Serveur d'exploration sur la mycorhize

Attention, ce site est en cours de développement !
Attention, site généré par des moyens informatiques à partir de corpus bruts.
Les informations ne sont donc pas validées.

Plant responses to abiotic stresses: heavy metal-induced oxidative stress and protection by mycorrhization.

Identifieur interne : 003A61 ( Main/Corpus ); précédent : 003A60; suivant : 003A62

Plant responses to abiotic stresses: heavy metal-induced oxidative stress and protection by mycorrhization.

Auteurs : Andres Schützendübel ; Andrea Polle

Source :

RBID : pubmed:11997381

English descriptors

Abstract

The aim of this review is to assess the mode of action and role of antioxidants as protection from heavy metal stress in roots, mycorrhizal fungi and mycorrhizae. Based on their chemical and physical properties three different molecular mechanisms of heavy metal toxicity can be distinguished: (a) production of reactive oxygen species by autoxidation and Fenton reaction; this reaction is typical for transition metals such as iron or copper, (b) blocking of essential functional groups in biomolecules, this reaction has mainly been reported for non-redox-reactive heavy metals such as cadmium and mercury, (c) displacement of essential metal ions from biomolecules; the latter reaction occurs with different kinds of heavy metals. Transition metals cause oxidative injury in plant tissue, but a literature survey did not provide evidence that this stress could be alleviated by increased levels of antioxidative systems. The reason may be that transition metals initiate hydroxyl radical production, which can not be controlled by antioxidants. Exposure of plants to non-redox reactive metals also resulted in oxidative stress as indicated by lipid peroxidation, H(2)O(2) accumulation, and an oxidative burst. Cadmium and some other metals caused a transient depletion of GSH and an inhibition of antioxidative enzymes, especially of glutathione reductase. Assessment of antioxidative capacities by metabolic modelling suggested that the reported diminution of antioxidants was sufficient to cause H(2)O(2) accumulation. The depletion of GSH is apparently a critical step in cadmium sensitivity since plants with improved capacities for GSH synthesis displayed higher Cd tolerance. Available data suggest that cadmium, when not detoxified rapidly enough, may trigger, via the disturbance of the redox control of the cell, a sequence of reactions leading to growth inhibition, stimulation of secondary metabolism, lignification, and finally cell death. This view is in contrast to the idea that cadmium results in unspecific necrosis. Plants in certain mycorrhizal associations are less sensitive to cadmium stress than non-mycorrhizal plants. Data about antioxidative systems in mycorrhizal fungi in pure culture and in symbiosis are scarce. The present results indicate that mycorrhization stimulated the phenolic defence system in the Paxillus-Pinus mycorrhizal symbiosis. Cadmium-induced changes in mycorrhizal roots were absent or smaller than those in non-mycorrhizal roots. These observations suggest that although changes in rhizospheric conditions were perceived by the root part of the symbiosis, the typical Cd-induced stress responses of phenolics were buffered. It is not known whether mycorrhization protected roots from Cd-induced injury by preventing access of cadmium to sensitive extra- or intracellular sites, or by excreted or intrinsic metal-chelators, or by other defence systems. It is possible that mycorrhizal fungi provide protection via GSH since higher concentrations of this thiol were found in pure cultures of the fungi than in bare roots. The development of stress-tolerant plant-mycorrhizal associations may be a promising new strategy for phytoremediation and soil amelioration measures.

