The metabolism of the nicotinic acid (NA) moiety of d, l-α-tocopheryl nicotinate (TN) was investigated using radiolabeled TN, with the labeled moiety of the molecule being either NA or tocopherol, and labeled NA. After a single orally administered dose of TN to normal rats, the level of this radiolabeled compound increased gradually in the blood. After the oral administration of NA, the level increased and decreased rapidly initially before coming to a stable level of elevation. Urinary metabolites from rats administered TN were compared with those from rats administered NA. In the case of NA administration, the main metabolites in the urine were nicotinuric acid and NA, while NA was the main metabolite in the urine from rats given TN. These results indicate that the metabolism of the NA moiety of TN differs from that of free NA. The tocopherol moiety of TN was taken up by red blood cell membranes and the NA moiety was distributed among red blood cell contents. The main metabolite in both red blood cell contents and liver after a single orally administered dose of TN was nicotine amide.
To determine the metabolism and distribution of TN incorporated into the cellular organelles of the liver, TN was injected intravenously to normal rats and the livers subjected to cell fractionation. TN was distributed in nuclear, mitochondrial, lysosomal, microsomal and supernatant fractions in unchanged form. Several metabolites of TN were detected as minor components in these organelles as well.

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Spectral characterization of 5, 6-epoxyretinal isomers (II) prepared by a regioselective epoxidation of the parent retinal isomers have been described. High-performance liquid chromatographic separation of epoxyretinals and a photoisomerization behavior of all-trans-5, 6epoxyretinal (ha) have been investigated.

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Thermal isomerization of synthetic all-(E)-β-carotene yielded a multi-component mixture composed of more than sixteen (Z)-β-carotenes and two thermo-cyclized isomers. They were separated and purified by high-performance liquid chromatography. Ten of these were characterized by spectroscopic methods as four mono-(Z)-, five di-(Z)-, and one tri-(Z)-β-carotenes; the 7-(Z)-, 9-(Z)-, 13-(Z)-, 15-(Z)-, 9.13-(Z)-, 9.15-(Z)-, 9.13'-(Z)-, 13.15-(Z)-, 7.13'-(Z)-, and 9.9'.13-(Z)-isomers were included. Stereochemistry of six additional (Z)-isomers obtained is, as yet, unknown, though one of them might have the 9.9'-(Z)-geometry in the molecule. This is the first report on the formation and identification of the ‘sterically hindered’ 7-(Z)-isomers as well as the (5→10)-thermo-cyclized products in the field of alicyclic carotenoids

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A new radioisotopic assay for ornithine aminotransferase with [U-¹⁴C]ornithine as a substrate was developed. The dihydroquinazolinium compound formed was extracted from the reaction mixture with n-butanol and an addition of high concentration of sodium sulfate. This assay is sensitive and convenient and more than 50 assays can be done in one day without any special apparatus. The activities of ornithine aminotransferase in rat liver and human lymphoblastoid cells could be measured at nanomole levels by this method. Thus, the assay should be useful for measurement of OAT activity in cultured cells and for studies on the metabolic bases of the different types of ornithine aminotransferase deficiency: vitamin B₆-responsive and -nonresponsive types

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The effects of iron deficiency anemia and iron treatment on blood gas and acid-base balance at rest and during exercise were studied. Eight Sri Lankan males and 13 females were randomly divided into an iron treatment or placebo group. Their initial hemoglobin (Hb) levels were 6.2±0.5 and 5.5±0.7g/ 100ml (mean±SEM) with serum iron levels of 41±8 and 30±6μg/100ml, respectively. Hemoglobin concentration was increased significantly within 7 days after iron treatment to 7.2±0.4g/100ml. Resting lactate was higher than normal, while base excess, buffer base, and actual bicarbonate were lower, maintaining a normal pH. Heart rates during exercise at a given work load and lactate production following exercise decreased after the elevation of Hb. Venous blood PCO₂ rose as Hb concentration increased, preceeding a significant increase in resting O₂ content, 16 days after iron treatment. With anemia, O₂ delivery is potentially maintained by a shift of the O₂-dissociation curve to the right due, in part, to 2, 3-diphosphoglycerate. There was no significant change in PO₂ or Hb-O₂ % saturation following exercise or iron treatment. These data suggest that severe iron deficiency anemia results in lactate accumulation in blood even at rest but pH is maintained within normal limits. It was also suggested that severe anemia may impair CO₂ transport capacity of blood which could limit continuation of muscle metabolism.

