The vitamin A content (A_l, A₂, A_l aldehyde, A₂ aldehyde, and C₂₂ vitamin A) was determined in the liver oil of 5 species of Brazilian freshwater fish.

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By conducting a cross administration of Toc. nic and the combination of Toc. ace and 20% nicotinic acid to cases with insufficient micro-circulation and also by performing the cooling rewarming test during the administration, it was found that Toc. nic is more effective than the combination in reducing the MRT, and that the effectiveness of Toc. nic was not due to the synergic action of tocopherol and nicotinic acid but to the independent action of Toc. nic.

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Methylmalonic aciduria is a metabolic defect characterized by an ex-cessive excretion of methylmalonic acid in the urine.
The present paper reports the results obtained on rats fed a vitamin B₁₂-deficient diet to which were administered propionate or the amino acids L-valine, L-isoleucine, L-methionine, L-threonine. Detection of metabolites was carried out by gas chromatography. The results obtained showed that besides propionate only L-valine and L-isoleucine cause an increase in the daily excretion of methylmalonic acid, while L-methionine and L-threonine have no effect on the rat.

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Characteristics of the PaA uptake process in E. coil K-12 were studied. PaA uptake was energy-, temperature-, and pH-dependent, with an optimum pH of 6.5, and was markedly inhibited by sulfuhydryl reagents (N-ethylmaleimide, monoiodoacetamide) and uncouplers of oxidative phosphorylation (pentachlorophenol, 2, 4-dinitrophenol). Saturation of PaA uptake occurred with increasing substrate concentrations. The apparent K_m was 3.0×10^-7 M. PaA was transported into the cells of E. coli without phosphorylation, and the major intracellular metabolites accumulated were CoA and DP-CoA. The results suggest the presence of an active transport system for PaA in E. coli K-12.

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The uptake of ³H-pyridoxol by everted intestinal rings of the rat was studied mainly at concentrations of 0.1-4μM of the vitamin in the medium. Incubation of the tissue at 37°C for 60 min in Krebs-Ringer bicarbonate medium containing glucose and labelled pyridoxol resulted in intracellular accumulation of the labelled compounds. The total intracellular concentration of the compounds after the incubation was always higher than the extracellular concentration, and this accumu-lation was especially appreciable at relatively low external concentra-tions of the ³H-vitamin. The uptake under the same conditions was partially saturated with increasing concentration of ³H-pyridoxol in the medium, whereas the uptake during the initial 5 min of incubation increased in a linear manner with an increase of external concentration. The uptake was markedly depressed by lowering the temperature of incubation or addition of 4-deoxypyridoxol. The inhibition by 4-deoxypyridoxol affected the time course of uptake mainly in its later period, and also depressed both the linear and saturable components contained in the relation of uptake to the external concentration of the ³H-vitamin. However, a considerable uptake occurred even at the maximum inhibition with 4-deoxypyridoxol. Examination of the intracellular forms of the ³H-vitamin taken up revealed that the major components were three B₆ phosphates. This phosphorylating tendency was particularly extreme when the tissue was incubated under conditions allowing marked accumulation of the ³H-vitamin. Of these phosphate esters, ³H-pyridoxamine 5'-phosphate appeared most highly responsible for the accumulation. 4-Deoxypyridoxol remark-ably diminished the ³H-vitamin B₆ phosphates with a consequent de-crease of total intracellular ³H-vitamin B₆ compounds, although it permitted free ³H-pyridoxol increase. From these results it is con-cluded that pyridoxol enters the intracellular space by simple diffusion, is accumulated by metabolic conversion to the phosphate forms of the vitamin, and the converion is inhibited by 4-deoxypyridoxol.

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Male Wistar rats fed on a laboratory ration were fasted starting at 6 p. m., and the incorporation of the acyl molecules and acetate into glycerolipids was compared with that of fed rats.
1. The incorporation of ¹⁴C-palmitate and linoleate into hepatic glycerolipids at 0.5 to 6 hr after their injection intraperitoneally into rats that had been fasted for 15 hr was markedly depressed by fasting, whereas there was no remarkable difference in the incorporation of ¹⁴C-stearate. The fractional disappearance rate of ¹⁴C-linoleate from phosphatidylcholine (PC) and phosphatidylethanolamine and that of ¹⁴C-palmitate from triglyceride were greater in fasted than in fed rats. The incorporation of ¹⁴C-palmitate and stearate into the molecular species of PC was specifically altered. Desaturation by the liver of these precursors was depressed by fasting.
2. The synthesis by the liver slices of the acyl moieties from acetate was depressed by fasting.
3. When ¹⁴C-acetate was injected intraperitoneally at the beginning of fasting, the turnover of the labelled fatty acids in the liver between 3 and 6 hr after the injection was slower in fasted rats, that of the polyunsaturated acids being the slowest.
4. These results suggest that the specific changes in the turnover of individual fatty acids in hepatic glycerolipids are principal determinants of fasting-induced changes in the fatty acid compositions.

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The mechanism of acceleration of lipid peroxide formation in the liver homogenate of vitamin E-deficient mice was investigated. The quantities of unsaturated fatty acid, NADPH, ascorbate and hemo-protein, which have been so far thought to be the main factors of ac-celeration of lipid peroxidation, could not be considered the major reason for acceleration in vitamin E-deficient liver homogenate.
The phenomena resulting from the addition of a surfactant to normal liver homogenate and subcellular fractions resemble those obtained in E-deficient homogenate; (a) Though the rate of lipid peroxidation in E-deficient liver homogenate was 4.5-fold higher than that in normal one, the maximum rate of lipid peroxidation induced by the addition of Tween 80 was only little different in the above two homogenates. (b) Homogenate concentration of normal mouse liver in which maximum acceleration of lipid peroxidation was shown was lower than that of the E-deficient homogenate but shifted towards a higher concentration following the addition of Tween 80. (c) Vitamin E deficiency and the in vitro addition of Tween 80 resulted the decline of aminopyrine oxidation but in the activation of both the NADPH-linked enzymatical lipid peroxi-dation and the ascorbate-linked non-enzymatical one in microsomes and mitochondria.
These results indicate the possibility that the increase in lipid peroxida-tion in E-deficient liver was not a cause but a subsequence of membrane alteration, especially a change in tertiary structure of membrane-bound heme or non-heme iron protein.

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Studies were made on the cellular components of the blood, the serumiron concentration, and the circulating blood and plasma volumes of rats in pregnancy and on the iron transport from the maternal blood to the conception products (uterus and its contents) using radioactiveiron. Anemia of pregnancy developed and was most pronounced during late pregnancy when the conception products developed rapidly. The reticulocyte count did not increase significantly, so that there is no evidence for stimulation of hematopoiesis during pregnancy of rats. The circulating blood and plasma volumes increased significantly during late pregnancy, but the total hemoglobin and red cell volume did not increase.
The anemia in pregnancy of rats was due to hemodilution, but this hemodilution occurred in different grades in comparison with human pregnancy. The iron concentration of the serum decreased most during late pregnancy when development of the conception products was greatest and placental transport of iron to the fetus was largest.

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