4-β-Hydroxyethylamino-5-aminouracil (VII), 8-N-hydroxyethyl-6, 7-dimethyllumazine (VIII) and 9-hydroxyethylflavin (IX) were chemically synthesized. The following reactions, VII→VIII→IX, were successfully proved by the growing cells of Cl. acetobutylicum and the enzyme preparations of both A. aerogenesand Er. ashbyii, although the conversion of 8-N-methyl-6, 7-dimethyllumazine into lumiflavin was negative. This represents the model experiments of the riboflavin synthesis from 4-N-ribitylamino-5-aminouracil as one of the possible intermediates. The enzymic activity toward the conversion of VIII to IX was much lower than that of 6, 7-dimethylribolumazine to riboflavin. The mechanisms of the ribityl side chain synthesis were discussed.

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A switch of an ordinary to a vegetable diet resulted in an increase both in the fecal PaA and in the PaA synthesized and it resulted in a further increase with an addition of cellulose. On the contrary, a switch from the ordinary to a meat diet resulted in a reduction in the fecal PaA and the PaA synthesized, but they were definitely enhanced when cellulose was added to the meat diet. The total amount of PaA excreted in urine and feces was constantly and definitely larger than that of PaA ingested. The synthesis of PaA by intestinal bacteria was, therefore, very marked.

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1. The apoenzyme activity of Pyruvate oxidase system in the tissue of B₁₂-deficient rats was studied in vitro under various additions of B₁₂, cytochrome c, niacinamide, DPN, DPT, lipoic acid, CoA, ATP, FAD, glutathione as well as fumaric acid. The decrease of the apoenzyme activity in B₁₂-eficient rats was always recognized in the uptake of O₂ and the evolution of CO₂ after adding pyruvate.
FIG. 3 Difference in Activities for Pyruvate Oxidation between Washed Liver Homogenate and Untreated Whole Homogenate.
FIG. 4 Effect of FAD and Fumarate on the Activity of Pyruvate Oxidation in Washed Liver Homogenate of B₁₂-deficient Rats.
2. The animals receiving 0.2μg of B₁₂ per os daily before experiments showed always an increased apoenzyme activity of pyruvate oxidase system.
3. The results seem to lead to the conclusion that vitamin B₁₂ contributes to the activation of the apoenzyme in pyruvate oxidase system in rats.

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1. Metabolic conversion of β-carotene to vitamin A was studied by oral administration to rats, rabbits as well as frogs, and several unknown compounds were found on paper chromatograms.
2. Further studies on metabolic conversion of β-carotene to vitamin A in vitro by rat tissue homogenate, revealed two metabolic intermediates in paper chromatograms.
Compound I with an absorption maximum at 296mμ in ethanol was identified as β-ionone, and the Compound II with an absorption maximum at 365mμ in petroleum ether was identified as a kind of vitamin A aldehyde-proteincomplex.
These findings lead to the plausible conclusion that vitamin A aldehydeprotein-complex may be an intermediate in the metabolic conversion of β-carotene to vitamin A alcohol.

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1. The enzyme activity of the purified thiaminase II was examined from 1 to 30 minutes.
2. The purified thiaminase II showed only a single boundary curve by the ultracentrifuge sedimentation. The sedimentation coefficient of the thiaminase was 3.7×10^-13.

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1. Running fit-inducing agents characteristically inhibit the activity of brain glutamic decarboxylase and this inhibition is closely related to the occurrence of the running fit.
2. The enzyme is not affected by convulsants, e.g., strychnine, cardiazol and ammonium chloride, which do not incite the running fit.
3. The inhibitory action of carbonyl reagents is stronger than that of OMP group substances.
4. The site of origin of the running fit was discussed.

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1. When mice are raised on a vitamin B₆-deficient diet, there is a decrease in activity of the enzyme involved in the transamination reaction between γ-aminobutyric acid and α-ketoglutaric acid in the brain and the activity is restored by administration of vitamin B₆.
2. This enzyme is inhibited by carbonyl reagents and is restored by pyridoxal phosphate. There is no increase in activity, however, in normal animal brain when pyridoxal phosphate is added.
3. The activity of the enzyme is lost by dialysis and restored by addition of pyridoxal phosphate.
4. Pyridoxal phosphate is considered to be involved as a coenzyme of this enzyme.

