Abstract
The level of succinyl-CoA synthetase in rat liver mitochondria was not appreciably increased by the administration of allylisopropylacetamide (AIA), while the activity of δ-aminolevulinate synthetase in liver mitochondria was increased more than ten times in these rats. The synthesis of δ-aminolevulinate by liver mitochondria was significantly increased by the addition of ATP in the assay system. The ATP-stimulated increase of the δ-aminolevulinate synthesis in mitochondria from control rats was completely abolished by the further addition of atractyloside, but the ATP-stimulated synthesis of δ-aminolevulinate by mitochondria from AIA-treated rats was far less sensitive to atractyloside. The atractyloside barrier itself appeared to be not affected by the AIA administration as far as examined with respect to the α-ketoglutarate oxidation system and the ATPase system.
