Possible action of chlortetracycline (CTC) to provoke ariboflavinosis was examined using albino rats. Body weight gain and flavin contents of the liver and kidney were measured with 7 groups of animals: animals of group a were fed with riboflavin-deficient diet, animals in groups b-g were supplemented daily for a rat with 10μg of riboflavin (group b), CTC 5mg (group c), riboflavin 2μg plus CTC 5mg (group d), riboflavin 2μg plus CTC 10mg (group e), riboflavin 5μg plus CTC 10mg (group f), riboflavin 10μg plus CTC 10mg (group g). The results showed that CTC promotes the appearance of ariboflavinosis. As to the cause of this effect, it is noted that riboflavin and CTC act in competition with each other. This may be explained, at least partly, by the previously reported fact that CTC forms a complex with flavins and inhibits flavin enzyme in competition with the apoenzyme as studied by using D-amino acid oxidase.

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1. The CoQ content of whole rat liver increased significantly as compared with the control after the intramuscular administration of CoQ₇, CoQ₉ or CoQ₁₀, but increased slightly after the administration of CoQ₂ or CoQ₆. In the mitochondrial fraction, CoQ content increased only after the administration of CoQ₇ or CoQ₉. After the administration of CoQ compounds, paper chromatography of the liver extract showed a corresponding increase of CoQ.
2. Twenty-four hours after giving CoQ₇-¹⁴C to rats, the percentage recovery in the liver administered was found to be 12.3±0.47% of the dose of ¹⁴C administered intramuscularly or 11.8±1.37% of those given orally. When the CoQ fraction was developed paperchromatographically, the radioactivity on the actigram was found in the CoQ₇ portion exclusively.

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Free forms of B₆ are actively transported into the erythrocytes against a concentration gradient, especially, pyridoxal reaches quickly a level large enough to include permeation of all the cell water. Small amounts of pyridoxine and pyridoxal transported in the cells are in the phosphorylated forms. Decreasing the hydrogen ion concentration results in a decreased transportation of pyridoxine and pyridoxamine, but no decreased transportation of pyridoxal. Transported pyridoxine in the cells scarcely leaked out by the washing process, but a small amount of transported pyridoxal was eluted in the washing saline solution. The transported amounts of pyridoxine and pyridoxamine into the cells increase in accordance with the acceleration of intracellular glycolysis induced by the uptake of phosphate, while the transported amount of pyridoxal does not. Furthermore, the concentration of pyridoxal phosphate in the cells after an incubation with various forms of vitamin B₆ is decreased in parallel with the decreased amount of phosphate in the medium. In contrast, the transported amount of phosphorylated forms of B₆ into erythrocytes are much smaller than that of their free forms, although the transportation of pyridoxal phosphate in the cells increases in parallel with the elevation of the amount in the medium. The binding of pyridoxine and pyridoxal by the ghost cells is not observed. The ghost cells liberate enzymatically about 24% of pyridoxal from pyridoxal phosphate.

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1. Aminothiamine inhibits the growth of thiamine requiring L. fermenti by competing with thiamine, the inhibition index being 450 to 470.
2. Aminothiamine inhibits competitively uptake of thiamine by resting cells of baker's yeast and L. fermenti.
3. Aminothiamine inhibits baker's yeast thiamine kinase.
4. As one of the sites of antithiamine action of aminothiamine on microorganism the competition between thiamine antagonist and thiamine in the process of permeation into cell membrane was discussed.

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1. Distribution of flavokinase and FAD-pyrophosphorylase in various organs and the cell fractionations were described.
2. Flavokinase and FAD-pyrophosphorylase were separated from the same starting tissue by DEAE-Sephadex column chromatography.
3. Several properties of the purified enzymes were investigated. The most effective metal ion, optimum pH, activation energy and Michaelis constant were determined.
4. Inhibition of flavin enzymes by D-araboflavin showed a competitive one which was distinctly observed on flavokinase and no effect was found on FAD-pyrophosphorylase. This would suggest that the inhibition of araboflavin occurred on the first phosphorylation step of free riboflavin in the body.

