A single dose of 2 microCi [3H] aflatoxin B1 (AFB1) containing 20 micrograms AFB1 was administered to the lactating rat. This resulted in the excretion of AFB1-metabolites in the milk, which were transferred and distributed in many tissues of the offspring consuming milk for 48 h. An equal distribution of radioactivity in liver and lung of suckling rats as well as in their sub-cellular fractions was observed. No AFB1 metabolite binding was apparent with tissue DNA. However, considerable binding of aflatoxin residues was observed with protein followed by RNA. Three metabolites have been detected in the milk sample derived from the stomach of the suckling rats on thin layer chromatogram with Rf values of 0.2, 0.4 and 0.8. Pretreatment of lactating rats with phenobarbitone (PB: 80 mg/kg/3 days) prior to the administration of [3H]AFB1 caused an overall decrease in the radioactivity in the neonatal tissues, particularly lung and intestine (P less than 0.05). The fluorescent bands with Rf values of 0.2 and 0.4 were not visualized in the milk sample from the PB group. Subsequently, the binding of AFB1 residues to cellular macromolecules of neonatal tissues was decreased. PB treatment further resulted in lowering the glucuronide/sulphate conjugates of AFB1 in the milk consumed by suckling rats; AFB1-glutathione (GSH) conjugates were slightly increased. These results point out the possibility that aflatoxin metabolites bind to the tissues of offspring fed by mothers consuming aflatoxin contaminated diets thus leading to chronic effects.