Metabolic changes associated with acid-base regulation during hypercarbia in the CO2-tolerant chondrostean, white sturgeon (Acipenser transmontanus).
Identifieur interne : 000326 ( PubMed/Corpus ); précédent : 000325; suivant : 000327Metabolic changes associated with acid-base regulation during hypercarbia in the CO2-tolerant chondrostean, white sturgeon (Acipenser transmontanus).
Auteurs : Daniel W. Baker ; Colin J. BraunerSource :
- Comparative biochemistry and physiology. Part A, Molecular & integrative physiology [ 1531-4332 ] ; 2012.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Carbon Dioxide.
- metabolism : Fishes, Liver, Muscle, Skeletal.
- Acid-Base Equilibrium, Animals, Hydrogen-Ion Concentration, Oxygen Consumption.
Abstract
CO(2) tolerance in white sturgeon is associated with the ability to tightly regulate intracellular pH (pHi) despite a large reduction in extracellular pH (pHe) termed preferential pHi regulation. How this regulatory response affects whole animal metabolic rate is unknown. Accordingly, we characterized oxygen consumption rate ( [Formula: see text] ) and metabolically-relevant organismal and cellular responses in white sturgeon during exposure to hypercarbia. White sturgeon were able to protect intracellular pH (pHi) in liver and white muscle as early as 6h (the earliest time period investigated) following exposure to severe (sub-lethal) hypercarbia (45 and 90 mm Hg PCO(2)). Sturgeon exposed to 15 and 30 mm Hg PCO(2) exhibited pHe compensation and significant increases in [Formula: see text] (up to 80% greater than control values). In contrast, severe hypercarbia (≥45 mm Hg PCO(2)) elicited an uncompensated reduction in pHe (up to ~1.0 pH units) and red blood cells (as great as ~0.5 pH units), and was accompanied by 30 and 60% reductions in [Formula: see text] , respectively. While behavioral, respiratory and cellular responses to hypercarbia were observed, none corresponded well with the pattern or magnitude of changes in [Formula: see text] . The findings of this research provide empirical support for the hypothesis that preferential pHi regulation is not metabolically costly, and thus may have been a strategy strongly selected for in fishes encountering short-term hypercarbia.
DOI: 10.1016/j.cbpa.2011.09.002
PubMed: 21945112
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pubmed:21945112Le document en format XML
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Brauner</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2012">2012</date><idno type="RBID">pubmed:21945112</idno><idno type="pmid">21945112</idno><idno type="doi">10.1016/j.cbpa.2011.09.002</idno><idno type="wicri:Area/PubMed/Corpus">000326</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000326</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Metabolic changes associated with acid-base regulation during hypercarbia in the CO2-tolerant chondrostean, white sturgeon (Acipenser transmontanus).</title><author><name sortKey="Baker, Daniel W" sort="Baker, Daniel W" uniqKey="Baker D" first="Daniel W" last="Baker">Daniel W. Baker</name><affiliation><nlm:affiliation>Department of Zoology, University of British Columbia, Vancouver, B.C., Canada. dan.baker@auckland.ac.nz</nlm:affiliation></affiliation></author><author><name sortKey="Brauner, Colin J" sort="Brauner, Colin J" uniqKey="Brauner C" first="Colin J" last="Brauner">Colin J. Brauner</name></author></analytic><series><title level="j">Comparative biochemistry and physiology. Part A, Molecular & integrative physiology</title><idno type="eISSN">1531-4332</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acid-Base Equilibrium</term><term>Animals</term><term>Carbon Dioxide (metabolism)</term><term>Fishes (metabolism)</term><term>Hydrogen-Ion Concentration</term><term>Liver (metabolism)</term><term>Muscle, Skeletal (metabolism)</term><term>Oxygen Consumption</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carbon Dioxide</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Fishes</term><term>Liver</term><term>Muscle, Skeletal</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Acid-Base Equilibrium</term><term>Animals</term><term>Hydrogen-Ion Concentration</term><term>Oxygen Consumption</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">CO(2) tolerance in white sturgeon is associated with the ability to tightly regulate intracellular pH (pHi) despite a large reduction in extracellular pH (pHe) termed preferential pHi regulation. How this regulatory response affects whole animal metabolic rate is unknown. Accordingly, we characterized oxygen consumption rate ( [Formula: see text] ) and metabolically-relevant organismal and cellular responses in white sturgeon during exposure to hypercarbia. White sturgeon were able to protect intracellular pH (pHi) in liver and white muscle as early as 6h (the earliest time period investigated) following exposure to severe (sub-lethal) hypercarbia (45 and 90 mm Hg PCO(2)). Sturgeon exposed to 15 and 30 mm Hg PCO(2) exhibited pHe compensation and significant increases in [Formula: see text] (up to 80% greater than control values). In contrast, severe hypercarbia (≥45 mm Hg PCO(2)) elicited an uncompensated reduction in pHe (up to ~1.0 pH units) and red blood cells (as great as ~0.5 pH units), and was accompanied by 30 and 60% reductions in [Formula: see text] , respectively. While behavioral, respiratory and cellular responses to hypercarbia were observed, none corresponded well with the pattern or magnitude of changes in [Formula: see text] . The findings of this research provide empirical support for the hypothesis that preferential pHi regulation is not metabolically costly, and thus may have been a strategy strongly selected for in fishes encountering short-term hypercarbia.