Cardiac lesions of selenium-vitamin E deficiency in animals

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Abstract
Necrosis of myocardium and skeletal muscle is a consistent finding in the numerous animal species in which spontaneous or experimental selenium-vitamin E (Se-E) deficiency has been described. Etiologic factors in the development of these lesions include: (1) low dietary levels of Se, vitamin E, and sulfur-containing amino acids; (2) high dietary concentrations of polyunsaturated fats; (3) exposure to prooxidant conditions (toxicity by O2, O3, Fe, doxorubicin, and radiation injury); and (4) intake of Se antagonists (Ag, Cu, Co, Cd, Te, Sb, and Zn). Myocardial lesions in Se-E deficient animals are most frequently seen in calves, lambs, turkey poults, and ducklings. In calves and lambs with cardiac lesions, the clinical finding usually is sudden death after vigorous exercise. At necropsy, affected calves have areas of necrosis and calcification in the left ventricular free wall and ventricular septum, while in lambs these lesions are seen in the right ventricular subendocardium. Histologically, areas of myocardial damage have hyaline necrosis with or without calcification, subsequent macrophagic invasion, and eventural fibrosis. In growing pigs, the hearts may have scattered pale streaks in the ventricular myocardium, but the most striking alterations are widespread epicardial and myocardial hemorrhages (“mulberry heart”). Histologically, both vascular and myocyte lesions are present. Vascular changes include fibrinoid necrosis of small arteries and arterioles and fibrin microthrombi in capillaries. The myocyte lesions in pigs and in birds consist of multifocal hyaline necrosis with calcification, followed by macrophagic invasion and fibrosis. Ultrastructural study of these lesions reveals myocyte alterations, which include mitochondrial swelling and mineralization, myofibrillar lysis, and necrosis with contraction bands.