Sodium selenite and selenomethionine were investigated as possible causative factors for the induction of Degnala disease syndrome in twelve buffalo (Bubalus bubalis) calves divided into three groups of four. Group 1 was the control group and received no additional selenium. Sodium selenite and selenomethionine were given daily as intramuscular injections on a selenium-equivalent basis, with a weekly increment in the dose of 0.05 mg Se/kg live weight from 0.05 to 0.20 mg Se/kg live weight per day, in groups 2 and 3 respectively. Only one animal from group 3 manifested the lesions of Degnala disease. The blood Se concentration and erythrocyte glutathione peroxidase (EC 1.11.1.9; GSH-Px) activity were both greater in groups 2 and 3 than in control group 1. The overall blood Se concentration was 0.22 (se 0.01), 0.38 (se 0.12) and 0.77 (se 0.20) μg Se/ml in groups 1 to 3 respectively with corresponding GSH-Px activities of 63.84 (se 7.38), 88.37 (se 12.38) and 165.32 (se 40.62) enzyme units/mg protein. Erythrocyte glutathione reductase (NAD(P)H) (EC 1.6.4.2) activity was not affected by treatment but reduced glutathione content was lower in groups 2 and 3. Liver adenosylmethionine, estimated at autopsy, was lowest (22.87 (se 6.17) μmol/g) in group 3, and greatest (102.63 (se 9.39) μmol/g) in group 1 (P < 0.01). Organic Se sources seemed to accumulate in tissues more than inorganic sources, and might be the causative toxic factors of Degnala disease.