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Physiological response in the European flounder (Platichthys flesus) to variable salinity and oxygen conditions
Physiological mechanisms involved in acclimation to variable salinity and oxygen levels and their interaction were studied in European flounder. The fish were acclimated for 2 weeks to freshwater (1[per thousand] salinity), brackish water (11[per thousand]) or full strength seawater (35[per thousand...
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Published in: | Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology Biochemical, systemic, and environmental physiology, 2008-09, Vol.178 (7), p.909-915 |
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creator | Lundgreen, Kim Kiilerich, Pia Tipsmark, Christian K Madsen, Steffen S Jensen, Frank B |
description | Physiological mechanisms involved in acclimation to variable salinity and oxygen levels and their interaction were studied in European flounder. The fish were acclimated for 2 weeks to freshwater (1[per thousand] salinity), brackish water (11[per thousand]) or full strength seawater (35[per thousand]) under normoxic conditions (water Po₂ = 158 mmHg) and then subjected to 48 h of continued normoxia or hypoxia at a level (Po₂ = 54 mmHg) close to but above the critical Po₂. Plasma osmolality, [Na⁺] and [Cl⁻] increased with increasing salinity, but the rises were limited, reflecting an effective extracellular osmoregulation. Muscle water content was the same at all three salinities, indicating complete cell volume regulation. Gill Na⁺/K⁺-ATPase activity did not change with salinity, but hypoxia caused a 25% decrease in branchial Na⁺/K⁺-ATPase activity at all three salinities. Furthermore, hypoxia induced a significant decrease in mRNA levels of the Na⁺/K⁺-ATPase α1-subunit, signifying a reduced expression of the transporter gene. The reduced ATPase activity did not influence extracellular ionic concentrations. Blood [Hb] was stable with salinity, and it was not increased by hypoxia. Instead, hypoxia decreased the erythrocytic nucleoside triphosphate content, a common mechanism for increasing blood O₂ affinity. It is concluded that moderate hypoxia induced an energy saving decrease in branchial Na⁺/K⁺-ATPase activity, which did not compromise extracellular osmoregulation. |
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The fish were acclimated for 2 weeks to freshwater (1[per thousand] salinity), brackish water (11[per thousand]) or full strength seawater (35[per thousand]) under normoxic conditions (water Po₂ = 158 mmHg) and then subjected to 48 h of continued normoxia or hypoxia at a level (Po₂ = 54 mmHg) close to but above the critical Po₂. Plasma osmolality, [Na⁺] and [Cl⁻] increased with increasing salinity, but the rises were limited, reflecting an effective extracellular osmoregulation. Muscle water content was the same at all three salinities, indicating complete cell volume regulation. Gill Na⁺/K⁺-ATPase activity did not change with salinity, but hypoxia caused a 25% decrease in branchial Na⁺/K⁺-ATPase activity at all three salinities. Furthermore, hypoxia induced a significant decrease in mRNA levels of the Na⁺/K⁺-ATPase α1-subunit, signifying a reduced expression of the transporter gene. The reduced ATPase activity did not influence extracellular ionic concentrations. Blood [Hb] was stable with salinity, and it was not increased by hypoxia. Instead, hypoxia decreased the erythrocytic nucleoside triphosphate content, a common mechanism for increasing blood O₂ affinity. It is concluded that moderate hypoxia induced an energy saving decrease in branchial Na⁺/K⁺-ATPase activity, which did not compromise extracellular osmoregulation.