Nitric oxide acts as an antioxidant and inhibits programmed cell death induced by aluminum in the root tips of peanut (Arachis hypogaea L.).
Identifieur interne : 000102 ( Main/Exploration ); précédent : 000101; suivant : 000103Nitric oxide acts as an antioxidant and inhibits programmed cell death induced by aluminum in the root tips of peanut (Arachis hypogaea L.).
Auteurs : Huyi He [République populaire de Chine] ; Thet Lwin Oo [République populaire de Chine] ; Wenjing Huang [République populaire de Chine] ; Long-Fei He [République populaire de Chine] ; Minghua Gu [République populaire de Chine]Source :
- Scientific reports [ 2045-2322 ] ; 2019.
Descripteurs français
- KwdFr :
- Aluminium (toxicité), Analyse de regroupements (MeSH), Antioxydants (métabolisme), Apoptose (effets des médicaments et des substances chimiques), Arachis (métabolisme), Ascorbate peroxidases (métabolisme), Complexe IV de la chaîne respiratoire (métabolisme), Espèces réactives de l'oxygène (métabolisme), Malonaldéhyde (métabolisme), Mitochondries (effets des médicaments et des substances chimiques), Mitochondries (métabolisme), Monoxyde d'azote (métabolisme), Nitroprussiate (pharmacologie), Peroxydation lipidique (effets des médicaments et des substances chimiques), Peroxyde d'hydrogène (métabolisme), Racines de plante (métabolisme), Régulation négative (effets des médicaments et des substances chimiques), Régulation positive (effets des médicaments et des substances chimiques).
- MESH :
- effets des médicaments et des substances chimiques : Apoptose, Mitochondries, Peroxydation lipidique, Régulation négative, Régulation positive.
- métabolisme : Antioxydants, Arachis, Ascorbate peroxidases, Complexe IV de la chaîne respiratoire, Espèces réactives de l'oxygène, Malonaldéhyde, Mitochondries, Monoxyde d'azote, Peroxyde d'hydrogène, Racines de plante.
- pharmacologie : Nitroprussiate.
- toxicité : Aluminium.
- Analyse de regroupements.
English descriptors
- KwdEn :
- Aluminum (toxicity), Antioxidants (metabolism), Apoptosis (drug effects), Arachis (metabolism), Ascorbate Peroxidases (metabolism), Cluster Analysis (MeSH), Down-Regulation (drug effects), Electron Transport Complex IV (metabolism), Hydrogen Peroxide (metabolism), Lipid Peroxidation (drug effects), Malondialdehyde (metabolism), Mitochondria (drug effects), Mitochondria (metabolism), Nitric Oxide (metabolism), Nitroprusside (pharmacology), Plant Roots (metabolism), Reactive Oxygen Species (metabolism), Up-Regulation (drug effects).
- MESH :
- chemical , metabolism : Antioxidants, Ascorbate Peroxidases, Electron Transport Complex IV, Hydrogen Peroxide, Malondialdehyde, Nitric Oxide, Reactive Oxygen Species.
- chemical , pharmacology : Nitroprusside.
- chemical , toxicity : Aluminum.
- drug effects : Apoptosis, Down-Regulation, Lipid Peroxidation, Mitochondria, Up-Regulation.
- metabolism : Arachis, Mitochondria, Plant Roots.
- Cluster Analysis.
Abstract
Aluminum (Al) causes programmed cell death (PCD) in plants. Our previous studies have confirmed that nitric oxide (NO) inhibits Al-induced PCD in the root tips of peanut. However, the mechanism by which NO inhibits Al-induced PCD is unclear. Here the effects of NO on mitochondrial reactive oxygen species (ROS), malondialdehyde (MDA), activities of superoxide dismutase (SOD) and ascorbate peroxidase (APX), expression of alternative oxidase (AhAOX) and cytochrome oxidase (AhCOX) were investigated in peanut (Arachis hypogaea L.) root tips treated with Al. The results showed that Al stress induced rapid accumulation of H2O2 and MDA and increased the ratio of SOD/APX. The up-regulation of AhAOX and AhCOX expressions was not enough to inhibit PCD occurrence. Sodium nitroprusside (SNP, a NO donor) decreased the ratio of SOD/APX and eliminated excess H2O2 and MDA, thereby inhibiting Al-induced PCD in the root tips of peanut. The expression of AhAOX and AhCOX was significantly enhanced in Al-induced PCD treated with SNP. But cPTIO (a NO specific scavenger) supply had the opposite effect. Taken together, these results suggested that lipid peroxidation induced by higher levels of H2O2 was an important cause of Al-induced PCD. NO-mediated inhibition of Al-induced PCD was related to a significant elimination of H2O2 accumulation by decreasing the ratio of SOD/APX and up-regulating the expression of AhAOX and AhCOX.
