Histopathologic and ultrastructural myocardial alterations in calves deficient in vitamin E and selenium and fed polyunsaturated fatty acids.

We developed an experimental model of nutritional degenerative myopathy in ruminant cattle. Fourteen experimental calves were fed a diet low in vitamin E and selenium for 127 to 137 days. Six of these calves were then euthanatized. After 127 days, a dietary additive of linseed oil that had been treated to protect it against ruminal hydrogenation was added to the low vitamin E and selenium diet of the eight remaining calves as a source of polyunsaturated fatty acids. Six of these animals were euthanatized after 6 to 11 days of polyunsaturated fatty acid feeding; the other two died after 6 and 8 days. Macroscopic myocardial alterations were seen in five polyunsaturated fatty acid-fed calves but not in any other experimental calf. Microscopic lesions, comprising multifocal or diffuse cardiocyte degeneration and necrosis, were seen in atrial and ventricular myocardium of all experimental calves. These changes were more severe in polyunsaturated fatty acid-fed calves than in animals that did not receive polyunsaturates. Ultrastructurally, sublethally damaged cardiocytes had lysed contractile material; vacuolated sarcoplasm; altered mitochondria, sarcoplasmic myelin figures, and lipofuscin granules; and multiple nuclei. Necrotic cardiocytes had contracted myofibrils, pyknotic nuclei, mineralized mitochondria, and plasmalemmal disruption; the external lamina remained largely intact. Necrosis was followed by macrophage invasion and phagocytosis of necrotic debris. Repair of the lesions was by deposition of collagen and elastin fibers. No alterations were seen in the hearts of control calves fed vitamin E and selenium-supplemented diet. The induced myocardial lesions are similar to those of spontaneous nutritional degenerative myopathy in ruminant cattle.     

Vitamin E, selenium, and polyunsaturated fatty acid concentrations and glutathione peroxidase activity in tissues from pigs with dietetic microangiopathy (mulberry heart disease)

Tissues of 27 pigs with spontaneous dietetic microangiopathy (DM) and of 27 control pigs that died of causes unrelated to vitamin E and selenium (E-Se) deficiency were analyzed for alpha-tocopherol, Se and polyunsaturated fatty acid (PUFA) concentrations and for glutathione perioxidase (GSH-Px) activity. These variables (except for GSH-Px) also were measured in rations fed to control pigs and pigs with DM. Swine with DM had lower heart and liver alpha-tocopherol concentrations than did control pigs. Heart and kidney Se concentrations and heart and liver PUFA concentrations were similar in pigs of either group. Diets fed to both groups of pigs contained similar content of alpha-tocopherol, Se, oil, and PUFA; alpha-tocopherol and Se concentrations in the diets of both groups of pigs were high. In spite of apparently adequate amount of dietary alpha-tocopherol, results indicate that pigs with DM had lower tissue alpha-tocopherol concentration than did control pigs. Spontaneous DM is associated with altered alpha-tocopherol metabolism, but is unrelated to alterations in dietary Se and PUFA contents and tissue Se and PUFA concentrations and GSH-Px activity.