The albino rats were kept on a riboflavin-deficient diet for one week to lower the riboflavin level in the intestinal mucosa. The intestine was excised and was soaked in Ringer's solution containing 5μg/ml each of riboflavin, FMN or FAD to observe the pictures of resorption. The following results were obtained.
1. Riboflavin is resorbed from the jejunum, whereby it is partly phosphorylated into FMN in the area between Goligi and basal mitochondria in the mucous epithelia.
2. FMN is resorbed fairly well as riboflavin, but FMN is not phosphorylated in the mucous epithelia.
3. FAD is resorbed from the intestinal mucosa, though it is relatively small in amount.

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1. γ-aminobutyric acid was used in an attempt to suppress the running fit incited by 2-methyl-4-amino-5-hydroxymethylpyrimidine (OMP) but proved ineffective. This was due to the fact that γ-aminobutyric acid is not transfered to the brain in an effective form when given from outside.
2. The running fit caused by OMP is suppressed by β-hydroxy-γ-aminobutyric acid. It must, however, be administered for more than 5 hours after injection of OMP.
3. The reason for the need for prolonged administration of β-hydroxy-γ-aminobutyric acid is its short duration of action, i.e., 30 to 40 minutes, and its prolonged inhibition of brain glutamic decarboxylase.

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1. Fractional separation of α-and β-carotene is not possible by use of alumina chromatography. Slaked lime chromatography is suited for this purpose.
2. For fractionating the isomers of β-carotene, slaked lime chromatography developed with p-cresyl-methyl ether in petroleum benzine is adequate. Neo-β-carotene B and U are found besides all-trans β-carotene, but no other isomers are observed.
3. α-Carotene appears in the B fraction in the procedure of the fractional determination of β-carotene isomers. It should therefore be previously removed by slaked lime chromatography, followed by development with petroleum benzine.
4. No difference was observed in the ratio of the isomers, whether the saponification was perfomed for 15 minutes or for 30 hours, provided the procedures are carried out in the dark.
5. An improved procedure for fractional determination of the stereoisomers of β-carotene in foodstuffs is described.
6. The distribution of β-carotene isomers in foodstuffs which are ingested in this country as the main sources of carotene was examined. The majority was all-trans form (80-90%), whereas the quantities of B and U were relatively insignificant (less than 10%). No significant difference in the ratio of the isomers between fresh and dried materials were observed in the samples, which were examined in the present study.

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Investigation was made on the fluorometric determination of nicotinamide and N¹-methylnicotinamide using column chromatography of ion exchange resins according to Kato. The urinary excretion of nicotinamide and N¹-methylnicotinamide was estimated by this improved method in the 24-hour urines of healthy and diabetic subjects.

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1. Various quantities of β-carotene and vitamin A palmitate were given orally in a healthy male subject and changes in serum vitamin A and carotene levels were investigated. The maximal rise in vitamin A level after ingesting β-carotene was 25% of that after ingesting vitamin A of the same I. U.
2. The changes in serum vitamin A and carotene levels were examined successively after ingesting various quantities of cooked squash and the rise in the highest vitamin A and carotene levels was compared with those obtained after ingesting β-carotene in oil. For a rise in serum vitamin A level equal to that obtained with β-carotene in oil, 2.1-2.8 times the amount of carotene in squash was required. For a rise in serum carotene level equal to that of β-carotene in oil, 1.4-2 times as much carotene in squash was required.
3. Similar experiments with the carrot showed that 3 times as much carrot was required as β-carotene in oil for an equal rise in serum vitamin A levels and twice as much carotene in carrot was required for an equal rise in serum carotene levels.
4. Similar experiments with spinach showed that 1.8 times as much carotene in spinach was required for a rise in serum vitamin A level and twice as much carotene in spinach was required for a rise in serum carotene level equal to that of pure β-carotene solution.
5. From these findings, it is assumed that the absorption of the carotene in food is 31 to 55% that of β-carotene in oil in man and this coincides well with the absorption rate estimated from the carotene in food and in the feces, suggesting an insignificant decomposition of carotene in the digestive tract.
6. Though almost all of the β-carotene in oil is absorbed, the increase in serum vitamin A level is about 1/3 that occurring with vitamin A palmitate, so that 6 times as much I. U. of carotene in food must be taken as vitamin A in order to obtain an equal effect. However, a rise in serum carotene level also takes place after ingesting β-carotene. Considering this fact, the effect of β-carotene may be greater than 1/3 of vitamin A of the same I. U., but possibly less than 1/2. The effect of the carotene in food is considered to be at most 1/4 that of vitamin A.

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1. Male weaning rats were divided into three groups and maintained for several weeks on a low fat, vitamin E-free diet.
2. Two of the groups termed control and E-excess groups were given, respectively, daily supplements of 0.5mg and 100ml α-tocopherol.
3. The third group termed E-deficient received no α-tocopherol.
4. The E-excess group had significantly higher concentration of DNA in liver than the control or E-deficient groups.
5. On the basis of an assumed constant amount of DNA per cell, it has been possible to compute the number of cells per unit weight of tissue and per liver, as well as the cell mass.
6. It is concluded that α-tocopherol in excess amounts stimulates hyperplasia in rat liver in the young animal.

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1. Male weaning rats, maintained on a low fat, vitamin E-free diet for several weeks were divided into three groups, termed respectively, vitamin E-deficient, control and vitamin E-excess.
2. As a daily dietary supplement 0.5mg α-tocopherol was added to the diet of each animal in the control group, and 100mg α-tocopherol was added to the diet of each in the E-excess group.
3. Glutamic-aspartic transaminase, glutamic dehydrogenase activities, and free amino acids and protein were determined in the liver tissue of all the experimental animals.
4. On a wet weight basis, excess vitamin E reduced only the free amino acids of liver tissue, while vitamin E deficiency increased only glutamic-aspartic transaminase activity.
5. On a cellular basis, excess vitamin E brought about a reduction in glutamic-aspartic transaminase activity, glutamic dehydrogenase activity, protein and free amino acids; on the same basis deprivation of vitamin E caused a significant increase in glutamic-aspartic transaminase activity only.
6. The significance of selecting a proper reference base is discussed.

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1. Flavin mononucleotide inhibits the initiation and shortens the duration of convulsions caused by phenol. Flavin mononucleotide previously injected is more effective than when injected at the same time as phenol for the inhibition of phenol convulsions, and they are similarly effective in shortening the duration of phenol convulsions.
2. A similar experiment was also carried out with flavin-adenine dinucleotide, and the results showed the same tendency. These results suggest that the riboflavin part of flavin nucleotide may be an active component in the above-mentioned effect.
3. Since the dissociation constant of flavin mononucleotide and phenol complex was measured to be 0.12 moles per liter, it was considered that 1/6 of phenol formed the complex with flavin mononucleotide in this experiment. This may partly explain the effect of flavins on the phenol convulsion.

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The areas of melanic pigmentation were found to contain much thiamine and riboflavin. Thiamine and riboflavin detected in these areas are mostly in the free form and flavinmononucleotide. The role of thiamine played in melanogenesis was further investigated. Thiamine, added to tyrosine-tyrosinase reaction is assumed to act as follows: it interferes in the action of dopa or dopaquinone, inhibits the production of dopa, extends the lag period of this reaction, and is in itself oxidized to thiamine disulfide.
The inhibitory action of thiamine in melanogenesis would not be so strong as that of reducing agents, such as ascorbic acid or cysteine; it would be just enough to adjust the progress of melanogenesis in such a way that it may not proceed too fast.

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