Rats of four groups were fed vitamin E deficient or supplemented diets containing 5.6 or 15.6% linoleic acid for 100 days. The rats fed vitamin E deficient diets displayed signs of vitamin E deficiency as shown in erythrocytes hemolysis value and blood tocopherol content. The rats fed vitamin E supplemented (2mg/100g) diet containing 15.6% linoleic acid displayed borderline deficiency signs. The amounts of lipid peroxides in blood and liver were higher in rats fed vitamin E deficient diets and were significantly increased by dietary linoleic acid. Morphologically the most striking changes in the hepatocytes of vitamin E deficient rats were occurrence of large numbers of microbodies. lysosomes. lipofuscin. lipid droplets and enlarged mitochondria. The number of micro-bodies per hepatocyte increased and was 1.5 times greater than that in E-supplemented rats. The mitochondria were enlarged with dense matrix and indistinct outer membrane. The number of lysosomes and microbodies were further increased in the hepatocytes of rats fed vitamin E deficient diets containing 15.6% linoleic acid. Peroxidase reaction product was histochemically found in microbodies and in a rim of lipid droplets. Acid phosphatase reaction was found in primary lysosomes and weak reaction in the matrix of residual bodies or lipofuscin. The increases in activities of peroxidase and acid phosphatase in hepatocytes of rats fed vitamin E deficient diet containing linoleic acid appear to be in response to the increased lipid peroxidation which occurred in the liver of these rats.

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Rats of four groups were fed vitamin E deficient or supplemented diets containing 5.6 or 15.6% linoleic acid for 100 days. The amounts of lipid peroxides in cardiac muscle were higher in rats fed vitamin E deficient diet containing 15.6% linoleic acid than that of E supplemented rats. In the vitamin E deficient rats. a large amount of PAS-positive lipofuscin granules occurred in the perinuclear region and periphery of muscle fibers. Two types of lipofuscin. large droplet-like form and small granular type, were observed in the cardiac muscle of rats fed vitamin E deficient diet containing 15.6% linoleic acid. The droplet form lipofuscin lying between mitochondria is considered to be formed by degeneration of mitochondria or degradation of lipid droplets. The granular type pigments were accumulated in the cisternae of sarcoplasmic reticulum. The disarrangement of myofilaments and indistinct Z bands were observed in some myofibrils lying close to the accumulation of lipofuscin. The mitochondria were hypertrophied with dense or swollen matrix. Acid phosphatase reaction products occurred in lysosomes lying in perinuclear zone and between mitochondria and in the cisternae of sarcoplasmic reticulum lying along the T systems. Peroxidase occurred in the microbodies between mitochondria and cristae of some enlarged mitochondria. The significance of these enzymes in formation of lipofuscin was discussed.

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B_1をBrCN-NaOH法で酸化し,反応産物をゲル濾過カラムクロマトグラフィーあるいは薄層ク団マトグラフィーで展開すると,螢光強度で判定してほぼ等量の2種の物質に分離し,また多量のB_1酸化産物をゲル濾過クロマトグラフィーで展開したときには更に極少量の第3の螢光物質が検出された.B_1をK_3Fe(CN)_6-NaOH法で酸化した場合,螢光物質としては唯一の反応産物(標準Thc)が認められた.B_1をBrCN-NaOH法で酸化して得た2物質(Thc I及びThc II)を結晶化し,薄層クロマトグラフィー,赤外吸収スペクトル,核磁気共鳴スペクトル,融点測定,マススペクトル等により標準Thcと比較したところ,Thc Iは標準Thcと同定され,Thc IIは別物質であった.なおThc I及びThc IIは紫外部吸収スペクトル及び螢光スペクトルにほとんど差がなく,B_1の螢光定量法としては唯一の反応産物を生じると見たして差し支えたいものと考えられた.

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Quantitative and qualitative changes in lung proteins after exposure to 100% oxygen for 40 hours were examined in the vitamin E deficient rats, as an indicator of severity of tissue damage. 1. A decrease in SH groups was observed in the lungs of oxygen exposure groups. It was more marked in the sediment fractions than in the supernatant fractions of the lung homogenates, especially in the vitamin E deficient group. 2. An increase in lung protein content was observed only in the supernatant fractions of lungs after exposure to oxygen. It was more marked in the vitamin E deficient group than in the supplemented group. 3. Hemoglobin content in the supernatant fractions of lungs paralleled with changes in protein content. 4. On the basis of eledtrophoretic analysis, changes in lung protein content resulted from increase in serum proteins and hemolysate proteins in the supernatant fractions, apart from lung tissue protein itself. 5. A decrease in DNA content was observed in the lung tissues after exposure to oxygen. It was more marked in the vitamin E deficient group than in the supplemented group.

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