VITAMINS

Regulation of reactive oxygen species actions via ascorbic acid metabolism

Takanori Maruta

Article type: Article
2014 Volume 88 Issue 1 Pages 1-10
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_1

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Reactive oxygen species (ROS) act not only as toxic compounds, but also as signaling molecules associated with responses to abiotic and biotic stresses in living organisms. The cellular redox state consisting of a delicate balance between ROS-production and ROS-scavenging must be strictly controlled. Ascorbic acid (AsA) is the most abundant water-soluble antioxidant in plants. Biochemical and molecular genetic approaches we have found by that AsA is mainly synthesized via a D-mannose/L-galactose pathway and that the pathway is regulated by light/dark and plastid-derived signals. AsA peroxidase (APX) plays a central role in controlling cellular H_2O_2 levels. We have demonstrated that cytosolic and chloroplastic APXs are required for plant tolerance and response to various types of stresses. Furthermore, using a conditional APX silencing system, we have found that chloroplastic H_2O_2 acts as a specific signal and regulates plant response to stress and hormones. Thus, our findings revealed a central role of AsA metabolism for regulating the cytotoxic effect and the signaling function of ROS in plants.

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Studies on neuroprotective effect of tocotrienol

Koji Fukui, Hirokatsu Takatsu, Taisuke Koike, Shiro Urano

Article type: Article
2014 Volume 88 Issue 1 Pages 11-17
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_11

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Cognitive dysfunction is induced in vitamin E-deficient and normal old rats. Previously, we found neuronal apoptosis in the hippocampal CA1 region which plays an important role in cognitive function. In this point, however it is difficult to treatment of cognitive function because the neurons have already died. It is necessary to find early sign before induction of cell death in vitamin E-deficient and normal old rats. We found beads formation in the axon and dendrite as neuronal degeneration. This neurite degeneration was discovered in not only cell line model but also primary cultured cells. Furthermore, we found the induction of axonal degeneration in the hippocampal CA1 region of vitamin E-deficient and normal old mice using silver staining. Treatment with tocotrienols significantly inhibited hydrogen peroxide-induced neurite degeneration in neuro2a and granule cells. These results indicate that tocotrienols have neuroprotective function. Next, we examined the mechanism of induction of neurite degeneration in vitamin E-deficient and normal old mice. Treatment with 2,2'-azobis(2-methylpropion amide) dihydorochloride (AAPH), which is one of water-soluble free radical generators, induced neurite degeneration in neuro2a cells. The expression of collapsin response mediator protein (CRMP)-2 which plays a role in microtubule assembly decreased in the brain of vitamin E-deficient and normal old mice. Furthermore, autophagy function also attenuated in the brain of vitamin E-deficient and normal old mice. These alterations were improved by treatment with tocotrienols. These results show the possibility that one of the mechanisms of the neuroprotective effects of tocotrienols may be involved in their antioxidant and non-antioxidant functions.

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[title in Japanese]

[in Japanese]

Article type: Article
2014 Volume 88 Issue 1 Pages 17-
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_17

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Vitamin K and bone metabolism

Sachiko Shiba, Satoshi Inoue

Article type: Article
2014 Volume 88 Issue 1 Pages 18-24
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_18

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Vitamin K (VK) is a fat-soluble vitamin that is essential for blood coagulation as well as bone metabolism. VK consists of 3 forms due to the difference of side chains bound to naphtoquinone ring: VK_1 (phylloquinone), VK_2 (menaquinone) and, VK_3 (menadione). In Japan, VK_2 is clinically used as a therapeutic agent for osteoporosis. VK functions as a co-factor of VK-dependent γ-glutamyl carboxylase (GGCX) in mediating post-translational modifications. As GGCX-dependent γ-carboxylated (Gla) proteins expressed in bone, osteocalcin (OC) and matrix Gla protein (MGP) are known to play modulatory roles in bone metabolism. On the other hand, VK_2 also regulates the transcription of bone-related genes in osteoblasts through activating steroid X receptor (SXR)/pregnane X receptor (PXR), as well as enhancing the phosphorylation of protein kinase A (PKA). Recent studies have revealed that osteoblast-derived OC also exerts a hormone-like action that controls bone metabolism and energy metabolism. Overall, VK is an essential nutrient for bone metabolism through modulating multiple signaling pathways mediated by GGCX, SXR, PKA, and VK-dependent proteins

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Functions and pathobiology of liver as a target organ of vitamin A

Goshi Shiota

Article type: Article
2014 Volume 88 Issue 1 Pages 25-30
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_25

