Abstract
A chemical porphyria was induced in rat by feeding allylisopropylacetamide (AIA) and activities in liver mitochondria to synthesize aminoketones were studied.
It was shown that the activity to synthesize δ-aminolevulinic acid (δ-ALA) was high in liver mitochondria from AIA-induced porphyria rat, while it was very low in normal rat. In contrast, both mitochondria from normal and AIA-treated rats produced large amounts of aminoacetone and no activity difference was noticed between normal and porphyria rats. The δ-ALA synthesizing activity of liver mitochondria varied significantly according to the reaction conditions employed; particularly the yield of δ-ALA was increased by omitting ADP or Pi from the reaction system under anaerobic conditions.
Activities of terminal respiration systems in AIA-treated rat were found to be unaffected. δ-ALA was scarcely catabolyzed by liver mitochondrial preparations from either of normal and porphyria rats.
Significance of succinyl-CoA supplying system in controling the activity of δ-ALA synthesis was discussed in relation to chemical porphyria.