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This study was conducted to investigate whether a moderate running exercise would enhance or prevent the lipid peroxidation in animal body and also stimulate or depress the degradation-excretion of lipid peroxides (LIPOX, thiobarbituric acid reactive substances determined as malon dialdehyde) in young female rats. Compared with sedentary rats, voluntary wheel-running exercised rats did not show any significant difference in total LIPOX contents in plasma and several tissues including brain, and whole body during 4 weeks of experiment with a vitamin E-free low LIPOX diet. On the contrary, when rats were previously fed a high LIPOX diet and then allowed voluntary exercise with a vitamin E-added low LIPOX diet, total LIPOX contents per whole body reduced significantly faster in the exercised rats than in the sedentary controls during 2 weeks of exercise. At that period, LIPOX were progressively increased in the brain in both groups of animals, but was significantly greater in the exercised group. Interestingly, more than 80% of total LIPOX contents in whole body were found to be stored in carcass portions regardless of greater or lesser amounts of LIPOX contents in rats. These data suggest that a moderate exercise of several weeks might enhance the degradation-excretion of LIPOX but not the formation-accumulation of LIPOX in rats. Exercise also seems to modulate LIPOX transference among tissues.

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In order to clarify the mechanism of the adverse effects of dietary amaranth, trisodium 1-(4-sulfo-l-naphthylazo)-2-naphthyl-3, 6 disulfonic acid, the effects of amaranth in vitro and in a jejunum perfusion in vivo on intestinal sucrase were investigated in rats. The inhibitory effect of amaranth in vitro on the sucrase activity was not detected even at the concentration of 1%, whereas the remarkable release of intestinal sucrase from intestine was observed with the jejunum perfusion of Ringer bicarbonate solution (RBS) containing amaranth at the 1% level. On the other hand, the perfusion of RBS containing tris(hydroxymethyl)aminomethane, a strong inhibitor of intestinal disaccharidase activities, did not produce the release of intestinal alkaline phosphatase. These findings suggest that the toxicity of dietary amaranth is due to the exfoliating or solubilizing effects of amaranth on the brush border membrane of the small intestine.

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Seeds of winged bean (Psophocarpus tetragonolobus) were stored under four different sets of conditions; 65% relative humidity (RH) at 5°C, 35% RH at 37°C, 65% RH at 37°C, and 85% RH at 37°C. After storage for. three and five months, samples were taken out to explore quality changes during storage. The germination capacity decreased during storage at high temperatures. Although little change was found in content in extractable oil, a decrease in the iodine value and an increase in the acid value and in the TBA value were significant during storage at high temperature and high moisture, indicating deterioration of oil. Aldehyde in defatted bean extract increased under all conditions for storage. Protein extractability was greatly reduced at 36°C and 85% RH, while no reduction was observed at other conditions.

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The effect of energy on nitrogen balance was examined in young men given amino acid mixture. The minimum amino acid nitrogen requirement for nitrogen equilibrium was determined together with the egg protein requirement. In experiment 1, the nitrogen sparing effect of energy was evaluated in four male students receiving diet containing an amino acid mixture and a constant nitrogen intake of 3.5gN/day, which was equivalent to the nitrogen requirement with excess energy intake determined by Rose and Wixom (1). When the dietary energy supply was 45kcal/kg, which is approximately the maintenance level, the mean nitrogen balance was negative, being -23.9±9.3mg N/kg. However, with an excess energy intake of 55kcal/kg, the nitrogen balance improved significantly, being -6.1±7.7mg N/kg. In experiment 2, the nitrogen requirement of egg-pattern amino acid mixture for apparently zero balance was evaluated at maintenance energy intake in 28 Japanese young men and was compared with that of egg protein. After receiving standard diet, the subjects were given a semi-purified experimental diet containing egg-pattern amino acid mixture at nitrogen intake levels of 60, 75, 100, and 130mg N/kg for two weeks. Then all groups except the 60mg N/kg group were given isonitrogenous egg protein diet for another week. Energy intake was kept constant at approximately the maintenance level of 44.4±1.4 kcal/kg throughout the experiment. Nitrogen balance was not significantly different in groups given egg-pattern amino acid mixture and intact egg protein in each nitrogen intake level. From regression analysis, the nitrogen requirement for nitrogen equilibrium of the amino acid mixture was calculated to be 110.1±50.2mg N/kg, which was not significantly different from the value of 88.4±40.6mg N/kg of egg protein. It was concluded that the total amino acid requirement estimated by Rose and Wixom (1) was too low because they gave excess energy, and that there was no difference between the nitrogen requirement of egg protein and that of the corresponding amino acid mixture.