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Retinoids are known to be involved in suppression of several kinds of cancers, including hepatocellular carcinoma (HCC). To test the hypothesis that shortage of vitamin A in hepatic stellate cells causes HCC during the course of chronic liver disease, we reported the transgenic mice, in which retinoic acid (RA) signaling is suppressed in a hepatocyte-specific manner, developed liver cancer at a high rate. Retinoids play an important role in liver pathophysiology including iron metabolism, insulin resistance, fatty acid oxidation and regulation of oxidative stress. These data suggest that exploring the metabolism of retinoids in liver diseases and their target genes provides us with useful information to understand the liver functions and diseases. The metabolism of retinoids was altered in liver diseases, including non-alcoholic fatty liver disease. We identified 26 genes using in silico analysis based on the gene information of a DR5 in the 5-Kb upstream of 36,341 EST clusteres. Of these genes, expression of OTUD7B, an upregulated by ATRA, serves as an indicator of cancer-specific survival in HCC patients. These efforts will hopefully improve the prognosis of the patients with liver diseases in the near future.

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Biotin responsive metabolic and neurological diseases

Yoichi Suzuki

Article type: Article
2014 Volume 88 Issue 1 Pages 31-35
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_31

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Biotin is a water-soluble vitamin and a cofactor of several types of carboxylases. Insufficient intake of biotin and a congenital deficiency of enzymes that are required for biotin to act in the cell cause clinical symptoms called multiple carboxylase deficiency (MCD). In recent years, there have been several reports of infants with food allergy and/or atopic eczema who developed MCD after being fed with peptide formula. We investigated the incidence of nutritional biotin deficiency and congenital enzyme deficiency in Japan. For the estimated incidence of biotin deficiency, there were at least 70 cases in the last 10 years. Since the first diagnosis of holocarboxylase synthetase deficiency (HCSD) in 1982, HCSD and biotinidase deficiency were confirmed in 28 and 2 cases, respectively. These data suggest that the incidence of congenital enzyme deficiency is about 1 case per year. Biotin-responsive basal ganglia disease (BBGD) is an encephalopathy of children whose symptoms are ameliorated by biotin administration. Mutations in the SLC19A3 gene were identified in the patients. SLC19A3 shows transporter activity for thiamin but not for biotin. The mechanism of biotin-responsiveness in BBGD is not yet elucidated. Further, patients with Leigh-like syndromes have been shown to have mutations in this gene. Currently, the relationship between biotin and SLC19A3 is largely unknown.

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Effect of tocotrienol intake on brain function

Koji Fukui

Article type: Article
2014 Volume 88 Issue 1 Pages 36-39
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_36

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Regulation of epigenetics by vitamin C

Yuki Kishimoto, Akihito Ishigami

Article type: Article
2014 Volume 88 Issue 1 Pages 40-43
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_40

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[title in Japanese]

[in Japanese], [in Japanese]

Article type: Article
2014 Volume 88 Issue 1 Pages 44-45
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_44

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[title in Japanese]

[in Japanese], [in Japanese], [in Japanese], [in Japanese]

Article type: Article
2014 Volume 88 Issue 1 Pages 45-46
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_45

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[title in Japanese]

[in Japanese], [in Japanese], [in Japanese], [in Japanese]

Article type: Article
2014 Volume 88 Issue 1 Pages 46-47
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_46

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[title in Japanese]

[in Japanese]

Article type: Article
2014 Volume 88 Issue 1 Pages 47-48
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_47

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[title in Japanese]

[in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...

Article type: Article
2014 Volume 88 Issue 1 Pages 48-49
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_48

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[title in Japanese]

[in Japanese]

Article type: Article
2014 Volume 88 Issue 1 Pages 49-50
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_49

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[title in Japanese]

[in Japanese], [in Japanese], [in Japanese], [in Japanese], [in Japane ...

Article type: Article
2014 Volume 88 Issue 1 Pages 50-51
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_50

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[title in Japanese]

[in Japanese], [in Japanese], [in Japanese], [in Japanese]

Article type: Article
2014 Volume 88 Issue 1 Pages 51-52
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_51

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[title in Japanese]

[in Japanese], [in Japanese], [in Japanese]

Article type: Article
2014 Volume 88 Issue 1 Pages 52-53
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_52

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[title in Japanese]

[in Japanese]

Article type: Article
2014 Volume 88 Issue 1 Pages 53-
Published: January 25, 2014
Released on J-STAGE: August 10, 2017

DOIhttps://doi.org/10.20632/vso.88.1_53

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