A chemical porphyria was induced in the rat by feeding allylisopropylacetamide (ALA) and activities in liver mitochondria to synthesize aminoketones were studied. It was shown that the activity to synthesize [delta] -aminolevulinic acid ([delta]-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 [delta] -ALA synthesizing activity of liver mitochondria varied significantly according to the reaction conditions employed; particularly the yield of [delta] -ALA was increased by omitting ADP or Pi from the reaction system under anerobic conditions. Activities of terminal respiration systems in AIA-treated rat were found to be unaffected, [delta] -ALA was scarcely catabolized by liver mitochondrial preparations from either of normal and porphyria rats. Significance of succinyl-CoA supplying system in controlling the activity of [delta] -ALA synthesis was discussed in relation to chemical porphyria.