Luteoskyrin, one of the anthraquinoid metabolites of Pcnicilliunr is/uitdicunr Sopp, affects selectively the livers of mice and rats and causes both acute and chronic disorders including centrolobular necrosis, fatty metamorphosis, cirrhosis and hepatoma depending upon the dose and duration of administration (1-3).In order to elucidate the processes of development of the acute injury into a chronic intoxication, the authors performed toxicological studies of the acute stage of luteoskyrin intoxication, and found that this mycotoxin exhibits varying degrees of toxicity depending on the species, strain, sex and age of experimental animals; the susceptibility of nice is higher than that of rats, and in mice it is higher in males and infants than in females and adults (4).Pharmacokinetic studies with 3H-luteoskyrin (5) showed that the hepatotoxicity in mice is ascribable to the selective concentration of the mycotoxin in the liver. Biochemi cal investigations revealed further that luteoskyrin acts as an inhibitor of the respiratory enzyme system (6) and the coupled phosphorylation (7) of liver mitochondria, and binds to DNA (8-10) with resultant suppression of RNA synthesis (I1).In an attempt to confirm the possibility that luteoskyrin or its metabolites directly attack the cellular components of the liver to cause the above mentioned biochemical al terations in the course of the intoxication, intracellular distribution of the radioactivity derived from 3H-luteoskyrin in the liver of mice of different ages and sexes was examined. It was found that the large portion of the tritium label taken up by the liver was distribut