Rats fed a vitamin E-deficient diet containing 10% "stripped" corn oil had reduced growth rate and elevated platelet count by 12 weeks of age, and a normocytic anemia with elevated reticulocytes by 16 weeks of age. After 5 months, rats became emaciated and developed kyphoscoliosis. Some rats developed skin ulcers and tremors, and mortality was high. Neuromuscular lesions included a chronic necrotizing myopathy and localized axonal dystrophy. There was also a selective activation of lysosomes in the central nervous system microcirculation. Liver ascorbic acid of deficient rats was the same as in those receiving vitamin E. Urinary excretion of p-hydroxyphenylpyruvate after a tyrosine load was also the same in deficient and control rats. It was concluded that neither vitamin C synthesis or utilization was affected the E-deficient rats.

Young guinea pigs were fed a purified diet containing vitamin E for 3 weeks and then fed the diet without vitamin E for 8 weeks. Levels of vitamin E in plasma and liver decreased to low values within a week. Depletion rates for heart and muscle were much slower, whereas the rate of loss from fat was negligible. In experiments with more mature guinea pigs and a depletion period of 4 months, the depletion rate of tocopherol from fat was also barely detectable. Both yound and mature guinea pigs developed myopathy after 8 weeks of depletion. Apparently, tocopherol in adipose tissue is not sufficiently available to maintain plasma tocopherol levels or to prevent signs of vitamin E deficiency. Even during fasting, adipose tissue tocopherol was not mobilized readily. During a 4 day fast, adipose tissue mass diminished considerably, but there was no appreciable loss of tocopherol.

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Weanling rats were fed either a vitamin E-deficient diet or the deficient diet supplemented with vitamin E or the antioxidant ethoxyquin. Ethoxyquin was not effective in preventing the elevation in platelet number or percent aggregation. However, ethoxyquin was as effective as vitamin E in maintaining body weight, testes weight, pigmentation of the incisors and in preventing myopathy, observed either histologically or by an elevation in plasma glutamic oxalacetic transaminase (GOT) activity. Removal of ethoxyquin from the diet after 19 weeks of feeding resulted in a rapid onset of myopathy. These observations permitted us to study the requirement for vitamin E at various ages without the complication of any cumulative pathological effects of vitamin E deficiency. Ethoxyquin was deleted from the diet at 8, 20, 44 and 64 weeks of age. The requirement for vitamin E to reduce plasma GOT and pyruvate kinase (PK) activity was measured at 12, 24, 48 and 68 weeks of age. The requirement for vitamin E did not change significantly during this time period.