Nicotinamide; antioxidative and DNA hypomethylation effects in plant cells.
Identifieur interne : 001291 ( Main/Exploration ); précédent : 001290; suivant : 001292Nicotinamide; antioxidative and DNA hypomethylation effects in plant cells.
Auteurs : Torkel Berglund [Suède] ; Anders Wallström [Suède] ; Tuong-Van Nguyen [Viêt Nam] ; Cecilia Laurell [Suède] ; Anna B. Ohlsson [Suède]Source :
- Plant physiology and biochemistry : PPB [ 1873-2690 ] ; 2017.
Descripteurs français
- KwdFr :
- ADN des plantes (métabolisme), Aconitate hydratase (métabolisme), Cassures de l'ADN (MeSH), Cellules végétales (métabolisme), Fumarate hydratase (métabolisme), Métabolisme énergétique (effets des médicaments et des substances chimiques), Méthylation de l'ADN (effets des médicaments et des substances chimiques), Nicotinamide (pharmacologie), Protéines végétales (métabolisme), Régulation de l'expression des gènes végétaux (effets des médicaments et des substances chimiques), Épigenèse génétique (effets des médicaments et des substances chimiques).
- MESH :
- effets des médicaments et des substances chimiques : Métabolisme énergétique, Méthylation de l'ADN, Régulation de l'expression des gènes végétaux, Épigenèse génétique.
- métabolisme : ADN des plantes, Aconitate hydratase, Cellules végétales, Fumarate hydratase, Protéines végétales.
- pharmacologie : Nicotinamide.
- Cassures de l'ADN.
English descriptors
- KwdEn :
- Aconitate Hydratase (metabolism), DNA Breaks (MeSH), DNA Methylation (drug effects), DNA, Plant (metabolism), Energy Metabolism (drug effects), Epigenesis, Genetic (drug effects), Fumarate Hydratase (metabolism), Gene Expression Regulation, Plant (drug effects), Niacinamide (pharmacology), Plant Cells (metabolism), Plant Proteins (metabolism).
- MESH :
- chemical , metabolism : Aconitate Hydratase, DNA, Plant, Fumarate Hydratase, Plant Proteins.
- drug effects : DNA Methylation, Energy Metabolism, Epigenesis, Genetic, Gene Expression Regulation, Plant.
- metabolism : Plant Cells.
- chemical , pharmacology : Niacinamide.
- DNA Breaks.
Abstract
The effects of nicotinamide (NIC) and its natural plant metabolites nicotinic acid (NIA) and trigonelline (TRIG) were studied with respect to defense in plant cell cultures. NIC and NIA could protect against oxidative stress damage caused by 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH), which generates free radicals. Damage was analyzed as DNA strand breaks in cell cultures of Pisum sativum (garden pea), Daucus carota (carrot), Populus tremula L. × P. tremuloides (hybrid aspen) and Catharanthus roseus (Madagascar periwinkle), monitored by single cell gel electrophoresis (comet assay), and assays of cell leakage in C. roseus. The activities of aconitase and fumarase enzymes, which have key roles in energy metabolism, were analyzed in P. sativum cultures after treatment with NIC or NIA. Aconitase activity was increased by NIA, and fumarase activity was increased by both compounds. These compounds were shown to promote glutathione metabolism in P. sativum cultures, and NIC was shown to have a global DNA hypomethylating effect. Neither TRIG nor poly(ADP-ribose) polymerase (PARP) inhibitor 3-aminobenzamide offered any protection against DNA damage or cell leakage, nor did they promote aconitase or fumarase activities, or glutathione metabolism. By this broad approach addressing multiple biochemical factors and different plant species, we demonstrate that NIC and NIA protect plant cells from oxidative stress, and that NIC clearly exerts an epigenetic effect; decreased DNA methylation. This indicates that these compounds have important roles in the regulation of metabolism in plant cells, especially in connection to stress.
DOI: 10.1016/j.plaphy.2017.07.023
PubMed: 28780454
Affiliations:
Links toward previous steps (curation, corpus...)
