ビタミン

酸化ストレスと老化により発現する退行性変化・認識機能低下とビタミンEによる防御

浦野四郎

原稿種別: 本文
2009 年 83 巻 3 号 p. 85-93
発行日: 2009/03/25
公開日: 2017/10/10

DOIhttps://doi.org/10.20632/vso.83.3_85

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Oxidative stress during aging, which is caused by the imbalance between reactive oxygen species (ROS) generation and antioxidant defense, leads to many physiological dysfunctions. Senescence is speculated to be mediated by ROS-induced oxidative damage through chronic oxidative stress experienced over a long period during aging, so that this study has carried out to clarify whether oxidative stress implicates in neurodegeneration especially cognitive decline during aging, and whether vitamin E prevents the changes that occur during brain aging. The results revealed that when young rats were subjected to oxidative stress, their physiopathological, biochemical and behavioral changes were observed similarly to phenomena observed in normal aged rats. It was found that vitamin E inhibits markedly these abnormalities caused by oxidative stress and aging.

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ビタミンB_<12>補酵素関与酵素の再活性化タンパク質に関する研究

森光一

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2009 年 83 巻 3 号 p. 95-110
発行日: 2009/03/25
公開日: 2017/10/10

DOIhttps://doi.org/10.20632/vso.83.3_95

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Adenosylcobalamin-dependent enzymes tend to inactivate holoenzyme accompanying the modification of the coenzyme. We identified reactivating factors for inactivated holoenzymes of adenosylcobalamin-dependent diol dehydratase (DD), glycerol dehydratase (GD), and ethanolamine ammonia-lyase (EAL), i.e., DDR, GDR, and EALR, respectively. DDR hydrolyzes ATP to ADP and induces its conformational change. Then, DDR facilitates the dissociation of the damaged coenzyme from the inactivated holoDD through formation of tight DD-DDR-ADP complex. This complex is dissociated into apoDD and DDR by replacing ADP on DDR with ATP, and then active holoenzyme is reconstituted. Crystal structures of DDR allow us to construct a model of DD-DDR complex. DD should be bind to DDR with concomitant displacement of a DDR β subunit by a DD β subunit. It induces steric repulsion between DD α and DDR α subunits that would lead to the release of a damaged coenzyme from inactivated holoDD. GDR reactivates inactivated holoGD by similar mechanism.

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真核生物のD-アスパラギン酸代謝に関係するビタミンB_2およびB_6酵素の研究

高橋祥司

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2009 年 83 巻 3 号 p. 111-124
発行日: 2009/03/25
公開日: 2017/10/10

DOIhttps://doi.org/10.20632/vso.83.3_111

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Free D-aspartate has been recently found in a large amount in several animals and plays an important role in various physiological processes. The D-amino acid is considered to be synthesized and degraded mainly by aspartate racemase (AspR) and D-aspartate oxidase (DDO), respectively, in eukaryote. However, the synthetic pathway of the amino acid in eukaryote and the structure and physiological function of DDO in microorganisms remained to be elucidated. We thus purified and characterized AspR from the bivalve Scapharca broughtonii and cloned the encoding gene. The first eukaryotic AspR is the first example of pyridoxal 5'-phosphate (PLP)-dependent AspR and belongs to the fold-type II PLP enzyme family, and had unique characteristics, including the regulation of its activity by nucleotides. We next cloned the first microbial DDO gene from the yeast Cryptococcus humicola, analyzed its expression profile and constructed DDO gene-disrupted strain. The primary structure contains several common features conserved among DDO and D-amino acid oxidase (DAO), and showed a more close relation to fungal DAO. The DDO expression profile and the disrupted strain showed its role in not only the utilization of but also the protection from acidic D-amino acids for cell growth.

