition of glutamic-oxaloacetic transaminase is discussed with reference to hydrazine induced hyperlactatemia and hypoglycemia.