DOI: 10.1038/s41598-019-46036-8
PubMed: 31267033
PubMed Central: PMC6606607
Affiliations:
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China.</nlm:affiliation><country xml:lang="fr" wicri:curation="lc">République populaire de Chine</country><wicri:regionArea>College of Agronomy, Guangxi University, Nanning, 530004</wicri:regionArea><wicri:noRegion>530004</wicri:noRegion></affiliation></author></analytic><series><title level="j">Scientific reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aluminum (toxicity)</term><term>Antioxidants (metabolism)</term><term>Apoptosis (drug effects)</term><term>Arachis (metabolism)</term><term>Ascorbate Peroxidases (metabolism)</term><term>Cluster Analysis (MeSH)</term><term>Down-Regulation (drug effects)</term><term>Electron Transport Complex IV (metabolism)</term><term>Hydrogen Peroxide (metabolism)</term><term>Lipid Peroxidation (drug effects)</term><term>Malondialdehyde (metabolism)</term><term>Mitochondria (drug effects)</term><term>Mitochondria (metabolism)</term><term>Nitric Oxide (metabolism)</term><term>Nitroprusside (pharmacology)</term><term>Plant Roots (metabolism)</term><term>Reactive Oxygen Species (metabolism)</term><term>Up-Regulation (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Aluminium (toxicité)</term><term>Analyse de regroupements (MeSH)</term><term>Antioxydants (métabolisme)</term><term>Apoptose (effets des médicaments et des substances chimiques)</term><term>Arachis (métabolisme)</term><term>Ascorbate peroxidases (métabolisme)</term><term>Complexe IV de la chaîne respiratoire (métabolisme)</term><term>Espèces réactives de l'oxygène (métabolisme)</term><term>Malonaldéhyde (métabolisme)</term><term>Mitochondries (effets des médicaments et des substances chimiques)</term><term>Mitochondries (métabolisme)</term><term>Monoxyde d'azote (métabolisme)</term><term>Nitroprussiate (pharmacologie)</term><term>Peroxydation lipidique (effets des médicaments et des substances chimiques)</term><term>Peroxyde d'hydrogène (métabolisme)</term><term>Racines de plante (métabolisme)</term><term>Régulation négative (effets des médicaments et des substances chimiques)</term><term>Régulation positive (effets des médicaments et des substances chimiques)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antioxidants</term><term>Ascorbate Peroxidases</term><term>Electron Transport Complex IV</term><term>Hydrogen Peroxide</term><term>Malondialdehyde</term><term>Nitric Oxide</term><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Nitroprusside</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Aluminum</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Down-Regulation</term><term>Lipid Peroxidation</term><term>Mitochondria</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Apoptose</term><term>Mitochondries</term><term>Peroxydation lipidique</term><term>Régulation négative</term><term>Régulation positive</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Arachis</term><term>Mitochondria</term><term>Plant Roots</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antioxydants</term><term>Arachis</term><term>Ascorbate peroxidases</term><term>Complexe IV de la chaîne respiratoire</term><term>Espèces réactives de l'oxygène</term><term>Malonaldéhyde</term><term>Mitochondries</term><term>Monoxyde d'azote</term><term>Peroxyde d'hydrogène</term><term>Racines de plante</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Nitroprussiate</term></keywords><keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Aluminium</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cluster Analysis</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de regroupements</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Aluminum (Al) causes programmed cell death (PCD) in plants. Our previous studies have confirmed that nitric oxide (NO) inhibits Al-induced PCD in the root tips of peanut. However, the mechanism by which NO inhibits Al-induced PCD is unclear. Here the effects of NO on mitochondrial reactive oxygen species (ROS), malondialdehyde (MDA), activities of superoxide dismutase (SOD) and ascorbate peroxidase (APX), expression of alternative oxidase (AhAOX) and cytochrome oxidase (AhCOX) were investigated in peanut (Arachis hypogaea L.) root tips