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ビタミンCと老化制御,疾患研究

石神昭人

原稿種別: 本文
2009 年 83 巻 3 号 p. 125-130
発行日: 2009/03/25
公開日: 2017/10/10

DOIhttps://doi.org/10.20632/vso.83.3_125

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Senescence Marker Protein-30 (SMP30) was originally identified as a novel protein in the rat liver, the expression of which decreases with aging. Recently, we identified SMP30 as the lactone-hydrolyzing enzyme gluconolactonases (GNL) of animal species. GNL was a key enzyme which involve in vitamin C biosynthesis, and the essential role of SMP30 in this synthetic process was verified by a nutritional study. SMP30 knockout mice developed symptoms of scurvy when fed a vitamin C-deficient diet, verifying the pivotal role of SMP30 in vitamin C biosynthesis. Moreover, SMP30 knockout mice were shorter in life span than the wild type when fed autoclaved mouse chow contained 〜55mg/kg of vitamin C, which we now know contains too little vitamin C to maintain normal levels of vitamin C in tissues. These results demonstrate that vitamin C deficiency accelerates aging. Aging and smoking are considered as major contributing factors for the development of pulmonary emphysema. We evaluated whether SMP30/GNL knockout mice are susceptible to oxidative stress associated with aging and smoking. In the lungs of SMP30/GNL knockout mice, airspace enlargement of pulmonary alveolus occurred when fed a vitamin C-deficient diet. Moreover, cigarette smoke exposure generated marked airspace enlargement with significant parenchymal destruction in the SMP30/GNL knockout mice but not in the wild type mice. Our results suggest that vitamin C protects mice lungs from oxidative stress associated with aging and smoking. The SMP30/GNL knockout mice could be useful animal models for investigating age-related lung diseases including cigarette smoke-induced chronic obstructive pulmonary disease (COPD).

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腸内細菌のパントテン酸前駆体の投与がパントテン酸欠乏幼若ラットの成長とパントテン酸の尿中排泄量におよぼす影響

福渡努, 三木啓子, 東野勲, 柴田克己

原稿種別: 本文
2009 年 83 巻 3 号 p. 131-137
発行日: 2009/03/25
公開日: 2017/10/10

DOIhttps://doi.org/10.20632/vso.83.3_131

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Pantothenic acid is very unstable under acid or alkaline conditions to be hydrolyzed to pantolactone and β-alanine. There is no information of the pantothenate deficiency which might be caused by hydrolysis with gastric acid. It may be possible that pantothenate is synthesized again from pantolactone and β-alanine by enterobacteria. Accordinngly when pantolactone and β-alanine was administered to pantothenate-deficient infant rats, the growth and pantotheate content in liver and urine were compared with normal rats. Consequently pantolactone and β-alanine has not supported the growth similar to pantothenate-deficiency.

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トコトリエノールは3T3-L1未分化脂肪細胞において脂肪分化とAktのリン酸化を抑制する

近藤春美, 大森玲子, 清瀬千佳子, 岸本良美, 斉藤尚子, 五十嵐脩, 近藤和雄

原稿種別: 本文
2009 年 83 巻 3 号 p. 139-140
発行日: 2009/03/25
公開日: 2017/10/10

DOIhttps://doi.org/10.20632/vso.83.3_139

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チアミンが薬を運ぶ

田鶴谷(村山) 恵子, 三嶋基弘, 山田和子

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2009 年 83 巻 3 号 p. 141-144
発行日: 2009/03/25
公開日: 2017/10/10

DOIhttps://doi.org/10.20632/vso.83.3_141

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機能性ペプチド研究の展開

二川健, 寺尾純二, 岡達三

原稿種別: 本文
2009 年 83 巻 3 号 p. 145-146
発行日: 2009/03/25
公開日: 2017/10/10

DOIhttps://doi.org/10.20632/vso.83.3_145

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組織選択的ビタミンD受容体モジュレーターへの展望

高野真史, 橘高敦史

原稿種別: 本文
2009 年 83 巻 3 号 p. 147-149
発行日: 2009/03/25
公開日: 2017/10/10

DOIhttps://doi.org/10.20632/vso.83.3_147

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Transketolaseと角膜

竹内亨, 堀内正久

原稿種別: 本文
2009 年 83 巻 3 号 p. 150-151
発行日: 2009/03/25
公開日: 2017/10/10

DOIhttps://doi.org/10.20632/vso.83.3_150

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D-ガラクツロン酸/L-ガラクトン酸経路は光合成生物に普遍的なアスコルビン酸生合成経路だろうか?

西川仁, 石川孝博

原稿種別: 本文
2009 年 83 巻 3 号 p. 152-154
発行日: 2009/03/25
公開日: 2017/10/10

DOIhttps://doi.org/10.20632/vso.83.3_152

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