Journal of Nutritional Science and Vitaminology
Online ISSN : 1881-7742
Print ISSN : 0301-4800
ISSN-L : 0301-4800
Volume 44, Issue 4
Displaying 1-9 of 9 articles from this issue
  • Tokumitsu OKAMURA, Hiroko NODA, Shoko FUKUDA, Masahiro OHSUGI
    1998 Volume 44 Issue 4 Pages 483-490
    Published: 1998
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    We found a new reaction of aspartic acid dehydrogenation, catalyzed by NADP+ -dependent aspartate dehydrogenase, in vitamin B12-producing Klebsiella pneumoniae IFO 13541. The enzyme, which was purified from a crude extract of K. pneumoniae IFO 13541, catalyzes the oxidative deamination of aspartic acid to form oxaloacetic acid. This enzyme had a molecular mass of about 124 kDa consisting of two identical subunits. L-Aspartic acid was a substrate, although D-aspartic acid and L-glutamic acid were inactive. The enzyme showed maximal activity at about pH 7.0-8.0 for the oxidative deamination of L-aspartic acid, and it required NADP+ as a coenzyme, while NAD+ was inactive.
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  • Vandana PATHANIA, Nidhi SYAL, Chander Mohan PATHAK, Krishan Lal KHANDU ...
    1998 Volume 44 Issue 4 Pages 491-502
    Published: 1998
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    For the past decade there has been emphasis on the immunomodulatory effects of vitamin E apart from its established role as a free radical scavenger. In alveolar macrophages (AMs), the role of vitamin E supplementation has not yet been investigated sufficiently. In the present study we have evaluated the effects of high vitamin E (DL-α-tocopheryl acetate, α-TA) supplementation for 10 d on rat-alveolar macrophageal antioxidant defense and reactive oxygen species (ROS) release. There was an increase in plasma vitamin E content from 5.22±1.30, at 50mg to 12.23±1.06 and 22.32±2.02μg/mL at 250 and 1, 250mg α-TA/kg dietary supplementation. Alveolar macrophage-vitamin E content enhanced by 56 to 75% at 250 and 1, 250mg α-TA diet as compared with control diet. Superoxide dismutase activity decreased and catalase and glutathione peroxidase activities increased significantly in AMs of 250 and 1, 250mg α-TA diet-fed rats. Reduced glutathione, total glutathione, and glutathione-S-transferase activity in AMs did not change significantly at any of the high doses of α-TA supplementation. On stimulation of AMs by phorbol-12-myristate-13-acetate (PMA), there was 2.8 and 3.5-fold enhancement in superoxide (O2_??_) and H2O2 production, respectively, at 50mg α-TA dose. But this increase by PMA could not take place in AMs from animals supplemented with 250 and 1, 250mg α-TA. It may therefore be concluded that high a-TA supplementation in diet may equip the AMs with a stronger defense against oxygen-free radical mediated damage to them.
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  • Seiichi KASAOKA, Takao KITANO, Miho HANAI, Makoto FUTATSUKA, Takatoshi ...
    1998 Volume 44 Issue 4 Pages 503-514
    Published: 1998
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    We studied the extent of kidney calcification by varying dietary levels of Mg, based on pathological examinations and calcium (Ca) and magnesium (Mg) balance tests. AIN-76 diets containing varying levels of Mg-0.3 (-M), 1.3 (1 /20M), 2.4 (1/10M), 9.2 (1/5M), 19 (control), 38 (2M), 102 (5M), and 187 (10M) mmol/kg diet-were fed to 3-week-old male Fischer-344 rats for 14 d. Although the magnitude of abnormality was highest in kidney of rats fed the M diet, the damage was normalized as the dietary level of Mg increased, with increasing serum Mg concentration and urinary excretion of Mg. We found almost no deposition of Ca in rats fed the 1OM diet. The mechanism by which the high dietary Mg induces these effects most likely involves a competition between Mg and Ca for reabsorption in proximal and/or distal tubules, since these diets increased the urinary excretion of Ca. However, these high Mg diets decreased food intake and body weight gain compared with the control diet, although these indices were not decreased in rats fed the 2M diet. The results suggest that a dietary magnesium level approximately twice the normal level effectively reduces kidney calcification while maintaining normal growth in rats.
