Participation of the mitochondrial permeability transition pore in nitric oxide-induced plant cell death.
Identifieur interne : 000044 ( Ncbi/Merge ); précédent : 000043; suivant : 000045Participation of the mitochondrial permeability transition pore in nitric oxide-induced plant cell death.
Auteurs : Elzira E. Saviani [Brésil] ; Cintia H. Orsi ; Jusceley F P. Oliveira ; Cecília A F. Pinto-Maglio ; Ione SalgadoSource :
- FEBS letters [ 0014-5793 ] ; 2002.
English descriptors
- KwdEn :
- Apoptosis (drug effects), Cell Death (drug effects), Cell Division (drug effects), Cells, Cultured, Citrus (cytology), Citrus (drug effects), Citrus (metabolism), Cyclosporine (pharmacology), DNA Fragmentation, Intracellular Membranes (drug effects), Intracellular Membranes (physiology), Ion Channels, Membrane Potentials (drug effects), Membrane Proteins (drug effects), Membrane Proteins (metabolism), Mitochondria (drug effects), Mitochondria (metabolism), Mitochondrial Membrane Transport Proteins, Nitric Oxide (toxicity), Nitric Oxide Donors (toxicity), Nitroprusside (toxicity), S-Nitroso-N-Acetylpenicillamine (toxicity), Signal Transduction (drug effects), Signal Transduction (physiology).
- MESH :
- chemical , drug effects : Membrane Proteins.
- chemical , metabolism : Membrane Proteins.
- chemical , pharmacology : Cyclosporine.
- cytology : Citrus.
- drug effects : Apoptosis, Cell Death, Cell Division, Citrus, Intracellular Membranes, Membrane Potentials, Mitochondria, Signal Transduction.
- metabolism : Citrus, Mitochondria.
- physiology : Intracellular Membranes, Signal Transduction.
- chemical , toxicity : Nitric Oxide, Nitric Oxide Donors, Nitroprusside, S-Nitroso-N-Acetylpenicillamine.
- Cells, Cultured, DNA Fragmentation, Ion Channels, Mitochondrial Membrane Transport Proteins.
Abstract
In the present study, we investigated the involvement of the mitochondrial permeability transition pore (PTP) in nitric oxide (NO)-induced plant cell death. NO donors such as sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine inhibited growth and caused death in suspension-cultured cells of Citrus sinensis. Cells treated with SNP showed chromatin condensation and fragmentation, characteristic of apoptosis. SNP caused loss of the mitochondrial membrane electrical potential, which was prevented by cyclosporin A (CsA), a specific inhibitor of PTP formation. CsA also prevented the nuclear apoptosis and subsequent Citrus cell death induced by NO. These findings indicate that mitochondrial PTP formation is involved in the signaling pathway by which NO induces apoptosis in cultured Citrus cells.
PubMed: 11801241
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Orsi</name></author><author><name sortKey="Oliveira, Jusceley F P" sort="Oliveira, Jusceley F P" uniqKey="Oliveira J" first="Jusceley F P" last="Oliveira">Jusceley F P. Oliveira</name></author><author><name sortKey="Pinto Maglio, Cecilia A F" sort="Pinto Maglio, Cecilia A F" uniqKey="Pinto Maglio C" first="Cecília A F" last="Pinto-Maglio">Cecília A F. Pinto-Maglio</name></author><author><name sortKey="Salgado, Ione" sort="Salgado, Ione" uniqKey="Salgado I" first="Ione" last="Salgado">Ione Salgado</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2002">2002</date><idno type="RBID">pubmed:11801241</idno><idno type="pmid">11801241</idno><idno type="wicri:Area/PubMed/Corpus">000E82</idno><idno type="wicri:Area/PubMed/Curation">000E82</idno><idno type="wicri:Area/PubMed/Checkpoint">000E82</idno><idno type="wicri:Area/Ncbi/Merge">000044</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Participation of the mitochondrial permeability transition pore in nitric oxide-induced plant cell death.</title><author><name sortKey="Saviani, Elzira E" sort="Saviani, Elzira E" uniqKey="Saviani E" first="Elzira E" last="Saviani">Elzira E. Saviani</name><affiliation wicri:level="2"><nlm:affiliation>Departmento de Bioquímica, Instituto de Biologia, Universidade Estadual de Campinas, SP, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Departmento de Bioquímica, Instituto de Biologia, Universidade Estadual de Campinas, SP</wicri:regionArea><placeName><region type="state">État de São Paulo</region></placeName></affiliation></author><author><name sortKey="Orsi, Cintia H" sort="Orsi, Cintia H" uniqKey="Orsi C" first="Cintia H" last="Orsi">Cintia H. Orsi</name></author><author><name sortKey="Oliveira, Jusceley F P" sort="Oliveira, Jusceley F P" uniqKey="Oliveira