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1. Bacterial flavokinase has first been isolated from the dried cells of E. coli, and the properties of the enzyme were investigated.
2. The Optimum pH is found to be 6.8 and the optimum temperature 30° for the phosphorylation of riboflavin.
3. A metallic ion is required for full activity; Mg⁺⁺, Mn⁺⁺ and Fe⁺⁺ are each effective, whereas Ca⁺⁺ is inhibitory.
4. Evidence is presented that bacterial flavokinase phosphorylates quite well both araboflavin and isoriboflavin as riboflavin, producing the corresponding mononucleotides.
5. Flavokinase activity is found in all the bacterial species examined, and the role of the enzyme for the biosynthesis of flavin coenzymes is discussed.

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Range and average values were determined for the vitamin B₁₂ levels of the liver tissues obtained at laparotomy from 35 patients with chronic liver diseases and from 18 patients with peptic ulcer or gastroptosis. In cirrhosis the average value was 0.19μg per g, in cancer of the liver possibly developed from cirrhosis 0.13μg per g, in Banti's syndrome 0.62μg per g, and in peptic ulcer and gastroptosis 0.74μg per g. In cirrhosis and Banti's syndrome the liver B₁₂ levels of the cases receiving parenterally B₁₂ did not rise significantly with a few exceptions, the average values remaining on the similar levels described above.
Following the operation of portacaval anastomosis the liver B₁₂ levels of the patients with cirrhosis or Banti's syndrome fell even during parenteral administration of the vitamin. The fall following the operation was not remarkable in cases whose pre-operation levels of the liver B₁₂ were low.

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1. A study was made on the physiological rôle of ascorbic acid when a living body is subjected to decompression with or without previous treatment of pure oxygen inhalation.
2. After a non-hypoxic decompression of 200mmHg was loaded on rats for 20 minutes, the animals showed severe symptoms and at the same time the ascorbic acid levels in adrenals, liver, blood and urine showed 81.9, 72.2, 133.8 and 292.6% respectively as compared with that in the control groups. This shows that this form of stress causes a disturbance in the utilization of ascorbic acid in the periphery and gives rise to a mobilization of the vitamin, which in turn causes a stagnation of the vitamin in the blood stream. The excess ascorbic acid is excreted in the urine resulting in the increase of urinary excretion of the vitamin.
3. When the animals had been allowed to inhale pure oxygen under normal pressure for two hours in order to replace nitrogen beforehand, and the similar decompression were loaded, they exhibited practically no abnormal symptoms. Ascorbic acid levels in the adrenals, liver, blood and urine showed 58.3, 62, 31 and 97.5% respectively as compared with that of the control groups, suggesting that the inhalation of pure oxygen prior to decompression not only prevents the formation of nitrogen bubbles and symptoms due to decompression, but also has a favorable influence on the oxidation of ascorbic acid in the peripheral tissues and enhances its utilization, thus increasing tolerance to low pressure.

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1. The saturation level of total ascorbic acid in the whole blood was found to be 1.1mg per 100ml as estimated by dinitrophenyl hydrazine method, a value lower than that estimated by indophenol method.
2. A linear negative correlation was found between the total ascorbic acid level in whole blood and the amount of ascorbic acid required for saturation.
3. Daily ascorbic acid consumption by adults in a saturation state was 95mg on an average. The amount of the vitamin consumed in the body increased with the rise of the amount ingested. After attaining a maximum level in a saturation state, the level in blood remain unchanged. For the concept of saturation with ascorbic acid, the increase of consumption in the body is regarded as important.
4. In a saturation state of pregnant and lactating women, the difference between the daily amount of ascorbic acid ingested and the amount excreted in the urine was about 80mg in pregnants and about 130mg in lactating women. The increase in the latter corresponds to the amount secreted in the milk. The daily consumption of the vitamin in the former was somewhat less than that in healthy adults, possibly due to the specificity of ascorbic acid metabolism in pregnants. The increase in ascorbic acid consumption in the body was not observed in pregnant and lactating women.

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