Journal of Nutritional Science and Vitaminology
Online ISSN : 1881-7742
Print ISSN : 0301-4800
ISSN-L : 0301-4800
Volume 24, Issue 4
Displaying 1-10 of 10 articles from this issue
  • Sabu KASAI, Yoko KUBO, Shigeko YAMANAKA, Takako HIROTA, Hiroshi SATO, ...
    1978 Volume 24 Issue 4 Pages 339-350
    Published: 1978
    Released on J-STAGE: June 15, 2009
    JOURNAL FREE ACCESS
    Three new 8N-alkyl analogues of roseoflavin (MM), i.e., 8-ethylamino (EH), 8-methylethylamino (ME), 8-diethylamino-8-demethyl-D-riboflavin (EE), their tetraacetates, and 8-amino-8-demethyl-Driboflavin (HH) tetraacetate, were synthesized.
    A relation between the anti-riboflavin activity and the chemical structure of 8N-alkyl analogues (8N-methyl, ethyl) was studied by a restoration by riboflavin (RF) of inhibitory effect of the analogues on a growth of Grampositive bacteria, i.e., Sarcina lutea, Bacillus cereus, and Staphylococcus aureus. The inhibitory effect of most of the analogues was restored by RF. But in some cases, i.e., 8-methylamino-8-demethyl-D-riboflavin (MH) in Sar. lutea and MM in Staph. aureus, the effect was not completely restored. Apparently, the inhibition in early phase of growth was restored, but the maximum growth was still suppressed. The non-alkylated amino analogue (HH) showed only unrestorable suppression of maximum growth in Sar. lutea.
    Of restorable effect by RF of N-alkyl analogues, approximate decreasing orders of anti-RF activity were as follows. Dialkylated analogue>monoalkylated. HH showed insignificant anti-RF activity. In each group, methylated analogue>ethylated. In B. cereus monoalkylated analogues, and in Staph. aureus monoalkylated and EE showed no significant inhibitory effect.
    Redox potentials of the N-alkyl analogues were measured, and a definite relation between the chemical structure and the potential was found (RF=EE>ME>MM>>HH>EH>MH). But the anti-RF activity of the analogues was not completely explained by the difference of the redox potential from RF.
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  • Chi-Po CHEN
    1978 Volume 24 Issue 4 Pages 351-362
    Published: 1978
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    Rat hepatocytes were freshly prepared from adult animals using the collagenase-perfusion technique. The hepatic transport of thiamine was studied in isolated liver cells. The process was found to be saturable with an apparent Kt of 0.31mM and a Vmax of 0.7 μmoles/ml intracellular fluid/5 minutes. However, at higher substrate concentrations, the process proceeded in a linear fashion. Both pyrithiamine and oxythiamine were inhibitory on the hepatic uptake of thiamine, the latter showed much weaker activity than the former. The system required the presence of sodium ions and was sensitive to ouabain. Anaerobic condition and metabolic inhibitors, e.g., 2, 4-dinitrophenol, cyanide, and iodoacetate suppressed the uptake rate of thiamine. Addition of ethanol in the incubation medium also caused significant reduction of thiamine uptake. Efflux studies indicated that a portion of intracellular thiamine is readily available for exodus. Chromatographic analyses showed that thiamine was only slightly metabolically altered during the transport process. It is suggested that thiamine is transported into isolated hepatic cells by an active, sodium-dependent process.
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  • Misako TANIGUCHI, Torao YAMAMOTO, Motoomi NAKAMURA
    1978 Volume 24 Issue 4 Pages 363-381
    Published: 1978
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    Weanling male rats were fed a riboflavin deficient diet for 5 weeks and enlargement of the liver mitochondria and discontinuity of the outer membrane were observed. The content of phospholipids was slightly increased in the deficient mitochondria, and decrease in phosphatidylcholine and increase in phosphatidylethanolamine were shown respectively. In comparison with the mitochondria, the content and distribution of phospholipids in microsomes were not affected. The fatty acid composition of phosphatidylcholine in mitochondria and microsomes was remarkably altered by the deficiency, and increases in palmitic and linoleic acids and decrease in arachidonic acid were demonstrated. The incorporation of 32P into diphosphatidylglycerol in mitochondria was reduced by the deficiency. The incorporation into other phospholipids was not significantly altered, whereas the incorporation into the subspecies of phosphatidylcholine was variously affected.