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The effect of bilateral destruction of the ventromedial hypothalamus (VMH) on protein and energy intakes was examined in relation to protein utilization. In Experiment 1, rats with VMH lesions were allowed to select protein (either casein or wheat gluten) and energy from two diets containing 70% and 5% protein, respectively. In Experiment 2, they were restricted to 0, 100 and 200mg N/day of protein and given free access to protein-free diet. In Experiment 3, they were restricted to 2 and 5g/day of protein-free diet but given 92% protein diet ad libitum.
Self-selecting rats with VMH lesions consumed about 100kcal/day regardless of the protein source, in contrast to sham-operated controls which consumed 75kcal/day. They showed increased non-protein energy intake with constant protein consumption resulting in normal protein retention with increased body fat. When protein intake was restricted to 200mg N/ day, energy intake was reduced in animals given diet containing wheat gluten more than in those given diet containing casein, resulting in lower protein utilization. Therefore, food intake depended upon the amount of dietary protein. Rats with VMH lesions showed an exaggerated response to the ratio of protein to energy in the diet and consumed more energy from balanced diet but showed more reduction in food intake than controls in response to diet with an inappropriate ratio of protein to energy.
The present study confirmed that the VMH was related to regulation of energy intake but not protein intake. It is suggested that protein intake is regulated in relation to maintenance of body protein in rats with VMH lesions as well as in normal rats.

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The nutritional quality of soy protein isolate (SPI) was evaluated in young men by the nitrogen balance method using fish protein as a standard. Twenty-one male university students were given SPI (Supro 620, Ralston Purina Co., St. Louis, Mo., U.S.A.), fish protein (cod fish) or a 50: 50 mixture of the two proteins as the sole source of protein. SPI and fish were prepared as paste products (kamaboko). Four experimental periods were used in which each subject received 0.35, 0.45, 0.55 and 0.65 g protein/kg/day, respectively, given in random order. Each period consisted of one day on protein-free diet and ten days on the experimental diet, with an interval of three days on a free-choice (ad libitum) diet between periods. Energy intake was constant for each individual to maintain their body weight (44.6±2.4 kcal/kg/day). The linear regression equations obtained between nitrogen intake (X: mg N/kg/day) and the apparent nitrogen balance (Y: mg N/kg/day) were as follows: SPI, Y=0.298X-35.2; fish protein, Y=0.365X-31.8; mixed protein, Y=0.423X-38.3. The nitrogen requirement for maintenance of nitrogen equilibrium determined from the regression equation was 118.1±15.4 mg N/kg/day for SPI, 87.1±17.2 mg N/kg/day for fish protein and 90.5±17.1 mg N/kg/day for mixed protein. The NPUs calculated at the respective maintenance nitrogen intakes were 38.9, 52.8 and 50.8 for SPI, fish protein and mixed protein, respectively. There was no significant difference between the nutritive values of mixed protein and fish protein. The nutritive value of SPI relative to fish protein was estimated as 82%, 74% and 74% by the slope-ratio method, and values for the nitrogen requirement and NPU, respectively.

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1. The effects of thiamin deficiency during pregnancy and/or lactation on brain cholinergic system in rat pups were studied. Dietary rehabilitation for a period of 5 weeks from the 28th day was instituted to study possible ‘catch-up’ in the brain acetylcholine levels. 2. Brain acetylcholine level was found to be significantly decreased on the 21st and 28th days in pups of the dams fed thiamin deficient diet during gestation and lactation, whereas it was decreased on the 28th day in pups of the dams fed thiamin deficient diet during lactation. Activities of Cholinergic enzymes remained unaltered in both the deficient groups. 3. Subsequent dietary rehabilitation was found to reverse the deficits in brain acetylcholine levels.

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