PubMed: 11997381

Links to Exploration step

pubmed:11997381

Le document en format XML

<record>
<TEI>
<teiHeader>
<fileDesc>
<titleStmt>
<title xml:lang="en">Plant responses to abiotic stresses: heavy metal-induced oxidative stress and protection by mycorrhization.</title>
<author>
<name sortKey="Schutzendubel, Andres" sort="Schutzendubel, Andres" uniqKey="Schutzendubel A" first="Andres" last="Schützendübel">Andres Schützendübel</name>
<affiliation>
<nlm:affiliation>Forstbotanisches Institut, Abteilung I, Forstbotanik und Baumphysiologie, Georg August Universität Göttingen, Büsgenweg 2, 37077 Göttingen, Germany.</nlm:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Polle, Andrea" sort="Polle, Andrea" uniqKey="Polle A" first="Andrea" last="Polle">Andrea Polle</name>
</author>
</titleStmt>
<publicationStmt>
<idno type="wicri:source">PubMed</idno>
<date when="2002">2002</date>
<idno type="RBID">pubmed:11997381</idno>
<idno type="pmid">11997381</idno>
<idno type="wicri:Area/Main/Corpus">003A61</idno>
<idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">003A61</idno>
</publicationStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title xml:lang="en">Plant responses to abiotic stresses: heavy metal-induced oxidative stress and protection by mycorrhization.</title>
<author>
<name sortKey="Schutzendubel, Andres" sort="Schutzendubel, Andres" uniqKey="Schutzendubel A" first="Andres" last="Schützendübel">Andres Schützendübel</name>
<affiliation>
<nlm:affiliation>Forstbotanisches Institut, Abteilung I, Forstbotanik und Baumphysiologie, Georg August Universität Göttingen, Büsgenweg 2, 37077 Göttingen, Germany.</nlm:affiliation>
</affiliation>
</author>
<author>
<name sortKey="Polle, Andrea" sort="Polle, Andrea" uniqKey="Polle A" first="Andrea" last="Polle">Andrea Polle</name>
</author>
</analytic>
<series>
<title level="j">Journal of experimental botany</title>
<idno type="ISSN">0022-0957</idno>
<imprint>
<date when="2002" type="published">2002</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Antioxidants (metabolism)</term>
<term>Ascorbate Peroxidases (MeSH)</term>
<term>Cadmium (chemistry)</term>
<term>Cadmium (metabolism)</term>
<term>Cadmium (pharmacology)</term>
<term>Catalase (metabolism)</term>
<term>Fungi (growth & development)</term>
<term>Glutathione Reductase (metabolism)</term>
<term>Hydrogen Peroxide (metabolism)</term>
<term>Metals, Heavy (chemistry)</term>
<term>Metals, Heavy (metabolism)</term>
<term>Metals, Heavy (pharmacology)</term>
<term>Models, Biological (MeSH)</term>
<term>Oxidative Stress (physiology)</term>
<term>Peroxidases (metabolism)</term>
<term>Plant Leaves (drug effects)</term>
<term>Plant Leaves (metabolism)</term>
<term>Plant Roots (drug effects)</term>
<term>Plant Roots (metabolism)</term>
<term>Plant Roots (microbiology)</term>
<term>Plant Shoots (drug effects)</term>
<term>Plant Shoots (metabolism)</term>
<term>Plants (drug effects)</term>
<term>Plants (metabolism)</term>
<term>Plants (microbiology)</term>
<term>Signal Transduction (MeSH)</term>
<term>Soil Microbiology (MeSH)</term>
<term>Stress, Mechanical (MeSH)</term>
<term>Superoxide Dismutase (metabolism)</term>
<term>Symbiosis (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en">
<term>Cadmium</term>
<term>Metals, Heavy</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en">
<term>Antioxidants</term>
<term>Cadmium</term>
<term>Catalase</term>
<term>Glutathione Reductase</term>
<term>Hydrogen Peroxide</term>
<term>Metals, Heavy</term>
<term>Peroxidases</term>
<term>Superoxide Dismutase</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en">
<term>Cadmium</term>
<term>Metals, Heavy</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en">
<term>Ascorbate Peroxidases</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en">
<term>Plant Leaves</term>
<term>Plant Roots</term>
<term>Plant Shoots</term>
<term>Plants</term>
</keywords>
<keywords scheme="MESH" qualifier="growth & development" xml:lang="en">
<term>Fungi</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en">
<term>Plant Leaves</term>
<term>Plant Roots</term>
<term>Plant Shoots</term>
<term>Plants</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en">
<term>Plant Roots</term>
<term>Plants</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en">
<term>Oxidative Stress</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Models, Biological</term>
<term>Signal Transduction</term>
<term>Soil Microbiology</term>
<term>Stress, Mechanical</term>
<term>Symbiosis</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">The aim of this review is to assess the mode of action and role of antioxidants as protection from heavy metal stress in roots, mycorrhizal fungi and mycorrhizae. Based on their chemical and physical properties three different molecular mechanisms of heavy metal toxicity can be distinguished: (a) production of reactive oxygen species by autoxidation and Fenton reaction; this reaction is typical for transition metals such as iron or copper, (b) blocking of essential functional groups in biomolecules, this reaction has mainly been reported for non-redox-reactive heavy metals such as cadmium and mercury, (c) displacement of essential metal ions from biomolecules; the latter reaction occurs with different kinds of heavy metals. Transition metals cause oxidative injury in plant tissue, but a literature survey did not provide evidence that this stress could be alleviated by increased levels of antioxidative systems. The reason may be that transition metals initiate hydroxyl radical production, which can not be controlled by antioxidants. Exposure of plants