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  • Tomoaki KIKUCHI, Hiroshi MATSUZAKI, Shigeru SATO, Yasutaka KAJITA, Hir ...
    1998 Volume 44 Issue 4 Pages 515-523
    Published: 1998
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    The effect of a magnesium-deficient diet on kidney function was studied in young male rats. The rats were fed a purified diet with a magnesium content of either 20.5 (control diet) or 2.6 mmol/kg (magnesium-deficient diet) for 21 d. In rats fed the magnesium-deficient diet, kidney wet and dry weights were significantly increased, and calcium and phosphorus concentrations in the kidney were significantly higher than in rats fed the control diet. Upon histological examination, an increase in the mesangial matrix of the glomeruli and injury to the brush border of the proximal tubules were observed in rats fed the magnesium-deficient diet. Also, a deposition of calcium was observed in the tubules of the corticomedullary junction and medulla of these rats. Total protein and albumin concentrations in serum were significantly decreased in rats fed the magnesium-deficient diet. Urinary albumin excretion was significantly higher, and N-acetyl-β-D-glucosaminidase activity in the urine was significantly increased in rats fed the magnesium-deficient diet. These findings indicate diminished glomerular and proximal tubular functions. We suggest that a magnesium-deficient diet not only induces nephrocalcinosis, but it also diminishes kidney function.
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  • Nobuhiro FUKUDA, Masanori FUKUI, Yasuko KAI, Anura P. JAYASOORIYA, Mas ...
    1998 Volume 44 Issue 4 Pages 525-535
    Published: 1998
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    To estimate the relative significance of exogenous vs. endogenous fatty acids in increasing hepatic triacylglycerol secretion following an inhibition of fatty acid oxidation by emeriamine, livers from 2-d-fasting rats were perfused with or without an inhibitor in the presence of a geometrical isomer of linoleate (linolelaidic acid, trans, trans-9, 12octadecadienoic acid). Emeriamine added to the perfusion medium at 2 h of the recirculating perfusion period caused immediate and complete cessation of ketone body production while it increased triacylglycerol and cholesterol secretion by the liver without affecting uptake of exogenous linolelaidic acid. The increase in the triacylglycerol secretion by emeriamine was accompanied by a marked increase in the proportion of linolelaidic acid in this lipid molecule in the perfusate and in the liver. The calculated amounts of exogenous linolelaidate, compared with those of endogenous fatty acids in the secretory triacylglycerol, suggested that the former compared with the latter contributes more to the drug-mediated increase in triacylglycerol secretion. This drug caused a marked reduction of mitochondrial carnitine palmitoyltransferase activity in perfused liver. These results suggest that a blockade of fatty acid oxidation by emeriamine, through an inhibition of carnitine palmitoyltransferase, diverts predominantly the exogenous free fatty acids from oxidation to the esterification pathway and subsequently stimulates the synthesis and secretion of triacylglycerol-rich lipoproteins.
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  • Masahiro KIMURA, Shigeko FUJIMOTO SAKATA, Yasuhiro MATOBA, Koichi MATS ...
    1998 Volume 44 Issue 4 Pages 537-546
    Published: 1998
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    Overlapping cDNAs encoding dihydropyrimidine dehydrogenase (DPD), the rate-limiting enzyme of pyrimidine degradation, were isolated from a rat liver cDNA library, and a 4, 353 by cDNA sequence with a 3, 075 by open reading frame encoding a polypeptide of 1, 025 residues with a molecular mass of 111, 458 Da was determined. Western blot analysis of COS-7 cells that were transfected with an RT-PCR-derived DPD cDNA showed that the product from the cDNA binds to an antiserum for DPD. Northern blot analysis was performed by using a partial fragment of the cloned cDNA as a probe. The mRNA level, the protein level, and the activity of DPD in the rat liver increased to the adult level by 3 mo of age. The levels of DPD in the liver of adrenalectomized rats increased 48 h after glucocorticoid administration. The increase of DPD after birth may be caused by the increase in glucocorticoid level.