    By the intraperitoneal injection of riboflavin to the deficient rats, normalization of the mitochondrial size and fatty acid composition of liver mitochondrial lipids was observed. However, decreased incorporation of 32P into diphosphatidylglycerol in mitochondria was not recovered completely at 40 hours after the injection, and in the mitochondrial lipids linoleic acid was higher and arachidonic acid was lower than respective controls at 60 hours.
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  • Makoto MIND, Yasuhiko NISHIDA, Kiku MURATA, Mitsuko TAKEGAWA, Goichiro ...
    1978 Volume 24 Issue 4 Pages 383-395
    Published: 1978
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    There seems to be a greater variation between laboratories in hydrogen peroxide hemolysis techniques than in other clinical laboratory procedures. In this report, factors influencing hemolytic values were examined and the effect of the combination of these factors on the results was analysed statistically by using the orthogonal array.
    Factors influencing hemolysis induced by hydrogen peroxide were as follows; the concentration of hydrogen peroxide, temperature in the peroxide reagent when added to the red cell suspension, the red cell concentration in the cell suspension and the addition of charcoal to the reaction mixture. However, addition of charcoal may not be essential to stabilize the hemolytic values and other factors such as keeping blood for 4 hours at room temperature before testing, the difference between investigators, a reaction time 2 or 3 hours and the technique of adding peroxide reagent to the cell suspension, had little effect on hemolysis. The most important factor was the temperature in hydrogen peroxide solution.
    The estimated hemolytic values by the orthogonal array linearly correlated with the plasma tocopherol levels.
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  • K. MOHANA, E. R. B. SHANMUGASUNDARAM
    1978 Volume 24 Issue 4 Pages 397-403
    Published: 1978
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    The effect of pyridoxine deficiency on fat metabolism was studied using mutant strains of Aspergillus nidulans requiring pyridoxine for growth. Under pyridoxine deficiency the mutants exhibited increased levels of total lipid, sterols, phospholipids, and triacylglycerols. Total fatty acids were found to decrease with pyridoxine deficiency. An increase in saturated fatty acids and decrease in unsaturated fatty acids were seen with deficiency. Pyridoxine deficiency also increased lower carbon chain fatty acids. A possible involvement of pyridoxine in the elongation of fatty acid chain and in the desaturation of fatty acids in Aspergillus nidulans is suggested.
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  • Setsuko NODA, Kura KUBOTA, Kazuhiko YAMADA, Setsuko YOSHIZAWA, Sachiko ...
    1978 Volume 24 Issue 4 Pages 405-418
    Published: 1978
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    The effect of vitamin D3 and dietary calcium level on the cadmium-induced changes was observed in the duodena of rats raised on various diets differing in vitamin D and calcium levels. Observation with scanning electron microscopy revealed that vitamin D and dietary calcium were required for normal intestinal villi and microvilli formation. The damaged cells were observed in the intestinall villi of cadmium-exposed rats. The length of microvilli was shortened in the cadmium-exposed rats. Furthermore, dietary cadmium reduced the enzyme activities in microvilli. Especially, alkaline phosphatase activity was reduced in the cadmium-exposed groups, even though it was still responsive to vitamin D3. These effects with cadmium were modulated by vitamin D3 and dietary calcium level. That is, in the presence of vitamin D3 and calcium, the effect of cadmium on intestinal villi and microvilli was reduced.