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Electronic address: vanngtg@gmail.com.</nlm:affiliation><country xml:lang="fr">Viêt Nam</country><wicri:regionArea>Institute of Biotechnology, Vietnam Academy of Science and Technology, 18 Hoang Quoc Viet Rd., Cau Giay, Hanoi</wicri:regionArea><wicri:noRegion>Hanoi</wicri:noRegion></affiliation></author><author><name sortKey="Laurell, Cecilia" sort="Laurell, Cecilia" uniqKey="Laurell C" first="Cecilia" last="Laurell">Cecilia Laurell</name><affiliation wicri:level="1"><nlm:affiliation>School of Biotechnology, KTH Royal Institute of Technology, AlbaNova University Center, SE-106 91 Stockholm, Sweden. 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NIC and NIA could protect against oxidative stress damage caused by 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH), which generates free radicals. Damage was analyzed as DNA strand breaks in cell cultures of Pisum sativum (garden pea), Daucus carota (carrot), Populus tremula L. × P. tremuloides (hybrid aspen) and Catharanthus roseus (Madagascar periwinkle), monitored by single cell gel electrophoresis (comet assay), and assays of cell leakage in C. roseus. The activities of aconitase and fumarase enzymes, which have key roles in energy metabolism, were analyzed in P. sativum cultures after treatment with NIC or NIA. Aconitase activity was increased by NIA, and fumarase activity was increased by both compounds. These compounds were shown to promote glutathione metabolism in P. sativum cultures, and NIC was shown to have a global DNA hypomethylating effect. Neither TRIG nor poly(ADP-ribose) polymerase (PARP) inhibitor 3-aminobenzamide offered any protection against DNA damage or cell leakage, nor did they promote aconitase or fumarase activities, or glutathione metabolism. By this broad approach addressing multiple biochemical factors and different plant species, we demonstrate that NIC and NIA protect plant cells from oxidative stress, and that NIC clearly exerts an epigenetic effect; decreased DNA methylation. This indicates that these compounds have important roles in the regulation of metabolism in plant cells, especially in connection to stress.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28780454</PMID><DateCompleted><Year>2017</Year><Month>12</Month><Day>26</Day></DateCompleted><DateRevised><Year>2020</Year><Month>09</Month><Day>30</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1873-2690</ISSN><JournalIssue CitedMedium="Internet"><Volume>118</Volume><PubDate><Year>2017</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Plant physiology and biochemistry : PPB</Title><ISOAbbreviation>Plant Physiol Biochem</ISOAbbreviation></Journal><ArticleTitle>Nicotinamide; antioxidative and DNA hypomethylation effects in plant cells.</ArticleTitle><Pagination><MedlinePgn>551-560</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0981-9428(17)30245-0</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.plaphy.2017.07.023</ELocationID><Abstract><AbstractText>The effects of nicotinamide (NIC) and its natural plant metabolites nicotinic acid (NIA) and trigonelline (TRIG) were studied with respect to defense in plant cell cultures. NIC and NIA could protect against oxidative stress damage caused by 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH), which generates free radicals. Damage was analyzed as DNA strand breaks in cell cultures of Pisum sativum (garden pea), Daucus carota (carrot), Populus tremula L. × P. tremuloides (hybrid aspen) and Catharanthus roseus (Madagascar periwinkle), monitored by single cell gel electrophoresis (comet assay), and assays of cell leakage in C. roseus. The activities of aconitase and fumarase enzymes, which have key roles in energy metabolism, were analyzed in P. sativum cultures after treatment with NIC or NIA. Aconitase activity was increased by NIA, and fumarase activity was increased by both compounds. These compounds were shown to promote glutathione metabolism in P. sativum cultures, and NIC was shown to have a global DNA hypomethylating effect. Neither TRIG nor poly(ADP-ribose) polymerase (PARP) inhibitor 3-aminobenzamide offered any protection against DNA damage or cell leakage, nor did they promote aconitase or fumarase activities, or glutathione metabolism. By this broad approach addressing multiple biochemical factors and different plant species, we demonstrate that NIC and NIA protect plant cells from oxidative stress, and that NIC clearly exerts an epigenetic effect; decreased DNA methylation. This indicates that these compounds have important roles in the regulation of metabolism in plant cells, especially in connection to stress.</AbstractText><CopyrightInformation>Copyright © 2017 The Authors. Published by Elsevier Masson SAS.. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Berglund</LastName><ForeName>Torkel</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>School of Biotechnology, KTH Royal Institute of Technology, AlbaNova University Center, SE-106 91 Stockholm, Sweden. Electronic address: torkelb@kth.se.