to non-redox reactive metals also resulted in oxidative stress as indicated by lipid peroxidation, H(2)O(2) accumulation, and an oxidative burst. Cadmium and some other metals caused a transient depletion of GSH and an inhibition of antioxidative enzymes, especially of glutathione reductase. Assessment of antioxidative capacities by metabolic modelling suggested that the reported diminution of antioxidants was sufficient to cause H(2)O(2) accumulation. The depletion of GSH is apparently a critical step in cadmium sensitivity since plants with improved capacities for GSH synthesis displayed higher Cd tolerance. Available data suggest that cadmium, when not detoxified rapidly enough, may trigger, via the disturbance of the redox control of the cell, a sequence of reactions leading to growth inhibition, stimulation of secondary metabolism, lignification, and finally cell death. This view is in contrast to the idea that cadmium results in unspecific necrosis. Plants in certain mycorrhizal associations are less sensitive to cadmium stress than non-mycorrhizal plants. Data about antioxidative systems in mycorrhizal fungi in pure culture and in symbiosis are scarce. The present results indicate that mycorrhization stimulated the phenolic defence system in the Paxillus-Pinus mycorrhizal symbiosis. Cadmium-induced changes in mycorrhizal roots were absent or smaller than those in non-mycorrhizal roots. These observations suggest that although changes in rhizospheric conditions were perceived by the root part of the symbiosis, the typical Cd-induced stress responses of phenolics were buffered. It is not known whether mycorrhization protected roots from Cd-induced injury by preventing access of cadmium to sensitive extra- or intracellular sites, or by excreted or intrinsic metal-chelators, or by other defence systems. It is possible that mycorrhizal fungi provide protection via GSH since higher concentrations of this thiol were found in pure cultures of the fungi than in bare roots. The development of stress-tolerant plant-mycorrhizal associations may be a promising new strategy for phytoremediation and soil amelioration measures.</div>
</front>
</TEI>
<pubmed>
<MedlineCitation Status="MEDLINE" Owner="NLM">
<PMID Version="1">11997381</PMID>
<DateCompleted>
<Year>2002</Year>
<Month>07</Month>
<Day>19</Day>
</DateCompleted>
<DateRevised>
<Year>2013</Year>
<Month>11</Month>
<Day>21</Day>
</DateRevised>
<Article PubModel="Print">
<Journal>
<ISSN IssnType="Print">0022-0957</ISSN>
<JournalIssue CitedMedium="Print">
<Volume>53</Volume>
<Issue>372</Issue>
<PubDate>
<Year>2002</Year>
<Month>May</Month>
</PubDate>
</JournalIssue>
<Title>Journal of experimental botany</Title>
<ISOAbbreviation>J Exp Bot</ISOAbbreviation>
</Journal>
<ArticleTitle>Plant responses to abiotic stresses: heavy metal-induced oxidative stress and protection by mycorrhization.</ArticleTitle>
<Pagination>
<MedlinePgn>1351-65</MedlinePgn>
</Pagination>
<Abstract>
<AbstractText>The aim of this review is to assess the mode of action and role of antioxidants as protection from heavy metal stress in roots, mycorrhizal fungi and mycorrhizae. Based on their chemical and physical properties three different molecular mechanisms of heavy metal toxicity can be distinguished: (a) production of reactive oxygen species by autoxidation and Fenton reaction; this reaction is typical for transition metals such as iron or copper, (b) blocking of essential functional groups in biomolecules, this reaction has mainly been reported for non-redox-reactive heavy metals such as cadmium and mercury, (c) displacement of essential metal ions from biomolecules; the latter reaction occurs with different kinds of heavy metals. Transition metals cause oxidative injury in plant tissue, but a literature survey did not provide evidence that this stress could be alleviated by increased levels of antioxidative systems. The reason may be that transition metals initiate hydroxyl radical production, which can not be controlled by antioxidants. Exposure of plants to non-redox reactive metals also resulted in oxidative stress as indicated by lipid peroxidation, H(2)O(2) accumulation, and an oxidative burst. Cadmium and some other metals caused a transient depletion of GSH and an inhibition of antioxidative enzymes, especially of glutathione reductase. Assessment of antioxidative capacities by metabolic modelling suggested that the reported diminution of antioxidants was sufficient to cause H(2)O(2) accumulation. The depletion of GSH is apparently a critical step in cadmium sensitivity since plants with improved capacities for GSH synthesis displayed higher Cd tolerance. Available data suggest that cadmium, when not detoxified rapidly enough, may trigger, via the disturbance of the redox control of the cell, a sequence of reactions leading to growth inhibition, stimulation of secondary metabolism, lignification, and finally cell death. This view is in contrast to the idea that cadmium results in unspecific necrosis. Plants in certain mycorrhizal associations are less sensitive to cadmium stress than non-mycorrhizal plants. Data about antioxidative systems in mycorrhizal fungi in pure culture and in symbiosis are scarce. The present results indicate that mycorrhization stimulated the phenolic defence system in the Paxillus-Pinus mycorrhizal symbiosis. Cadmium-induced changes in mycorrhizal roots were absent or smaller than those in non-mycorrhizal roots. These observations suggest that although changes in rhizospheric conditions were perceived by the root part of the symbiosis, the typical Cd-induced stress responses of phenolics were buffered. It is not known whether mycorrhization protected roots from Cd-induced injury by preventing access of cadmium to sensitive extra- or intracellular sites, or by excreted or intrinsic metal-chelators, or by other defence systems. It is possible that mycorrhizal fungi provide protection via GSH since higher concentrations of this thiol were found in pure cultures of the fungi than in bare roots. The development of stress-tolerant plant-mycorrhizal associations may be a promising new strategy for phytoremediation and soil amelioration measures.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y">
