Cellular Immunity and Tumor Growth in Vitamin E-Sufficient and -Deficient Mice
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Effects of vitamin E (VE) on tumor growth and in vitro lymphocyte proliferation as markers of cellular immunity in CDF1 mice were examined in the VE-deficient state as well as in the VE-sufficient state attained by pretreatment with VE. Oral (585mg of dl-α-tocopheryl nicotinate per 100g diet) or intraperitoneal (0.5ml of saline-diluted d-α-tocopherol every other day at a dose of 40mg/kg) supplementation with VE did not enhance in vitro lymphocyte proliferation to concanavalin A, phytohemagglutinin, or lipopolysaccharide, suppress the growth of Meth A fibrosarcoma, or prolong the survival of tumor-bearing animals, even though the serum VE value was maintained 1.5 to 2.4 times higher in the group fed the VE-sufficient diet and about 3 times higher in the group injected with VE than the value for the group fed the control diet. On the other hand, VE-deficiency produced by a basal VE-deficient diet (0.16mg of d-α-tocopherol per 100g diet) seemed to be disadvantageous for the tumor-bearing host in view of the decrease in in vitro lymphocyte proliferation to phytohemagglutinin or lipopolysaccharide, rapid tumor growth, and shortened survival of tumor-bearing mice.
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日本酸化ストレス学会 | 論文
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