VITAMINS
Online ISSN : 2424-080X
Print ISSN : 0006-386X
Volume 66, Issue 1
Displaying 1-15 of 15 articles from this issue
  • Kazuko YAMADA
    Article type: Article
    1992 Volume 66 Issue 1 Pages 1-24
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
    JOURNAL OPEN ACCESS
    Biosynthetic pathways of the pyrimidine moiety and thiazole moiety of thiamin were studied. Procaryotes and eucaryotes have different biosynthetic pathways for the pyrimidine. In procaryotes, the pyrimidine is formed by ring expansion of imidazole accompanied insertion of C-4', C-5' fragment of ribose of 5-aminoimidazole ribonucleotide, an intermediate of purine biosynthesis. In eucaryotes, N-3, C-4, and amino-N attached at C-4 of the pyrimidine are derived from N-1, C-2 and N-3 of the imidazole ring of histidine and the three carbon unit of C-6, C-5 and C-7 is originated from C-1, C-2 and C-3 of ribose. The precursor of C-2 and N-3 of the thiazole moiety is tyrosine in anaerobic microorganisms and glycine in aerobic microorganisms. Anaerobic microorganisms and aerobic microorganisms have different biosynthetic pathways for the thiazole. The origin of the S atom was established as being the S atom of cysteine in Escherichia coli and Saccharomyces cerevisiae. The origin of 5-carbons chain, C-4', 4, 5, 5' and 5" of the thiazole in anaerobic microorganisms was the compound drived from pyruvate and glycerol. The 5-carbons chain is derived from glucose via pentose phosphate shunt in aerobic microorganisms.
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  • Norihisa KATO
    Article type: Article
    1992 Volume 66 Issue 1 Pages 25-34
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
    JOURNAL OPEN ACCESS
    Effects of dietary addition of some xenobiotics on the metabolism of α-tocopherol in rats were studied with special reference to cholesterol metabolism. Dietary xenobiotics including PCB, DDT, Chloretone, phenobarbital, etc. caused an increase in serum α-tocopherol and cholesterol. The effects of dietary PCB on serum and tissue levels of α-tocopherol were influenced with dietary protein and copper. The increases in serum α-tocopherol and cholesterol due to the chemicals were attributed to the increases in the fraction of high-density-lipoproteins (HDL). Dietary PCB and Chloretone caused an increase in apparent absorption of α-tocopherol. Dietary clofibrate depressed the increases in serum and tissue α-tocopherol, and serum cholesterol and also suppressed the increase in apparent absorption of α-tocopherol by Chloretone. These results suggest that the increase in serum cholesterol due to xenobiotics relates to the increase in serum and tissue α-tocopherol. As well as xenobiotics, feeding of cystine excess and histidine excess diets which are known to cause hypercholesterolemia also increased serum α-tocopherol.
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  • Yoshinori ITOKAWA, Kohsuke NISHINO, Shogo IGARASHI
    Article type: Article
    1992 Volume 66 Issue 1 Pages 35-42
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
    JOURNAL OPEN ACCESS
    To evaluate the merits of commercially available leading thiamin derivatives, thiamin tetrahydrofurfuryl disulfide (TTFD), O-benzoylthiamin disulfide (BTDS), and S-benzoylthiamin O-monophosphate (BTMP), were studied in the following 3 experiments. The requirements of commercially available thiamin derivatives are also discussed from the point of view of effectiveness and safety. 1. Bioavailability Study in Human Subjects: Commercial tablets containing 100 mg of TTFD, or BTDS and a powder formulation containing 100 mg of thiamin were administered to healthy subjects and their bioavailability was evaluated by determining the blood concentration and urinary excretion of thiamin. It was found that the bioavailability of TTFD was better than that of BTDS or thiamin, according to the indices of C_<max>, T_<max>, AUC, and the 48-hour urinary excretion of thiamin. 2. Uptake into Human Blood Cells: An in vitro test was carried out to compare the uptake of TTFD, BTDS, BTMP, and thiamin into human blood cells. Most of the TTFD was incorporated by blood cells and converted into thiamin, but BTDS and thiamin largely remained in the supernatant. Most of the BTMP was not converted into thiamin under these experimental conditions. 3. Conversion to Thiamin by Rat Liver Homogenate: An in vitro test of the conversion of thiamin derivatives to thiamin by rat liver homogenate showed that TTFD was readily converted to thiamin by either fresh or boiled liver homogenate. BTDS was rapidly converted to O-benzoylthiamin (OBT), an intermediate metabolite, but conversion from O-benzoylthiamin to thiamin was very slow. BTMP was converted to thiamin fairly readily by fresh liver homogenate, but conversion was negligible when boiled liver homogenate was used.
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  • Masamichi IKEDA, Yutaka UNO, Midori IWAI, Hideko SATO, Hitomi KAWABE, ...
    Article type: Article
    1992 Volume 66 Issue 1 Pages 43-49
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
    JOURNAL OPEN ACCESS
    Germ-free (GF) and conventional (CV) mice were fed control and inositol-deficient diets containing 10% of palm oil and 60% of sucrose for 23 days. No significant differences in body weight were observed both in GF and CV mice between control and inositol-deficient groups. there was evidence of fatty liver in GF and CV mice fed inositol-deficient diets, and the degree of fatty liver was ;more evident in CV mice fed inositol-deficient diet than in GF ones. GF and CV mice fed inositol-deficient diet showed significant increases in the activities of malic enzyme, glucose 6-phosphate dehydrogenase and acetyl-CoA carboxylase compared with control animals. Plasma triglyceride level reduced significantly in CV mice fed inositol-deficient diet, and did not reduce significantly in GF ones. Plasma FFA level reduced significantly in GF mice fed inositol deficient diet, but didn't reduce in CV ones. These suggest that the fatty liver by inositol deficiency is due to increased lipid synthesis in liver, decreased lipid secretion and decreased FFA which is incorporated to liver, and that inositol synthesized by intestinal microflora do not contribute to depress fatty liver in conventional mice fed inositol-deficient diet.
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  • [in Japanese]
    Article type: Article
    1992 Volume 66 Issue 1 Pages 51-53
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
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  • [in Japanese]
    Article type: Article
    1992 Volume 66 Issue 1 Pages 53-
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
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  • [in Japanese]
    Article type: Article
    1992 Volume 66 Issue 1 Pages 54-
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
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  • [in Japanese]
    Article type: Article
    1992 Volume 66 Issue 1 Pages 55-
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
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  • [in Japanese]
    Article type: Article
    1992 Volume 66 Issue 1 Pages 55-56
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
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  • [in Japanese]
    Article type: Article
    1992 Volume 66 Issue 1 Pages 56-
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
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    Download PDF (196K)
  • [in Japanese]
    Article type: Article
    1992 Volume 66 Issue 1 Pages 56-57
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
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    Download PDF (341K)
  • [in Japanese]
    Article type: Article
    1992 Volume 66 Issue 1 Pages 57-58
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
    JOURNAL OPEN ACCESS
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  • [in Japanese]
    Article type: Article
    1992 Volume 66 Issue 1 Pages 58-59
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
    JOURNAL OPEN ACCESS
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  • [in Japanese]
    Article type: Article
    1992 Volume 66 Issue 1 Pages 59-
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
    JOURNAL OPEN ACCESS
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  • [in Japanese]
    Article type: Article
    1992 Volume 66 Issue 1 Pages 59-60
    Published: January 25, 1992
    Released on J-STAGE: March 30, 2018
    JOURNAL OPEN ACCESS
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