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Feeding of 14, 400, 28, 800, 57, 600 and 93, 600 I. U. of retinol respectively to adult rats significantly raised their hepatic vitamin A and esterified cholesterol contents as compared to control rats. The incorporation of acetate-1-¹⁴C radioactivity into hepatic total cholesterol was significantly increased in rats fed 93, 600 I. U. of retinol as compared to control. Incorporation of acetate-1-¹⁴C radioactivity was significantly higher in hepatic free cholesterol of all the retinol fed groups as compared to control.

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In order to obtain further informations on the mechanism of the decomposition of the cobalt-carbon bond of acetylcobalamin by nucleophilic agents, the reaction was carried out using an appropriate apparatus under either aerobic or anaerobic conditions.
By time-course study of the spectral changes, direct spectrophotometric evidence was presented for the formation of vitamin B_12S as the initial intermediate in these reactions. Formation of acetic acid was also detected in the case of alkaline cyanidedecomposition. These facts indicate that the cleavage of the cobalt-carbon bond of acetylcobalamin by alkaline cyanide is caused by OH^- ion generated from the hydrolysis of the cyanide in a similar way as in the case of β-cyanoethylcobalamin. Discussions on the mechanism of the conversion of vitamin B_12S into dicyanocobalamin were described.

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S-Pyrioxylthiamine disulfide was synthesized by acid hydrolysis of isopropyridene pyrioxylthiamine disulfide which was prepared from isopropyliene pyridoxine thiosulfate and thiamine.

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Pyridoxine disulfide and pyridoxamine disulfide were prepared by the reaction of their thiosuifate with mercaptans. The reaction of sodium hydrogensulfide with pyridoxine and pyridoxamine thiosulfate was also discussed.

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Various derivatives of γ-aminobutyric acid (GABA) including homopantothenic acid (HOPA) were prepared and their seizureand excitation-suppressing action and sleep-prolonging effect were examined. The followings were observed: 1. A degree of suppressive effect against the usual convulsants was found with α-OH-GABA, N-carbobenzoxy-GABA and pantoyl derivatives and the effect was most pronounced with β-OH-GABA. 2. A delay in the appearance of the 2-methyl-4-amino-5-hydoxymethyl pyrimidine-induced running fit was noted with the amino-radical bound forms and especially, HOPA completely suppressed the seizure in a dose of 3mg/g. 3. The amino radical bound forms also inhibited the maximal seizure induced by electric shock and of these compounds, the pantoyl derivatives showed a trend for decline in the seizure threshold value. 4. The excitation enhanced by Philopon and Ritalin was suppressed by HOPA and pantothenic acid and especially in the former its effect was remarkable. 5. A prolongation of the duration of sleep produced by Auropan-Na was observed with the pantoyl derivatives, α-SH-GABA and N-carbobenzoxy-GABA.

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The action of homopantothenic acid (HOPA) on the central nervous system was investigated on the basis of its effect on the transcallosal potential in the cat and spontaneous electroencephalogram in the rabbit. The antagonistic action against pentylenetetrazol- and picrotoxin-induced seizures was also examined electroencephalographically. The following results were obtained.
1. Intraarterial injection (carotid artery) and topical application on cortex of HOPA did not affect the transcallosal potential. 2. A slight alert pattern was obtained on the spontaneous electroencephalogram of the unanesthetized restrained rabbit with intravenous injection of 500mg/kg or intracysternal injection of 5mg/kg of HOPA. 3. An antagonistic effect against the electroencephalograms of pentylenetetrazol- and picrotoxin-induced seizures was not observed after intravenous injection of 500mg/kg of HOPA. These electroencephalograms were suppressed by the intracysternal injection of 5mg/kg of HOPA-Na, but complete disappearance of spike-and-wave discharges was not obtained.

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