J" first="Jusceley F P" last="Oliveira">Jusceley F P. Oliveira</name></author><author><name sortKey="Pinto Maglio, Cecilia A F" sort="Pinto Maglio, Cecilia A F" uniqKey="Pinto Maglio C" first="Cecília A F" last="Pinto-Maglio">Cecília A F. Pinto-Maglio</name></author><author><name sortKey="Salgado, Ione" sort="Salgado, Ione" uniqKey="Salgado I" first="Ione" last="Salgado">Ione Salgado</name></author></analytic><series><title level="j">FEBS letters</title><idno type="ISSN">0014-5793</idno><imprint><date when="2002" type="published">2002</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (drug effects)</term><term>Cell Death (drug effects)</term><term>Cell Division (drug effects)</term><term>Cells, Cultured</term><term>Citrus (cytology)</term><term>Citrus (drug effects)</term><term>Citrus (metabolism)</term><term>Cyclosporine (pharmacology)</term><term>DNA Fragmentation</term><term>Intracellular Membranes (drug effects)</term><term>Intracellular Membranes (physiology)</term><term>Ion Channels</term><term>Membrane Potentials (drug effects)</term><term>Membrane Proteins (drug effects)</term><term>Membrane Proteins (metabolism)</term><term>Mitochondria (drug effects)</term><term>Mitochondria (metabolism)</term><term>Mitochondrial Membrane Transport Proteins</term><term>Nitric Oxide (toxicity)</term><term>Nitric Oxide Donors (toxicity)</term><term>Nitroprusside (toxicity)</term><term>S-Nitroso-N-Acetylpenicillamine (toxicity)</term><term>Signal Transduction (drug effects)</term><term>Signal Transduction (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Membrane Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Membrane Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Cyclosporine</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Citrus</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Cell Death</term><term>Cell Division</term><term>Citrus</term><term>Intracellular Membranes</term><term>Membrane Potentials</term><term>Mitochondria</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Citrus</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Intracellular Membranes</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Nitric Oxide</term><term>Nitric Oxide Donors</term><term>Nitroprusside</term><term>S-Nitroso-N-Acetylpenicillamine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cells, Cultured</term><term>DNA Fragmentation</term><term>Ion Channels</term><term>Mitochondrial Membrane Transport Proteins</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In the present study, we investigated the involvement of the mitochondrial permeability transition pore (PTP) in nitric oxide (NO)-induced plant cell death. NO donors such as sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine inhibited growth and caused death in suspension-cultured cells of Citrus sinensis. Cells treated with SNP showed chromatin condensation and fragmentation, characteristic of apoptosis. SNP caused loss of the mitochondrial membrane electrical potential, which was prevented by cyclosporin A (CsA), a specific inhibitor of PTP formation. CsA also prevented the nuclear apoptosis and subsequent Citrus cell death induced by NO. These findings indicate that mitochondrial PTP formation is involved in the signaling pathway by which NO induces apoptosis in cultured Citrus cells.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">11801241</PMID><DateCreated><Year>2002</Year><Month>1</Month><Day>21</Day></DateCreated><DateCompleted><Year>2002</Year><Month>02</Month><Day>05</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0014-5793</ISSN><JournalIssue CitedMedium="Print"><Volume>510</Volume><Issue>3</Issue><PubDate><Year>2002</Year><Month>Jan</Month><Day>16</Day></PubDate></JournalIssue><Title>FEBS letters</Title><ISOAbbreviation>FEBS Lett.</ISOAbbreviation></Journal><ArticleTitle>Participation of the mitochondrial permeability transition pore in nitric oxide-induced plant cell death.</ArticleTitle><Pagination><MedlinePgn>136-40</MedlinePgn></Pagination><Abstract><AbstractText>In the present study, we investigated the involvement of the mitochondrial permeability transition pore (PTP) in nitric oxide (NO)-induced plant cell death. NO donors such as sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine inhibited growth and caused death in suspension-cultured cells of Citrus sinensis. Cells treated with SNP showed chromatin condensation and fragmentation, characteristic of apoptosis. SNP caused loss of the mitochondrial membrane electrical potential, which was prevented by cyclosporin A (CsA), a specific inhibitor of PTP formation. CsA also prevented the nuclear apoptosis and subsequent Citrus cell death induced by NO. These findings indicate that mitochondrial PTP formation is involved in the signaling pathway by which NO induces apoptosis in cultured Citrus cells.