</description><identifier>ISSN: 0174-1578</identifier><identifier>EISSN: 1432-136X</identifier><identifier>DOI: 10.1007/s00360-008-0281-9</identifier><identifier>PMID: 18536922</identifier><language>eng</language><publisher>Berlin/Heidelberg: Berlin/Heidelberg : Springer-Verlag</publisher><subject>Acclimatization ; Animal Physiology ; Animals ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Blood ; Brackish water ; Energy conservation ; Flounder - physiology ; Gills - enzymology ; Homeostasis ; Human Physiology ; Hypotheses ; Hypoxia ; Hypoxia - physiopathology ; Life Sciences ; Marine ; Original Paper ; Osmoregulation ; Oxygen - metabolism ; Physiology ; Platichthys flesus ; Salinity ; Seawater ; Sodium-Potassium-Exchanging ATPase - metabolism ; Water content ; Water-Electrolyte Balance - physiology ; Zoology</subject><ispartof>Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology, 2008-09, Vol.178 (7), p.909-915</ispartof><rights>Springer-Verlag 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c425t-da64d2b752c4cfc8262d7a9edecfeabe59b215cf49132ad725bf69b261cf220f3</citedby><cites>FETCH-LOGICAL-c425t-da64d2b752c4cfc8262d7a9edecfeabe59b215cf49132ad725bf69b261cf220f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18536922$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lundgreen, Kim</creatorcontrib><creatorcontrib>Kiilerich, Pia</creatorcontrib><creatorcontrib>Tipsmark, Christian K</creatorcontrib><creatorcontrib>Madsen, Steffen S</creatorcontrib><creatorcontrib>Jensen, Frank B</creatorcontrib><title>Physiological response in the European flounder (Platichthys flesus) to variable salinity and oxygen conditions</title><title>Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology</title><addtitle>J Comp Physiol B</addtitle><addtitle>J Comp Physiol B</addtitle><description>Physiological mechanisms involved in acclimation to variable salinity and oxygen levels and their interaction were studied in European flounder. The fish were acclimated for 2 weeks to freshwater (1[per thousand] salinity), brackish water (11[per thousand]) or full strength seawater (35[per thousand]) under normoxic conditions (water Po₂ = 158 mmHg) and then subjected to 48 h of continued normoxia or hypoxia at a level (Po₂ = 54 mmHg) close to but above the critical Po₂. Plasma osmolality, [Na⁺] and [Cl⁻] increased with increasing salinity, but the rises were limited, reflecting an effective extracellular osmoregulation. Muscle water content was the same at all three salinities, indicating complete cell volume regulation. Gill Na⁺/K⁺-ATPase activity did not change with salinity, but hypoxia caused a 25% decrease in branchial Na⁺/K⁺-ATPase activity at all three salinities. Furthermore, hypoxia induced a significant decrease in mRNA levels of the Na⁺/K⁺-ATPase α1-subunit, signifying a reduced expression of the transporter gene. The reduced ATPase activity did not influence extracellular ionic concentrations. Blood [Hb] was stable with salinity, and it was not increased by hypoxia. Instead, hypoxia decreased the erythrocytic nucleoside triphosphate content, a common mechanism for increasing blood O₂ affinity. It is concluded that moderate hypoxia induced an energy saving decrease in branchial Na⁺/K⁺-ATPase activity, which did not compromise extracellular osmoregulation.</description><subject>Acclimatization</subject><subject>Animal Physiology</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Blood</subject><subject>Brackish water</subject><subject>Energy conservation</subject><subject>Flounder - physiology</subject><subject>Gills - enzymology</subject><subject>Homeostasis</subject><subject>Human Physiology</subject><subject>Hypotheses</subject><subject>Hypoxia</subject><subject>Hypoxia - physiopathology</subject><subject>Life Sciences</subject><subject>Marine</subject><subject>Original Paper</subject><subject>Osmoregulation</subject><subject>Oxygen - metabolism</subject><subject>Physiology</subject><subject>Platichthys flesus</subject><subject>Salinity</subject><subject>Seawater</subject><subject>Sodium-Potassium-Exchanging ATPase - metabolism</subject><subject>Water content</subject><subject>Water-Electrolyte Balance - physiology</subject><subject>Zoology</subject><issn>0174-1578</issn><issn>1432-136X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNp9kUFrFDEUx4NY7Fr9AF40eND2MPryJsnMHKVULRQsaMFbyGSS3ZTZZJvMiPvtzTILBQ89BV5-_9_j8SfkDYNPDKD5nAFqCRVAWwG2rOqekRXjNVaslr-fkxWwhldMNO0peZnzPQBw1vIX5JS1opYd4orE280--zjGtTd6pMnmXQzZUh_otLH0ak5xZ3WgboxzGGyi57ejnrzZTCVXpjbP-YJOkf7Ryet-tDTr0Qc_7akOA41_92sbqIlh8JMv5lfkxOkx29fH94zcfb36dfm9uvnx7fryy01lOIqpGrTkA_aNQMONMy1KHBrd2cEaZ3VvRdcjE8bxjtWohwZF72SZSWYcIrj6jHxcvLsUH2abJ7X12dhx1MHGOatWMC4bxLqQH54kZceBd_IAvv8PvI9zCuUKhdgCCi5YgdgCmRRzTtapXfJbnfaKgTqUppbSVClNHUpTXcm8PYrnfmuHx8SxpQLgAuTyFdY2PW5-yvpuCTkdlV4nn9XdTwRWAxRny7D-B9_drO8</recordid><startdate>20080901</startdate><enddate>20080901</enddate><creator>Lundgreen, Kim</creator><creator>Kiilerich, Pia</creator><creator>Tipsmark, Christian