treated with Al. The results showed that Al stress induced rapid accumulation of H<sub>2</sub>O<sub>2</sub> and MDA and increased the ratio of SOD/APX. The up-regulation of AhAOX and AhCOX expressions was not enough to inhibit PCD occurrence. Sodium nitroprusside (SNP, a NO donor) decreased the ratio of SOD/APX and eliminated excess H<sub>2</sub>O<sub>2</sub> and MDA, thereby inhibiting Al-induced PCD in the root tips of peanut. The expression of AhAOX and AhCOX was significantly enhanced in Al-induced PCD treated with SNP. But cPTIO (a NO specific scavenger) supply had the opposite effect. Taken together, these results suggested that lipid peroxidation induced by higher levels of H<sub>2</sub>O<sub>2</sub> was an important cause of Al-induced PCD. NO-mediated inhibition of Al-induced PCD was related to a significant elimination of H<sub>2</sub>O<sub>2</sub> accumulation by decreasing the ratio of SOD/APX and up-regulating the expression of AhAOX and AhCOX.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31267033</PMID><DateCompleted><Year>2020</Year><Month>10</Month><Day>16</Day></DateCompleted><DateRevised><Year>2020</Year><Month>10</Month><Day>16</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2045-2322</ISSN><JournalIssue CitedMedium="Internet"><Volume>9</Volume><Issue>1</Issue><PubDate><Year>2019</Year><Month>07</Month><Day>02</Day></PubDate></JournalIssue><Title>Scientific reports</Title><ISOAbbreviation>Sci Rep</ISOAbbreviation></Journal><ArticleTitle>Nitric oxide acts as an antioxidant and inhibits programmed cell death induced by aluminum in the root tips of peanut (Arachis hypogaea L.).</ArticleTitle><Pagination><MedlinePgn>9516</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41598-019-46036-8</ELocationID><Abstract><AbstractText>Aluminum (Al) causes programmed cell death (PCD) in plants. Our previous studies have confirmed that nitric oxide (NO) inhibits Al-induced PCD in the root tips of peanut. However, the mechanism by which NO inhibits Al-induced PCD is unclear. Here the effects of NO on mitochondrial reactive oxygen species (ROS), malondialdehyde (MDA), activities of superoxide dismutase (SOD) and ascorbate peroxidase (APX), expression of alternative oxidase (AhAOX) and cytochrome oxidase (AhCOX) were investigated in peanut (Arachis hypogaea L.) root tips treated with Al. The results showed that Al stress induced rapid accumulation of H<sub>2</sub>O<sub>2</sub> and MDA and increased the ratio of SOD/APX. The up-regulation of AhAOX and AhCOX expressions was not enough to inhibit PCD occurrence. Sodium nitroprusside (SNP, a NO donor) decreased the ratio of SOD/APX and eliminated excess H<sub>2</sub>O<sub>2</sub> and MDA, thereby inhibiting Al-induced PCD in the root tips of peanut. The expression of AhAOX and AhCOX was significantly enhanced in Al-induced PCD treated with SNP. But cPTIO (a NO specific scavenger) supply had the opposite effect. Taken together, these results suggested that lipid peroxidation induced by higher levels of H<sub>2</sub>O<sub>2</sub> was an important cause of Al-induced PCD. NO-mediated inhibition of Al-induced PCD was related to a significant elimination of H<sub>2</sub>O<sub>2</sub> accumulation by decreasing the ratio of SOD/APX and up-regulating the expression of AhAOX and AhCOX.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>He</LastName><ForeName>Huyi</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>College of Agronomy, Guangxi University, Nanning, 530004, P.R. China.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Cash Crops Research Institute, Guangxi Academy of Agricultural Sciences, Nanning, 530007, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Oo</LastName><ForeName>Thet Lwin</ForeName><Initials>TL</Initials><AffiliationInfo><Affiliation>College of Agronomy, Guangxi University, Nanning, 530004, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Huang</LastName><ForeName>Wenjing</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>College of Agronomy, Guangxi University, Nanning, 530004, P.R. China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>He</LastName><ForeName>Long-Fei</ForeName><Initials>LF</Initials><AffiliationInfo><Affiliation>College of Agronomy, Guangxi University, Nanning, 530004, P.R. China. lfhe@gxu.edu.cn.