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Volume 83, Issue 3
Displaying 1-11 of 11 articles from this issue
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Shiro UranoArticle type: Article
2009 Volume 83 Issue 3 Pages 85-93
Published: March 25, 2009
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSOxidative 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.View full abstractDownload PDF (2793K) -
Koichi MoriArticle type: Article
2009 Volume 83 Issue 3 Pages 95-110
Published: March 25, 2009
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSAdenosylcobalamin-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.View full abstractDownload PDF (2354K) -
Shouji TakahashiArticle type: Article
2009 Volume 83 Issue 3 Pages 111-124
Published: March 25, 2009
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSFree 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.View full abstractDownload PDF (1773K) -
Akihito IshigamiArticle type: Article
2009 Volume 83 Issue 3 Pages 125-130
Published: March 25, 2009
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSSenescence 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).View full abstractDownload PDF (1329K) -
Tsutomu Fukuwatari, Keiko Miki, Isao Azumano, Katsumi ShibataArticle type: Article
2009 Volume 83 Issue 3 Pages 131-137
Published: March 25, 2009
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSPantothenic 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.View full abstractDownload PDF (779K) -
Harumi Uto-Kondo, Reiko Ohmori, Chikako Kiyose, Yoshimi Kishimoto, His ...Article type: Article
2009 Volume 83 Issue 3 Pages 139-140
Published: March 25, 2009
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (278K) -
Keiko Tazuya-Murayama, Motohiro Mishima, Kazuko YamadaArticle type: Article
2009 Volume 83 Issue 3 Pages 141-144
Published: March 25, 2009
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (498K) -
Ken Nikawa, Junji Terao, Tatsuzo OkaArticle type: Article
2009 Volume 83 Issue 3 Pages 145-146
Published: March 25, 2009
Released on J-STAGE: October 10, 2017
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Masashi Takano, Atsushi KittakaArticle type: Article
2009 Volume 83 Issue 3 Pages 147-149
Published: March 25, 2009
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (352K) -
Toru Takeuchi, Masahisa HoriuchiArticle type: Article
2009 Volume 83 Issue 3 Pages 150-151
Published: March 25, 2009
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (517K) -
Hitoshi Nishikawa, Takahiro IshikawaArticle type: Article
2009 Volume 83 Issue 3 Pages 152-154
Published: March 25, 2009
Released on J-STAGE: October 10, 2017
JOURNAL FREE ACCESSDownload PDF (435K)
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