K</creator><creator>Madsen, Steffen S</creator><creator>Jensen, Frank B</creator><general>Berlin/Heidelberg : Springer-Verlag</general><general>Springer-Verlag</general><general>Springer Nature B.V</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QG</scope><scope>7QR</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PATMY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PYCSY</scope><scope>7X8</scope><scope>F1W</scope><scope>H95</scope><scope>L.G</scope></search><sort><creationdate>20080901</creationdate><title>Physiological response in the European flounder (Platichthys flesus) to variable salinity and oxygen conditions</title><author>Lundgreen, Kim ; 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B, Biochemical, systemic, and environmental physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lundgreen, Kim</au><au>Kiilerich, Pia</au><au>Tipsmark, Christian K</au><au>Madsen, Steffen S</au><au>Jensen, Frank B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Physiological response in the European flounder (Platichthys flesus) to variable salinity and oxygen conditions</atitle><jtitle>Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology</jtitle><stitle>J Comp Physiol B</stitle><addtitle>J Comp Physiol B</addtitle><date>2008-09-01</date><risdate>2008</risdate><volume>178</volume><issue>7</issue><spage>909</spage><epage>915</epage><pages>909-915</pages><issn>0174-1578</issn><eissn>1432-136X</eissn><abstract>Physiological mechanisms involved in acclimation to variable salinity and oxygen levels and their interaction were studied in European flounder. The fish were acclimated for 2 weeks to freshwater (1[per thousand] salinity), brackish water (11[per thousand]) or full strength seawater (35[per thousand]) under normoxic conditions (water Po₂ = 158 mmHg) and then subjected to 48 h of continued normoxia or hypoxia at a level (Po₂ = 54 mmHg) close to but above the critical Po₂. Plasma osmolality, [Na⁺] and [Cl⁻] increased with increasing salinity, but the rises were limited, reflecting an effective extracellular osmoregulation. Muscle water content was the same at all three salinities, indicating complete cell volume regulation. Gill Na⁺/K⁺-ATPase activity did not change with salinity, but hypoxia caused a 25% decrease in branchial Na⁺/K⁺-ATPase activity at all three salinities. Furthermore, hypoxia induced a significant decrease in mRNA levels of the Na⁺/K⁺-ATPase α1-subunit, signifying a reduced expression of the transporter gene. The reduced ATPase activity did not influence extracellular ionic concentrations. Blood [Hb] was stable with salinity, and it was not increased by hypoxia. Instead, hypoxia decreased the erythrocytic nucleoside triphosphate content, a common mechanism for increasing blood O₂ affinity. It is concluded that moderate hypoxia induced an energy saving decrease in branchial Na⁺/K⁺-ATPase activity, which did not compromise extracellular osmoregulation.</abstract><cop>Berlin/Heidelberg</cop><pub>Berlin/Heidelberg : Springer-Verlag</pub><pmid>18536922</pmid><doi>10.1007/s00360-008-0281-9</doi><tpages>7</tpages></addata></record> |
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subjects | Acclimatization Animal Physiology Animals Biochemistry Biomedical and Life Sciences Biomedicine Blood Brackish water Energy conservation Flounder - physiology Gills - enzymology Homeostasis Human Physiology Hypotheses Hypoxia Hypoxia - physiopathology Life Sciences Marine Original Paper Osmoregulation Oxygen - metabolism Physiology Platichthys flesus Salinity Seawater Sodium-Potassium-Exchanging ATPase - metabolism Water content Water-Electrolyte Balance - physiology Zoology |
title | Physiological response in the European flounder (Platichthys flesus) to variable salinity and oxygen conditions |
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