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  • Yukiko MINAMIYAMA, Shigekazu TAKEMURA, Shinya TOYOKUNI, Yuko TANIMOTO, ...
    1998 Volume 44 Issue 4 Pages 547-559
    Published: 1998
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    Although various antioxidants have been tested as therapeutics for endotoxemic subjects, the results of their efficacy are conflicting. Antioxidant biofactor (AOB) is a unique processed grain food that exhibits strong antioxidant activity (Minamiyama et al, J Nutr Sci Vitaminol, 40: 467-477, 1994). The present study was carried out to test the effect of AOB on hepatic injury in rats induced by lipopolysaccharide (LPS). Intravenous administration of LPS induced liver injury with a concomitant increase in hepatic generation of nitric oxide (NO) and 4-hydroxy-2nonenal (HNE) modified proteins in the control group. The administration of AOB significantly inhibited the LPS-induced hepatic injury and generation of HNE-modified proteins and increased the survival rate of endotoxemic rats without affecting NO generation and plasma levels of tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ). AOB scavenged superoxide radicals without affecting NO production by LPS-stimulated macrophage cell line J 774.2 cells. AOB also inhibited lipid peroxidation induced by LPS in the cells. These results suggested that AOB might scavenge superoxide radicals and decrease toxic metabolites including HNE, thereby inhibiting liver injury in endotoxemic rats.
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  • Hiroko IWAOKA, Tetsuji YOKOYAMA, Takeo NAKAYAMA, Yasuhiro MATSUMURA, Y ...
    1998 Volume 44 Issue 4 Pages 561-568
    Published: 1998
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    The reliability and validity of two newly developed densitometric methods for determining the human body volume and percent body fat (%FAT), the sulfur hexafluoride dilution method (SHF) and air displacement plethysmography (ADP), were evaluated in comparison with the underwater weighing method (UWW). Seven healthy male volunteers (age 31 to 44, mean height 166.0 cm, weight 61.4 kg) participated in this study. The same-day test-retest coefficients of variation (CVs) for body volume and %FAT measurements were not significantly different among the three methods. SHF and UWW showed a strong correlation in terms of body volume and %FAT, with the correlation coefficients (r) being 0.9997 and 0.986, respectively. The correlation between ADP and UWW was slightly weaker (r=0.9997 for body volume and 0.907 for %FAT). However, body volumes measured by SHF and ADP were significantly different from that by UWW when compared by mean values. Such differences were also found for %FAT measurements. The regression lines of body volume measured by SHF and ADP on that by UWW were almost equivalent to the line of identity. However, those of %FAT measured by SHF and ADP on that by UWW were significantly different from the line of identity. Because the reliability of SHF and ADP appeared to be high, further validation and improvement are required and worth doing.
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  • James A. LEVINE, Norman L. EBERHARDT, Michael D. JENSEN, Timothy O'BRI ...
    1998 Volume 44 Issue 4 Pages 569-572
    Published: 1998
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    Adenoviral-mediated gene transfer has proven useful in several organ systems to understand gene action and to provide a potential therapeutic modality for localized, organ-specific gene overexpression. However, the application of adenoviral-mediated gene transfer to adipocytes and adipose tissue has not been evaluated. We evaluated the feasibility of in vitro and ex vivo transfer of the β-galactosidase gene to human adipocytes and adipose tissue by means of adenoviral vectors. The efficiency (percentage of cells transduced) of adenoviral-mediated gene transfer of the β-galactosidase gene to human adipocytes in vitro and to human adipose tissue ex vivo was 21±3% and 14±3%, respectively. Adenoviral-mediated gene transfer in a rabbit femoral adipose tissue was also demonstrated in vivo. Adenoviral-mediated gene transfer may facilitate studies on understanding the biology of adipocytes and provide a potential tool for the modulation of adipocyte function in vivo and thereby for the treatment of obesity.
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