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Saviani</LastName><ForeName>Elzira E</ForeName><Initials>EE</Initials><AffiliationInfo><Affiliation>Departmento de Bioquímica, Instituto de Biologia, Universidade Estadual de Campinas, SP, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Orsi</LastName><ForeName>Cintia H</ForeName><Initials>CH</Initials></Author><Author ValidYN="Y"><LastName>Oliveira</LastName><ForeName>Jusceley F P</ForeName><Initials>JF</Initials></Author><Author ValidYN="Y"><LastName>Pinto-Maglio</LastName><ForeName>Cecília A F</ForeName><Initials>CA</Initials></Author><Author ValidYN="Y"><LastName>Salgado</LastName><ForeName>Ione</ForeName><Initials>I</Initials></Author></AuthorList><Language>ENG</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>FEBS Lett</MedlineTA><NlmUniqueID>0155157</NlmUniqueID><ISSNLinking>0014-5793</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007473">Ion Channels</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008565">Membrane Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D033681">Mitochondrial Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020030">Nitric Oxide Donors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C120771">mitochondrial permeability transition pore</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>79032-48-7</RegistryNumber><NameOfSubstance UI="D026423">S-Nitroso-N-Acetylpenicillamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>83HN0GTJ6D</RegistryNumber><NameOfSubstance UI="D016572">Cyclosporine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016923" MajorTopicYN="N">Cell Death</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002455" MajorTopicYN="N">Cell Division</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002957" MajorTopicYN="N">Citrus</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016572" MajorTopicYN="N">Cyclosporine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053938" MajorTopicYN="N">DNA Fragmentation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007425" MajorTopicYN="N">Intracellular Membranes</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug 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Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009569" MajorTopicYN="N">Nitric Oxide</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020030" MajorTopicYN="N">Nitric Oxide Donors</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009599" MajorTopicYN="N">Nitroprusside</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D026423" MajorTopicYN="N">S-Nitroso-N-Acetylpenicillamine</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="N">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2002</Year><Month>1</Month><Day>22</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2002</Year><Month>2</Month><Day>6</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2002</Year><Month>1</Month><Day>22</Day><Hour>10</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">11801241</ArticleId><ArticleId IdType="pii">S0014579301032306</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Brésil</li></country><region><li>État de São Paulo</li></region></list><tree><noCountry><name sortKey="Oliveira, Jusceley F P" sort="Oliveira, Jusceley F P" uniqKey="Oliveira J" first="Jusceley F P" last="Oliveira">Jusceley F P. Oliveira</name><name sortKey="Orsi, Cintia H" sort="Orsi, Cintia H" uniqKey="Orsi C" first="Cintia H" last="Orsi">Cintia H. Orsi</name><name sortKey="Pinto Maglio, Cecilia A F" sort="Pinto Maglio, Cecilia A F" uniqKey="Pinto Maglio C" first="Cecília A F" last="Pinto-Maglio">Cecília A F. Pinto-Maglio</name><name sortKey="Salgado, Ione" sort="Salgado, Ione" uniqKey="Salgado I" first="Ione" last="Salgado">Ione Salgado</name></noCountry><country name="Brésil"><region name="État de São Paulo"><name sortKey="Saviani, Elzira E" sort="Saviani, Elzira E" uniqKey="Saviani E" first="Elzira E" last="Saviani">Elzira E. Saviani</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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