1. O-acetoglycolyl-S-furoyl thiamine (AFT)-³⁵S and thiamine (B₁)-³⁵S showed obvious differerences in radioactivity in the whole body autoradiogram.
2. Administration of AFT-³⁵S exhibited the higher radioactivity in the muscles (heart, skeletal, diaphram, masseter), stomach, brain, brown fat tissue and blood comparing with the case of B₁-³⁵S. In these organs, the radioactivity derived from AFT-³⁵S was found at higher concentration and was kept for a longer period as compared with B₁-³⁵S.
3. AFT converted into thiamine and its phosphoric acid esters within an hour after the administration, and the most abundant derivatives of thiamine was thiamine diphosphate.
4. As compared with B₁-³⁵S, AFT-³⁵S showed a considerably higher concentration of thiamine diphosphate in various organs.

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In the present paper the role of glucose cycloacetoacetate (GCA) in vitamin C synthesis of riboflavin-deficient rats was studied. It is evident from the results that GCA helps in maintaining vitamin C levels in blood and tissues of riboflavin-deficient rats.

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1. In the supernatant fraction isolated from the homogenate of scorbutic guinea pig gingiva, five lactate dehydrogenase (LDH) isoenzymes were always found by the starch gel electrophoresis, and the order of the activity was found to be LDH 2>LDH 1>LDH 3>LDH 4>LDH 5.
2. The activity of LDH 1 and LDH 2 in scorbutic gingiva was about 1.4- and 2-fold respectively of the normal. However, the activity of LDH 3, LDH 4 and LDH 5 was not increased.
3. In the supernatant fraction and the homogenate obtained from scorbutic gingiva, LDH activators were not found.

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A fat-soluble derivative of riboflavin, riboflavin-2′, 3′, 4′, 5′-tetrabutyrate was crystallized from methyl alcohol-water mixture (19:5, v/v), and the reddish yellow, rhombic crystals were obtained. Melting point of this recrystallized sample was found at 147-148° which is a little higher than that previously reported.
Infrared spectrum of this sample showed that 2′, 3′, 4′, 5′-tetrahydroxyl groups of riboflavin completely disappeared and that newly formed ester linkages between alcoholic hydroxyl group and carboxyl group of butyric acid appeared.
Absorption and fluorescence spectra of R-BUT were studied in water, ethyl alcohol and carbon tetrachloride, and molar extinction coefficients were determined. It was found that R-BUT is soluble in water at low concentration.

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1. Coenzyme B₁₂ content of liver and kidney was measured by the coenzyme B₁₂ activity in tne intramolecular oxidation-reduction reaction of α-glycol. According to Abeles the apoenzyme was prepared from Aerobacter aerogenes. Following Baker's method, coenzyme B₁₂ was extracted from the liver and kidneys of human and some animals.
2. The content of coenzyme B₁₂ was measured in rats, rabbits, guinea pigs and human subjects. The average value of coenzyme B₁₂ content in normal rat liver was 0.68±0.35μg/g wet weight and that of kidney was 1.88±1.08. The average value of rabbit liver was 1.18±0.25 and that of kidney 1.65±0.61, the values larger than those of rats and guinea pigs. The average value of coenzyme B₁₂ content of human liver without liver injury was 1.23±0.31. Coenzyme B₁₂ content of the liver and kidneys of the rat maintained on a vitamin B₁₂-deficient diet was smaller than those of the normal rat.
Coenzyme B₁₂ content of the liver and kidney of the rat saturated with 100mμg of vitamin B₁₂ did not differ so much from those of the normal rat. In the rats having acute liver injury due to carbon tetrachloride, the coenzyme B₁₂ in the liver and kidneys decreased remarkably from 6 to 9 hours after liver damage, and a sign of recovery of the coenzyme content was recognized 15 hours after damage. Thereafter, the coenzyme content approached to that of the normal rat.

