Published online by Cambridge University Press: 09 March 2007
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.