300mg of DAsA was administered orally to three subjects, and the vitamin C levels in the blood and urine were determined, and the results were compared with those after administering 300mg of AsA. The following findings were obtained in the present experiment.
1. In the case of DAsA administration, AsA alone increased in the urine, whereas DAsA and DKG remained almost unchanged. It was also the case with AsA administration.
2. In the case of DAsA administration, the rise of vitamin C levels in the blood and the urinary excretion of AsA were more rapid than in the case of AsA administration.
3. When the subject, having the same total vitamin C levels in the blood, is given the equivalent amounts of DAsA or AsA, about the same amounts of AsA is excreted in the urine.
4. DAsA is not only absorbed through the digestive tract more quickly than AsA, but also the levels of AsA in the erythrocytes increase rapidly.
5. In vitro experiment showed that the permeability of DAsA through the erythrocyte membrane was markedly greater than that of AsA, and that the DAsA in the erythrocytes was quickly reduced to AsA.

View full abstract

The distribution of riboflavin in normal organism was studied both phylogenically and ontogenically using histochemical techniques. Further the change of the distribution of the vitamin was observed on pathological materials of human corpses and on the animals poisoned experimentally with carbon tetrachloride. Following findings were obtained:
1. Marked differences in the distribution of riboflavin were observed according to the species and individuals of the animals tested.
2. There was specific distribution of the vitamin was observed according to the species of the animals. This specificity was discussed from the point of organ phylogenesis.
3. The vitamin was most abundantly detected in the organs with vigorous enzymatic activities in higher animals.
4. Observing ontogenically, definitely less vitamin was found in the materials of early fetal life. The vitamin increased gradually with the lapse of fetal life, especially marked in the end of pregnancy, but definitely less than after birth.
5. Observation on human corpse of sudden death revealed the same distribution pattern as found in normal mammals.
6. Changes of the distribution pattern of the vitamin in pathological cases, especially in liver cirrhosis were described and pointed out the disturbance of phosphorylation of the vitamin.
7. After giving carbon tetrachloride, a poison for various enzymes of citric acid cycle, reduction in the uptake of the vitamin was detected. Its cause was ascribed to the decrease of absorbability of the intestine, reduction of the uptake of the vitamin and of the phosphorylating activity in the liver and disturbance of the reabsorption of the vitamin from the epithelium of renal tubuli.

View full abstract

It has been demonstrated that extracts of human livers prepared with potassium ascorbate contain a derivative which is very active in supplying the FA requirement for L. casei, but only slightly so for P. cerevisiae or S. faecalis R. No autolytic or enzymatic treatment is required for the release of this activity.

View full abstract

1. In the present paper it was studied whether thiamine activated the oxidative phosphorylation of various substrates in the presence of the washed liver homogenate of thiamine-deficient rats.
TABLE II Oxidative Phosphorylation of Pyruvic Acid^a
TABLE III Qo₂(N) for the Phosphorylation of Various Substrates in the Presence of Washed Liver Homogenate
TABLE IV P/O Ratios for Various Substrates
2. To the reaction system pyruvic acid, α-ketoglutarate, L-proline, L-glutamic acid, and L-valine were added. The decrease of P/O ratio was seen in thiamine-deficient homogenate, but no such phenomenon occurred in thiaminepositive control animals.

View full abstract

1. Catalytic reduction was carried out with fresh (wet) Ca-5-keto-D-gluconate preparation isolated from the fresh broth, and it was found that Ca-L-idonate was obtained in a good yield, 94%.
2. The Ca-L-idonate thus obtained was studied for the confirmation of its properties by paper chromatography, potentiometric titration and by the change of specific rotation corresponding to the lactone formation.

View full abstract

1. Metabolic conversion of β-carotene to vitamin A was studied with the intestine homogenate of vitamin B₁-deficient rats. It was found that β-carotene was convertible to vitamin A alcohol in the rats receiving thiamine as well as those slightly B₁-deficient (scale 1-2), but complete failure of the conversion was seen in the severely deficient animals (scale 3-4).
2. The additive effects of various coenzymes revealed that the addition of FAD plus DPN or DPN plus cytochrome c contributed to the metabolic conversion of β-carotene to vitamin A, whereas other combinations of the coenzymes gave negative results.
3. In anaerobic experiments, it was confirmed that β-carotene was convertible to vitamin A in the rats receiving thiamine, but it was negative in B₁-deficient animals. In this case, FAD plus DPN contributed to the in vitro formation of vitamin A from β-carotene even in B₁-deficient intestine homogenate.
4. In the experiment on the conversion of synthetic vitamin A aldehyde to the alcohol, the rats receiving thiamine gave positive result and vitamin A ester was detected on a paper chromatogram, whereas it was completely negative in the B₁-deficient group. The addition of both FAD and DPN was effective for enzymatic conversion of vitamin A aldehyde to the alcohol.
5. Metabolic pathways of β-carotene te vitamin A may be divided into two systems, i.e., a system independent on FAD and DPN involving the conversion of β-carotene to vitamin A aldehyde and a system dependent on FAD and DPN involving the conversion of vitamin A aldehyde to A alcohol.

View full abstract

Using AsA bacterium No. 4 the mechanism of ascorbic acid degradation was studied with the following results.
1. The effects of substrate concentrations, nitrogen sources, organic acids and sugars on the degradation of ascorbic acid were tested.
2. An enzyme system degrading ascorbic acid was found to be adaptively produced under anaerobic conditions and an initial pathway of ascorbic acid degradation through dehydroascorbic acid and diketo-L-gulonic acid was confirmed.
3. An enzyme in nonadapted cells catalyzing a reaction: ascorbic acid→dehydroascorbic acid was assumed to exist and the effects of inhibitors such as 2, 4-dinitrophenol, NaF, KCN and NaN₃ were examined.

View full abstract

1. The reaction L-ascorbic acid→D-dehydroascorbic acid by adapted and unadapted cells is catalyzed by different enzymes, i.e.. by L-ascorbic acid oxidase in the former and L-ascorbic acid dehydrogenase in the latter.
2. The adaptive enzyme system in L-ascobic acid-adapted cells was inactivated by standing without the substrate, but is reactivated by adding L-ascorbic acid.
3. The relationship between the chemical structure of L-ascorbic acid and its degradation by the cells was investigated.

View full abstract

1. L-Ascorbic acid degradation by L-ascorbic acid-adapted cells is carried out by an intracellular enzyme.
2. The trial for extracting the enzyme system proved unsuccessful.
3. The effects of inhibitors for the degradation of L-ascorbic acid and glucose by the adapted cells were investigated.
4. Tricarboxylic acid cycle is assumed to be involved in the degradation of L-ascorbic acid in the L-ascorbic acid-adapted bacteria.

View full abstract

1. Brain γ-amino-butyric acid is reduced in the 2-methyl-4-amino-5-hydroxy-methylpyrimidine-induced running fit and the reduction is apparent prior to the seizure.
2. Brain γ-aminobutyric acid is not reduced when the seizure is prevented with pyridoxine or 2-methyl-4-amino-5-aminomethylpyrimidine.
3. Brain γ-aminobutyric acid is also reduced in the isonicotinic hyrazideinduced running fit. When pyridoxine is given concomittantly, the seizure occurs earlier and γ-aminobutyric acid is decreased earlier.
4. The reduction in γ-aminobutyric acid is believed to be the cause of the running fit.

View full abstract

It was clarified that the mechanism of chemical degradation of L-ascorbic acid was different from that by microorganism. The metabolic products were identified by paper chromatography and the mechanism of it was partially elucidated.

View full abstract