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Guangxi Key Laboratory for Agro-Environment and Agro-Product Safety, Nanning, 530004, P.R. China. lfhe@gxu.edu.cn.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gu</LastName><ForeName>Minghua</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>College of Agronomy, Guangxi University, Nanning, 530004, P.R. China.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>07</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Sci Rep</MedlineTA><NlmUniqueID>101563288</NlmUniqueID><ISSNLinking>2045-2322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000975">Antioxidants</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017382">Reactive Oxygen Species</NameOfSubstance></Chemical><Chemical><RegistryNumber>169D1260KM</RegistryNumber><NameOfSubstance UI="D009599">Nitroprusside</NameOfSubstance></Chemical><Chemical><RegistryNumber>31C4KY9ESH</RegistryNumber><NameOfSubstance UI="D009569">Nitric Oxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>4Y8F71G49Q</RegistryNumber><NameOfSubstance UI="D008315">Malondialdehyde</NameOfSubstance></Chemical><Chemical><RegistryNumber>BBX060AN9V</RegistryNumber><NameOfSubstance UI="D006861">Hydrogen Peroxide</NameOfSubstance></Chemical><Chemical><RegistryNumber>CPD4NFA903</RegistryNumber><NameOfSubstance UI="D000535">Aluminum</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.11.1.11</RegistryNumber><NameOfSubstance UI="D060387">Ascorbate Peroxidases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.9.3.1</RegistryNumber><NameOfSubstance UI="D003576">Electron Transport Complex IV</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000535" MajorTopicYN="N">Aluminum</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000975" MajorTopicYN="N">Antioxidants</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010367" MajorTopicYN="N">Arachis</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D060387" MajorTopicYN="N">Ascorbate Peroxidases</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016000" MajorTopicYN="N">Cluster Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003576" MajorTopicYN="N">Electron Transport Complex IV</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006861" MajorTopicYN="N">Hydrogen Peroxide</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015227" MajorTopicYN="N">Lipid Peroxidation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008315" MajorTopicYN="N">Malondialdehyde</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008928" MajorTopicYN="N">Mitochondria</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009569" MajorTopicYN="N">Nitric Oxide</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009599" MajorTopicYN="N">Nitroprusside</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018517" MajorTopicYN="N">Plant Roots</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>05</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>06</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>7</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>7</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>10</Month><Day>21</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31267033</ArticleId><ArticleId IdType="doi">10.1038/s41598-019-46036-8</ArticleId><ArticleId IdType="pii">10.1038/s41598-019-46036-8</ArticleId><ArticleId IdType="pmc">PMC6606607</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="He, Huyi" sort="He, Huyi" uniqKey="He H" first="Huyi" last="He">Huyi He</name></noRegion><name sortKey="Gu, Minghua" sort="Gu, Minghua" uniqKey="Gu M" first="Minghua" last="Gu">Minghua Gu</name><name sortKey="He, Huyi" sort="He, Huyi" uniqKey="He H" first="Huyi" last="He">Huyi He</name><name sortKey="He, Long Fei" sort="He, Long Fei" uniqKey="He L" first="Long-Fei" last="He">Long-Fei He</name><name sortKey="He, Long Fei" sort="He, Long Fei" uniqKey="He L" first="Long-Fei" last="He">Long-Fei He</name><name sortKey="Huang, Wenjing" sort="Huang, Wenjing" uniqKey="Huang W" first="Wenjing" last="Huang">Wenjing Huang</name><name sortKey="Oo, Thet Lwin" sort="Oo, Thet Lwin" uniqKey="Oo T" first="Thet Lwin" last="Oo">Thet Lwin Oo</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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