VITAMINS

Male rats of Sprague Dawley strain (5-week old) were divided into four groups and then fed thiamin-free, thiamin-free + 1% nicotinamide, normal (thiamin-free diet+0.59 mg%thiamin hydrochloride) and the normal + 1% nicotinamide diets for 24-29 days. Tryptophan metabolites in the liver, blood and urine, thiamin in the liver and urine and enzyme activities of tryptophan-NAD pathway and of transketolase were compared among the four groups. NAD level in the blood and liver was almost the same between the normal and the thiamin-free groups, while that in the group of the normal+nicotinamide diet was much higher than that in the group of the thiamin-free+nicotinamide diet. The activity of liver nicotinamide methyltransferase and amount of N^1- methylnicotinamide in both thiamin-free groups were significantly increased in comparison with those in both normal groups. Urinary thiamin excretion was significantly higher in the thiamin-free+nicotinamide group than in the thiamin-free group. The same relation of thiamin excretion was also observed between the groups of the normal and normal+nicotinamide.

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Aqueous solutions of thiamin hydrochloride were incubated with catechol at pH 7.4 and 50℃ for 24 hr. Additional solutions of thiamin and catechol were incubated separately. After incubation, remaining thiamin was analyzed by the thiochrome procedure which showed that the thiamin in the thiamin-catechol mixture was reduced by 82.5-90% and the thiamin incubated alone by 18-20%. The solutions were fed to groups of rats which had been kept on a thiamin free diet for 17 days. Body weight gains, erythrocyte transketolase (ETKA), thiamin pyrophosphate effect (TPPE) and thiamin in the liver and urine were measured. The results showed that the thiamin-catechol mixture produced thiamin deficiency in terms of TPPE values indicating that the thiamin was inactivated with catechol in vitro. However, no effect was observed in the rat groups given thiamin and catechol separately.

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Effects of retinyl palmitate, thyroxine and ethanol on hepatic uptake and release of vitamin A (A) were studied in rat liver perfused with fluorocarbon emulsion. The liver of growing rats fed a normal diet or A-deficient diet was perfused in situ with retiryl palmitate and the uptake of retinyl palmintate from the perfusate and the release of retinol to the perfusate were estimated by HPLC. A rapid uptake of retinyl palmitate by the liver in normal and A-deficient rats was shown. The release of retinol from the liver without retinyl palmitate was singificantly lower than that in the normal and A-deficient groups with retinyl palmitate. Rat retinol-binding protein (RBP) normally circulates in the serum as a protein-protein complex together with prealbumin (PA). And so, this study was conducted whether the retinol present in the perfusate of normal rat was also present in the form of RBP-A-PA or RBP-A. The perfusate from the normal rats were chromatographed of Sephadex G-100 columns, and the elution volume of immunoreactive RBP was determined. The results indicated the retinol in the perfusate in RBP-VA which may be rapidly converted to RBP-VA-PA in the blood. No effect of the thyroid hormone on uptake and release of A was observed. These data indicated that retinyl palmitate stimulates secretion of RBP-A from the liver. On the other hand, it was shown that ethanol had releasing effect of retinol from perfused liver in normal rats and this phenomena might suggest one of the mechanisms that a low level of vitamin A in the liver of alcoholism rats.

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