Pathophysiology of vitamin E deficiency in monkeys1,2

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Abstract
In a comparative study of vitamin E deficiency in Old and New World monkeys, 14 cynomolgus and 12 cebus monkeys were selected at 1 year of age from animals raised in our primate nursery and were fed either a diet containing 8% coconut oil or stripped safflower oil with or without added tocopherol. During the first year 0.2% cholesterol was added to all diets as an atherogenic stress. Plasma lipids, complete hematology, and plasma tocopherol values were monitored sequentially and complete histopathology, including electron microscopy, was performed terminally. Sudden death of undetermined cause occurred in 3 monkeys fed the safflower oil without vitamin E diet. After approximately 1 year, deficient cebus monkeys consuming safflower oil developed a progressive, macrocytic, hemolytic anemia. A similar, milder anemia was produced in the cynomolgus after 2 years and was accompanied in late stages with muscular weakness. Anemia did not occur with the coconut oil diet. Hemosiderosis resulting from the hemolysis was observed in the spleen, liver, and lung. In monkeys fed safflower oil without vitamin E a remarkable accumulation of lipofuscin and ceroid was observed in macrophages of the intestinal lamina propria, liver, lymph nodes, lung and spleen, and in hepatocytes, aortic and coronary artery endothelial cells, and retinal pigment epithelium. The latter was accompanied by macular degeneration of retinal photoreceptor outer segments. Despite the effect on vascular cells, tocopherol did not influence the extent or severity of atherogenesis induced by cholesterol feeding. Safflower oil was associated with more severe deficiency disease than coconut oil, and cebus monkeys were more adversely affected than cynomolgus even though the deficiency syndrome was similar in the two species.

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