After the oral administration of 5,6-O-isopropylidene-ascorbic acid (IAsA) and 5,6-O-isopropylidene-ascorbic acid 2-sulfate (IAsS), vitamin C levels in blood, liver, kidney, brain and muscle were determined to investigate the con-version of these two compounds into vitamin C in rainbow trout (body weight 160〜190g). Total vitamin C contents of these biological samples were deter-mined by the 2,4-dinitrophenylhydrazine method [J. Biol. Chem., 168, 197 (1947), Vitamins, 43, 210 (1971)]. Vitamin C levels in blood and these tissues were significantly increased in the IAsA-administered group, but slightly in the IAsS-administered group. Therefore, IAsA may be more effective than IAsS as dietary vitamin C source for rainbow trout.
The antioxidative effect of vitamin B_2 On the recovery of mitochondrial potential disorders induced by ultraviolet light exposure was studied by the method of fluorescence of 8-anilino-1-naphthalene sulfonate. Vitamin B_2 (free form) was injected intraperitoneally to rats during 6 days, after which mitochondria were prepared from rat liver. Ultraviolet irradiation upon the mitochondrial suspension resulted in the increase of fluorescence on the C-side of inner mitochondrial membrane. However vitamin B_2-administration was found to prevent the change of surface potential in the state of non-energized mitochondria and the respiratory disorders of mitochondria. The biochemical effect of vitamin B_2 to the surface potential of membrane was discussed by interaction with lipid peroxidation in mitochondria.
Four groups of rats were fed vitamin E deficient or supplemented diets containing 5.6% or 15.6% linoleic acid, respectively, for 100 days. The histological changes of the thyroid gland of these rats were light and electron microscopically examined. The results obtained are as follows: 1) The weight and cell height of the thyroid gland of vitamin E deficient rats did not show remarkable changes. The diameter of thyroid follicles was smaller in these rats than those of vitamin E supplemented control rats. 2) The follicular epithelial cells of the vitamin E deficient rats showed somewhat degenerated form and irregular arrangement. They contained small degenerated mitochondria, dilated sacs of endoplasmic reticulum, less developed Golgi apparatus and a large accumulation of lipofuscin granules. The re-absorptive figures of microvilli and absorbed lipid droplets disappeared in the deficiency. 3) The follicular epithelial cells of the vitamin E deficient rats treated with linoleic acid showed further remarkable degenerative changes; vacuolation of cells, increase of lysosomes and peroxisomes and accumulation of lipofuscin granules. Some follicular lumens contained cellular fragments fallen down from the follicular wall. 4) The thyrotrophic hormone cells of the pituitary gland of vitamin E, deficient rats were enlarged. The change resembles that in thyroidectomy.
The effect of nicotinic acid (NiA) on cerebroside synthesis in brain was studied with 8 weeks-old rats. In 62 days-old rats fed NiA deficient diet for last 50 days, the concentration of NiA and cerebroside in brain was significantly lower than those receiving NiA supplemented diet. NiA concentration in brain of the NiA deficient rat was recovered by the administration of NiA. However, cerebroside concentration was not recovered by the administration of NiA. The synthesis of cerebroside was followed in brain of 62 days-old rat after an intracerebral injection of (U-^<14>C)-L-serine. After myelination no remarkable difference of the total radioactivity incorporated into cerebroside fraction was observed by the administration of NiA to the NiA deficient rat. From these observations, it was suggested that cerebroside synthesis in brain after myelination was not affected by the administration of NiA.