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21945112</PMID><DateCreated><Year>2011</Year><Month>11</Month><Day>21</Day></DateCreated><DateCompleted><Year>2012</Year><Month>03</Month><Day>15</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-4332</ISSN><JournalIssue CitedMedium="Internet"><Volume>161</Volume><Issue>1</Issue><PubDate><Year>2012</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Comparative biochemistry and physiology. Part A, Molecular & integrative physiology</Title><ISOAbbreviation>Comp. Biochem. Physiol., Part A Mol. Integr. Physiol.</ISOAbbreviation></Journal><ArticleTitle>Metabolic changes associated with acid-base regulation during hypercarbia in the CO2-tolerant chondrostean, white sturgeon (Acipenser transmontanus).</ArticleTitle><Pagination><MedlinePgn>61-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.cbpa.2011.09.002</ELocationID><Abstract><AbstractText>CO(2) tolerance in white sturgeon is associated with the ability to tightly regulate intracellular pH (pHi) despite a large reduction in extracellular pH (pHe) termed preferential pHi regulation. How this regulatory response affects whole animal metabolic rate is unknown. Accordingly, we characterized oxygen consumption rate ( [Formula: see text] ) and metabolically-relevant organismal and cellular responses in white sturgeon during exposure to hypercarbia. White sturgeon were able to protect intracellular pH (pHi) in liver and white muscle as early as 6h (the earliest time period investigated) following exposure to severe (sub-lethal) hypercarbia (45 and 90 mm Hg PCO(2)). Sturgeon exposed to 15 and 30 mm Hg PCO(2) exhibited pHe compensation and significant increases in [Formula: see text] (up to 80% greater than control values). In contrast, severe hypercarbia (≥45 mm Hg PCO(2)) elicited an uncompensated reduction in pHe (up to ~1.0 pH units) and red blood cells (as great as ~0.5 pH units), and was accompanied by 30 and 60% reductions in [Formula: see text] , respectively. While behavioral, respiratory and cellular responses to hypercarbia were observed, none corresponded well with the pattern or magnitude of changes in [Formula: see text] . The findings of this research provide empirical support for the hypothesis that preferential pHi regulation is not metabolically costly, and thus may have been a strategy strongly selected for in fishes encountering short-term hypercarbia.</AbstractText><CopyrightInformation>Copyright © 2011 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Baker</LastName><ForeName>Daniel W</ForeName><Initials>DW</Initials><AffiliationInfo><Affiliation>Department of Zoology, University of British Columbia, Vancouver, B.C., Canada. dan.baker@auckland.ac.nz</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brauner</LastName><ForeName>Colin J</ForeName><Initials>CJ</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><ArticleDate DateType="Electronic"><Year>2011</Year><Month>09</Month><Day>16</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Comp Biochem Physiol A Mol Integr Physiol</MedlineTA><NlmUniqueID>9806096</NlmUniqueID><ISSNLinking>1095-6433</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>142M471B3J</RegistryNumber><NameOfSubstance UI="D002245">Carbon Dioxide</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000136" MajorTopicYN="Y">Acid-Base Equilibrium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002245" MajorTopicYN="N">Carbon Dioxide</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005399" MajorTopicYN="N">Fishes</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006863" MajorTopicYN="N">Hydrogen-Ion Concentration</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008099" MajorTopicYN="N">Liver</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018482" MajorTopicYN="N">Muscle, Skeletal</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010101" MajorTopicYN="N">Oxygen Consumption</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2011</Year><Month>07</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2011</Year><Month>09</Month><Day>08</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2011</Year><Month>09</Month><Day>08</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>9</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>9</Month><Day>29</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>3</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">21945112</ArticleId><ArticleId IdType="pii">S1095-6433(11)00266-2</ArticleId><ArticleId IdType="doi">10.1016/j.cbpa.2011.09.002</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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