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1, The clearance in the blood and the distribution in tissues of coenzyme B₁₂ were examined in comparison with cyanocabolamin in both cases of single and simultaneous administration.
2, Coenzyme B₁₂ disappeared faster from the blood and showed a stronger affinity for tissues than cyanocobalamin
3. By differential counting method with medical spectrometer coenzyme B₁₂ and cyanocobalamin did not show any competition when taken in tissues.
4. In the case of vitamin B₁₂ deficient rats the distribution in tissues of cyanocobalamin was not so different from normal rats, while that coenzyme B₁₂ was enhanced. Thus the coenzyme seems to be one of the storage form of the vitamin in the liver.
5. The coenzyme uptake in the vitamin suturated rats was reduced, suggesting the conversion of the vitamin into the coenzyme.
6. In case of an intravenous injection hydroxocobalamin showed a faster disappearance from the blood and a slower urinary excretion than cyanocobalamin, showing that hydroxocobalamin has a strong affinity for tissues. It was actually verified with a biological test.
7. Intrinc factor was found to have some influence on the hepatic uptake of the coenzyme, which showed a remarkable increase in a short time.

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1. The metabolism of vitamin B₁₂ in the body of rats and human subjects was examined.
2. Fractionation of three cobamides, CN-B₁₂, OH-B₁₂ and DBCC, and their identification were carried out.
3. The conversion from cyanocobalamin or hydroxocobalamin to coenzyme B₁₂ was found to take place in the liver and kidneys of rats and humans. Considerable quantities were converted in a short time. In fact, more than half of the administered derivatives were converted into the coenzyme in 48 hours.
4. The conversion from hydroxocobalamin to the coenzyme was faster than that from cyanocobalamin, which means that hydroxocobalamin is favorable for utilization of the vitamin.
5. The conversion rate in question was higher for the vitamin deficient rats than that for normal rats, showing that the requirement for the coenzyme is increased in the case of the deficient rats.
6. The conversion rate in the liver was lower in the carbon tetrachloride-injured rats and in the damaged human liver than that of normal ones. In these cases the conversion rate from hydroxocobalamin to the coenzyme was not changed appreciably as compared with the normal, showing that hydroxocobalamin is more available in the case of liver damage.
7. The intrinsic factor gives rise to an increase of the hepatic uptake and the quantity converted.

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Effect of different high fat diets on vitamin B₁₂ levels in plasma and liver in rats was studied, and the following findings were obtained.
1. High fat diet (35%) produced vitamin B₁₂ deficiency in rats after. 120 day-feeding.
2. The effect of saturated fats on vitamin B₁₂ levels in liver and plasma was more pronounced than that of the unsaturated ones.
3. Supplementation of linoleic acid in hydrogenated fat diet could improve the B₁₂ status.

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1. It was observed that in the medium containing E. coli K₁₂ dehydroascorbic acid was reduced as long as pyruvate existed.
2. The reduction is dependent upon a pyruvate oxidase system, but is independent of dehydroascorbic acid reductase.
3. Lipoic acid, dihydrolipoic dehydrogenase and CoA were found to be essential for the reduction in the pyruvate oxidase system of the cell-free extract, using reduced NAD as the hydrogen donor, but dihydrolipoic dehydrogenase was not essential in the absence of reduced NAD.
4. A plausible reaction mechanism is presented.

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1. As long as pyruvate existed in the medium containing the pyruvate oxidase isolated from pig heart muscle, dehydroascorbic acid was reduced, and the reducing activity was independent of dehydroascorbic acid reductase.
2. The reducing activity was dependent upon a pyruvate oxidase system, and the hydrogen donor was found to be dihydrolipoic acid.
3. As the non-enzymatic reduction of dehydroascorbic acid with dihydrolipoic acid was extremely rapid, participation of an enzyme catalyzing the hydrogen transfer from dihydrolipoic acid to dehydroascorbic acid was not determined.

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