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Three lots of cold-pressed soybean oil were treated with bubbling oxygen for 70, 80, and 180 hrs. at 70°C. and fed to rats at a level of 18% in diets which were nutritionally adequate but devoid of vitamin A. Untreated soybean oil was fed in similar control diets. Subgroups of 15 weanling rats each were given graded injections of vitamin A acetate intramuscularly each week. Diarrhea developed in the rats fed the diets containing oxidized oil. This condition soon subsided in the groups receiving vitamin A injections but not in the vitamin A-free group. Diarrhea was not noted in the rats receiving the untreated soybean oil, without respect to the amount of vitamin A they received. The rats on the vitamin A-free diets developed deficiency more rapidly when the diet contained oxidized rather than the untreated oil. The food efficiencies of the groups fed the oxidized oils were lower than the controls. The intestines of the groups receiving the oxidized oils were distended with fluid and were hemorrhagic. Enlarged kidneys were noted in the vitamin A-deficient control as well as in test rats. The retroperitoneal lipids of the groups on the oxidized oil were less unsaturated, had lower refractive indices, higher peroxide values, and higher carbonyl values than comparable groups fed the control oil. Vitamin A deficiency decreased the unsaturation of the kidney and liver lipids but increased that of the retroperitoneal lipids. Injections of increasing amounts of vitamin A produced increases in the unsaturation of the body lipids. The kidney lipids of the groups on the oxidized oil diets were less unsaturated and contained more peroxidic compounds than the controls. Vitamin A deficiency increased the peroxidic compounds in the kidney and liver lipids, even in rats fed the control oil. The liver lipids of the groups fed oxidized oil were less unsaturated, lower in vitamin A content, and higher in peroxide compounds than the controls. The vitamin A content of the whole blood varied in relation to the amounts injected. The content of tocopherol in the tissues were not affected significantly by the oxidized oil in the diet. The evidence indicates that severely oxidized oil may destroy vitamin A in the tissue of the rat, thereby hastening the development of deficiency on vitamin A-free diets, reducing the storage of injected vitamin A, and increasing the vitamin A requirement. These effects are with abused oil and should not be interpreted to mean that the mildly oxidized oils and fats, such as those in the diets of human beings in this country are toxic.