Abstract

Experimental tocopherol deficiency was produced in young male mink to study the subsequent gross and microscopic lesions and the extent to which they were altered or prevented by the addition of cod liver oil, selenium or α-tocopherol to the basal ration. The major gross lesions consisted of internal intercostal, adductor and cardiac myopathy, hepatic peripherolobular fatty infiltration and, in the cod liver oil-supplemented mink, yellow fat. Histologically, the tocopherol-deficiency myopathy was characterized by swollen, differentially stained fibers, vacuolar degeneration, sarcolemmal and myoblastic proliferation and calcification of the nonphagocytized myofibrillae. The myocarditis was focal calcified necrotic and the fatty hepatic infiltration was accompanied by centrolobular hepatic hemorrhage. Yellow, acid-fast pig-ment was deposited at the interstices of the adipose tissue from the cod liver oil-supplemented mink which also had coagulation necrosis and calcification of the renal tubules. Adipose tissue from chronically tocopherol-deficient mink had adipocyte-like, non-acid-fast spheres in its interstices. The basal tocopherol-deficient ration with 0.1 ppm of selenium as sodium selenite prevented all lesions except minor accumulations of amorphous non-acid-fast material at the adipose interstices. The basal mink ration with 25 ppm α-tocopherol prevented all the tocopherol deficiency lesions.

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