The LD50 (7 d) for aflatoxin B1(AFB1) in CD‐1 neonate mice (3.7 g; 5 d of age) was determined to be 13.3 mg/kg. The vehicle was dimethyl sulfoxide (DMSO), given intra‐peritoneally, at 0.01 ml/animal (7 mg/kg). The solvent was nontoxic and caused no significant change in body weight in animals during an 11‐d experimental period (17 d of age). Aflatoxin B1at 5.0 mg/kg and above caused reduced body weight gain. DMSO animals had a mean loss of more than 17% of the radiolabel over a 9‐d period. Aflatoxin treatments reversed the DMSO loss of54Mn in a concentration‐related fashion, and generally, AFB1caused a conservation of the radioisotope. The radiolabel was redistributed into the following organs/tissues: liver > brain > bone > muscle = lungs > blood. Aflatoxin‐treated animals showed a twofold increase of radiolabel in the liver as compared to controls. The DMSO itself failed to influence54Mn influx into the liver. In general, control neonate mice, by 17 d of age, were retaining and redistributing the54MnCl2and had not reached the time for sudden emergence of excretion common in rodents. DMSO was found not to be the most satisfactory solvent to use in the administration of aflatoxins, especially when manganese metabolism is being studied. Generally, both DMSO and AFB1influenced radiomanganese distribution, DMSO having a substantial influence.