<Author ValidYN="Y">
<LastName>Schützendübel</LastName>
<ForeName>Andres</ForeName>
<Initials>A</Initials>
<AffiliationInfo>
<Affiliation>Forstbotanisches Institut, Abteilung I, Forstbotanik und Baumphysiologie, Georg August Universität Göttingen, Büsgenweg 2, 37077 Göttingen, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Polle</LastName>
<ForeName>Andrea</ForeName>
<Initials>A</Initials>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList>
<PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
<PublicationType UI="D016454">Review</PublicationType>
</PublicationTypeList>
</Article>
<MedlineJournalInfo>
<Country>England</Country>
<MedlineTA>J Exp Bot</MedlineTA>
<NlmUniqueID>9882906</NlmUniqueID>
<ISSNLinking>0022-0957</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList>
<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000975">Antioxidants</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D019216">Metals, Heavy</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>00BH33GNGH</RegistryNumber>
<NameOfSubstance UI="D002104">Cadmium</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>BBX060AN9V</RegistryNumber>
<NameOfSubstance UI="D006861">Hydrogen Peroxide</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>EC 1.11.1.-</RegistryNumber>
<NameOfSubstance UI="D010544">Peroxidases</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>EC 1.11.1.11</RegistryNumber>
<NameOfSubstance UI="D060387">Ascorbate Peroxidases</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>EC 1.11.1.6</RegistryNumber>
<NameOfSubstance UI="D002374">Catalase</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>EC 1.15.1.1</RegistryNumber>
<NameOfSubstance UI="D013482">Superoxide Dismutase</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>EC 1.8.1.7</RegistryNumber>
<NameOfSubstance UI="D005980">Glutathione Reductase</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList>
<MeshHeading>
<DescriptorName UI="D000975" MajorTopicYN="N">Antioxidants</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D060387" MajorTopicYN="N">Ascorbate Peroxidases</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D002104" MajorTopicYN="N">Cadmium</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D002374" MajorTopicYN="N">Catalase</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D005658" MajorTopicYN="N">Fungi</DescriptorName>
<QualifierName UI="Q000254" MajorTopicYN="Y">growth & development</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D005980" MajorTopicYN="N">Glutathione Reductase</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="D019216" MajorTopicYN="N">Metals, Heavy</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D008954" MajorTopicYN="N">Models, Biological</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D010544" MajorTopicYN="N">Peroxidases</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D018515" MajorTopicYN="N">Plant Leaves</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D018517" MajorTopicYN="N">Plant Roots</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D018520" MajorTopicYN="N">Plant Shoots</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D010944" MajorTopicYN="N">Plants</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D012988" MajorTopicYN="N">Soil Microbiology</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D013314" MajorTopicYN="N">Stress, Mechanical</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D013482" MajorTopicYN="N">Superoxide Dismutase</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D013559" MajorTopicYN="N">Symbiosis</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<NumberOfReferences>114</NumberOfReferences>
</MedlineCitation>
<PubmedData>
<History>
<PubMedPubDate PubStatus="pubmed">
<Year>2002</Year>
<Month>5</Month>
<Day>9</Day>
<Hour>10</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline">
<Year>2002</Year>
<Month>7</Month>
<Day>20</Day>
<Hour>10</Hour>
<Minute>1</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez">
<Year>2002</Year>
<Month>5</Month>
<Day>9</Day>
<Hour>10</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList>
<ArticleId IdType="pubmed">11997381</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Bois/explor/MycorrhizaeV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 003A61 | SxmlIndent | more

Ou

HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 003A61 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Bois
   |area=    MycorrhizaeV1
   |flux=    Main
   |étape=   Corpus
   |type=    RBID
   |clé=     pubmed:11997381
   |texte=   Plant responses to abiotic stresses: heavy metal-induced oxidative stress and protection by mycorrhization.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Corpus/RBID.i   -Sk "pubmed:11997381" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd   \
       | NlmPubMed2Wicri -a MycorrhizaeV1 

Wicri

This area was generated with Dilib version V0.6.37.
Data generation: Wed Nov 18 15:34:48 2020. Site generation: Wed Nov 18 15:41:10 2020