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  • Miyako ABE
    1978 Volume 24 Issue 4 Pages 419-427
    Published: 1978
    Released on J-STAGE: June 15, 2009
    JOURNAL FREE ACCESS
    The correlation between the γ-aminobutyric acid (GABA) metabolism and convulsions by some vitamin B6 antagonists, DL-penicillamine (PeA), hydrazine (Hyd), thiosemicarbazide (TSC) were investigated. Glutamic acid decarboxylase (GAD) and γ-aminobutyric acid transaminase (GABA-T) activities were inhibited during convulsions by three antagonists, and GABA content was not changed by PeA, increased by Hyd and decreased by TSC in mice whole brain. In subcellular fractions of brain, GAD activity was inhibited and GABA content decreased in synaptosomes during convulsions by the above three drugs. Aminooxyacetic acid (AOAA), a potent GABA-elevating agent, showed an anticonvulsant property against convulsions by TSC for several hours after the injection of AOAA, but lost this property 16 hr after treatment. During the convulsions by TSC 16 hr after the AOAA-pretreatment, the GABA content in synaptosomes was less than that from the group treated with AOAA alone, though its GABA level was higher than the normal level. From the above results, the GABA content and GAD activity in synaptosomes might be deeply associated with convulsions by B6 antagonists.
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  • Akemichi BABA, Tsuneko BABA, Toshio MATSUDA, Heitaroh IWATA
    1978 Volume 24 Issue 4 Pages 429-435
    Published: 1978
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    Some metabolic changes induced by the intraventricular administration of 6-aminonicotinamide (6-AN) were studied in mice. Five or ten μg/animal of 6-AN produced a marked hyperglycemia, lowered glycogen content in the brain and liver, and reduced the adrenal epinephrine content. Adrenalectomy or hexamethonium prevented 6-AN induced hyperglycemia and decrease of glycogen content in the liver but not in the brain. Decrease of adrenal epinephrine content induced by 6-AN was overcome by hexamethonium. Pretreatment with 6-AN (10 /μg/animal) markedly lowered the toxic action, but not the hypoglycemic action, of a large dose of insulin.
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  • Hidetsugu FUWA, David V. GLOVER, Yoshimi SUGIMOTO, Mie TANAKA
    1978 Volume 24 Issue 4 Pages 437-448
    Published: 1978
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    Starch granules were prepared from kernels of eight single endosperm mutants, brittle-1 (bt1), brittle-2 (bt2), floury-1, floury-2, soft starch, opaque-1 (o1), shrunken-2 (sh2), and sugary-2 (su2), and their double-mutant combinations with opaque-2 (O2) of four inbred lines of maize (Zea mays L.), B37, C103, Oh43 and W64A. We compared the susceptibility of various starch granules to Rhizopus glucoamylase and pancreatin. Starch granules of the su2 and su2o2 mutants were digested by amylases much faster than those of the normal counterparts. Starch granules of the bt1, bt2, o1 and sh2 mutants tended to be digested by amylases faster than those of normal maize. Starch granules of doublemutant combinations with the o2 gene were, in general, digested to an extent very comparable to their respective non-opaque single mutant counterparts in each of their four inbred backgrounds. We followed the relative digestion of starch granules by using scanning electron microscopy. Starch granules of endosperm mutants susceptible to amylases showed numerous pin holes on the surface layer and the pores penetrated into the inner layers of the granules during the attack by amylases. In some of the granules the inner portion, which appeared terraced or step-shaped, could be seen. This may be indicative of layered internal structures of the granules.
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  • Michihiro SUGANO, Kimiko HIGUCHI-ASHIZAWA, Yasuo NAGATA, Takuo OKITA
    1978 Volume 24 Issue 4 Pages 449-458
    Published: 1978
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    Fasting serum aminograms were studied in rats fed a commercial stock diet or purified diets supplemented with or without 1 cholesterol and 0.25% sodium cholate. Sucrose, glucose or fructose served as a carbohydrate source for each purified diet. Accompanied by marked rises in serum cholesterol, the serum amino acid profile of rats fed glucose or fructose diets was modified significantly by dietary cholesterol. On feeding a glucose diet, dietary cholesterol caused decreases in Trp, Thr and Tyr and increase in Pro and Met. However, the concentration of total essential amino acids remained unchanged. Feeding a fructose diet resulted in a significant reduction of the amino acid level in comparison with that observed with glucose. This decrease was routinely compensated by the inclusion of cholesterol in the diet with the concentration of a number of amino acids being increased. Only Trp was decreased by this dietary manipulation. The serum aminogram of rats fed either a commercial stock diet or a sucrose diet was inconsiderably modified by dietary cholesterol. These data denote that dietary cholesterol influences the metabolic process of amino acids and that the response to cholesterol is modified by the carbohydrate source of the diet.
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