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wallström</LastName><ForeName>Anders</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Swedish Orphan Biovitrum AB, SE-112 76 Stockholm, Sweden. Electronic address: anders.wallstrom@sobi.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nguyen</LastName><ForeName>Tuong-Van</ForeName><Initials>TV</Initials><AffiliationInfo><Affiliation>Institute of Biotechnology, Vietnam Academy of Science and Technology, 18 Hoang Quoc Viet Rd., Cau Giay, Hanoi, Viet Nam. Electronic address: vanngtg@gmail.com.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Laurell</LastName><ForeName>Cecilia</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>School of Biotechnology, KTH Royal Institute of Technology, AlbaNova University Center, SE-106 91 Stockholm, Sweden. Electronic address: claurell@kth.se.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ohlsson</LastName><ForeName>Anna B</ForeName><Initials>AB</Initials><AffiliationInfo><Affiliation>School of Biotechnology, KTH Royal Institute of Technology, AlbaNova University Center, SE-106 91 Stockholm, Sweden. Electronic address: annao@biotech.kth.se.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>07</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Plant Physiol Biochem</MedlineTA><NlmUniqueID>9882449</NlmUniqueID><ISSNLinking>0981-9428</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018744">DNA, Plant</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010940">Plant Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>25X51I8RD4</RegistryNumber><NameOfSubstance UI="D009536">Niacinamide</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 4.2.1.2</RegistryNumber><NameOfSubstance UI="D005649">Fumarate Hydratase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 4.2.1.3</RegistryNumber><NameOfSubstance UI="D000154">Aconitate Hydratase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000154" MajorTopicYN="N">Aconitate Hydratase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053960" MajorTopicYN="N">DNA Breaks</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019175" MajorTopicYN="N">DNA Methylation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018744" MajorTopicYN="N">DNA, Plant</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004734" MajorTopicYN="N">Energy Metabolism</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D044127" MajorTopicYN="N">Epigenesis, Genetic</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005649" MajorTopicYN="N">Fumarate Hydratase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018506" MajorTopicYN="N">Gene Expression Regulation, Plant</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009536" MajorTopicYN="N">Niacinamide</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D059828" MajorTopicYN="N">Plant Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010940" MajorTopicYN="N">Plant Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Cell leakage</Keyword><Keyword MajorTopicYN="N">Citric acid cycle enzymes</Keyword><Keyword MajorTopicYN="N">DNA damage</Keyword><Keyword MajorTopicYN="N">DNA methylation</Keyword><Keyword MajorTopicYN="N">EC 2.4.2.30)</Keyword><Keyword MajorTopicYN="N">Nicotinic acid</Keyword><Keyword MajorTopicYN="N">Oxidative stress</Keyword><Keyword MajorTopicYN="N">PARP (poly(ADP-ribose) polymerase</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>06</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>07</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>07</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>8</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>12</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>8</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28780454</ArticleId><ArticleId IdType="pii">S0981-9428(17)30245-0</ArticleId><ArticleId IdType="doi">10.1016/j.plaphy.2017.07.023</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Suède</li><li>Viêt Nam</li></country></list><tree><country name="Suède"><noRegion><name sortKey="Berglund, Torkel" sort="Berglund, Torkel" uniqKey="Berglund T" first="Torkel" last="Berglund">Torkel Berglund</name></noRegion><name sortKey="Laurell, Cecilia" sort="Laurell, Cecilia" uniqKey="Laurell C" first="Cecilia" last="Laurell">Cecilia Laurell</name><name sortKey="Ohlsson, Anna B" sort="Ohlsson, Anna B" uniqKey="Ohlsson A" first="Anna B" last="Ohlsson">Anna B. Ohlsson</name><name sortKey="Wallstrom, Anders" sort="Wallstrom, Anders" uniqKey="Wallstrom A" first="Anders" last="Wallström">Anders Wallström</name></country><country name="Viêt Nam"><noRegion><name sortKey="Nguyen, Tuong Van" sort="Nguyen, Tuong Van" uniqKey="Nguyen T" first="Tuong-Van" last="Nguyen">Tuong-Van Nguyen</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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