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Complete intracellular pH protection during extracellular pH depression is associated with hypercarbia tolerance in white sturgeon, Acipenser transmontanus

Identifieur interne : 000137 ( PascalFrancis/Checkpoint ); précédent : 000136; suivant : 000138

Complete intracellular pH protection during extracellular pH depression is associated with hypercarbia tolerance in white sturgeon, Acipenser transmontanus

Auteurs : D. W. Baker [Canada] ; V. Matey [États-Unis] ; K. T. Huynh [Canada] ; J. M. Wilson [Portugal] ; J. D. Morgan [Canada] ; C. J. Brauner [Canada]

Source :

RBID : Pascal:09-0252976

Descripteurs français

English descriptors

Abstract

Sturgeons are among the most CO2 tolerant of fishes investigated to date. However, the basis of this exceptional CO2 tolerance is unknown. Here, white sturgeon, Acipenser transmontanus, were exposed to elevated CO2 to investigate the mechanisms associated with short-term hypercarbia tolerance. During exposure to 1.5 kPa PCO2, transient blood pH [extracellular pH (pHe)] depression was compensated within 24 h and associated with net plasma HCO-3 accumulation and equimolar Cl- loss, and changes in gill morphology, such as a decrease in apical surface area of mitochondrial-rich cells. These findings indicate that pHe recovery at this level of hypercarbia is accomplished in a manner similar to most freshwater teleost species studied to date, although branchial mechanisms involved may differ. White sturgeon exposed to more severe hypercarbia (3 and 6 kPa PCO2) for 48 h exhibited incomplete pH compensation in blood and red blood cells. Despite pHe depression, intracellular pH (pHi) of white muscle, heart, brain, and liver did not decrease during a transient (6 h of 1.5 kPa PCO2) or prolonged (48 h at 3 and 6 kPa PCO2) blood acidosis. This pHi protection was not due to high intrinsic buffering in tissues. Such tight active cellular regulation of pHi in the absence of pHe compensation represents a unique pattern for non-air-breathing fishes, and we hypothesize that it is the basis for the exceptional CO2 tolerance of white sturgeon and, likely, other CO2 tolerant fishes. Further research to elucidate the specific mechanisms responsible for this tremendous pH regulatory capacity in tissues of white sturgeon is warranted.


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Pascal:09-0252976

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<term>Hydrogencarbonates</term>
<term>Intracellular</term>
<term>Pisces</term>
<term>Plasma</term>
<term>Protection</term>
<term>Short term</term>
<term>Tolerance</term>
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<term>Protection</term>
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<term>Tolérance</term>
<term>Pisces</term>
<term>Court terme</term>
<term>Sang</term>
<term>Plasma</term>
<term>Hydrogénocarbonate</term>
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<div type="abstract" xml:lang="en">Sturgeons are among the most CO
<sub>2</sub>
tolerant of fishes investigated to date. However, the basis of this exceptional CO
<sub>2</sub>
tolerance is unknown. Here, white sturgeon, Acipenser transmontanus, were exposed to elevated CO
<sub>2</sub>
to investigate the mechanisms associated with short-term hypercarbia tolerance. During exposure to 1.5 kPa PCO
<sub>2</sub>
, transient blood pH [extracellular pH (pHe)] depression was compensated within 24 h and associated with net plasma HCO
<sup>-</sup>
<sub>3</sub>
accumulation and equimolar Cl
<sup>-</sup>
loss, and changes in gill morphology, such as a decrease in apical surface area of mitochondrial-rich cells. These findings indicate that pHe recovery at this level of hypercarbia is accomplished in a manner similar to most freshwater teleost species studied to date, although branchial mechanisms involved may differ. White sturgeon exposed to more severe hypercarbia (3 and 6 kPa PCO
<sub>2</sub>
) for 48 h exhibited incomplete pH compensation in blood and red blood cells. Despite pHe depression, intracellular pH (pHi) of white muscle, heart, brain, and liver did not decrease during a transient (6 h of 1.5 kPa PCO
<sub>2</sub>
) or prolonged (48 h at 3 and 6 kPa PCO
<sub>2</sub>
) blood acidosis. This pHi protection was not due to high intrinsic buffering in tissues. Such tight active cellular regulation of pHi in the absence of pHe compensation represents a unique pattern for non-air-breathing fishes, and we hypothesize that it is the basis for the exceptional CO
<sub>2</sub>
tolerance of white sturgeon and, likely, other CO
<sub>2</sub>
tolerant fishes. Further research to elucidate the specific mechanisms responsible for this tremendous pH regulatory capacity in tissues of white sturgeon is warranted.</div>
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<s0>Sturgeons are among the most CO
<sub>2</sub>
tolerant of fishes investigated to date. However, the basis of this exceptional CO
<sub>2</sub>
tolerance is unknown. Here, white sturgeon, Acipenser transmontanus, were exposed to elevated CO
<sub>2</sub>
to investigate the mechanisms associated with short-term hypercarbia tolerance. During exposure to 1.5 kPa PCO
<sub>2</sub>
, transient blood pH [extracellular pH (pHe)] depression was compensated within 24 h and associated with net plasma HCO
<sup>-</sup>
<sub>3</sub>
accumulation and equimolar Cl
<sup>-</sup>
loss, and changes in gill morphology, such as a decrease in apical surface area of mitochondrial-rich cells. These findings indicate that pHe recovery at this level of hypercarbia is accomplished in a manner similar to most freshwater teleost species studied to date, although branchial mechanisms involved may differ. White sturgeon exposed to more severe hypercarbia (3 and 6 kPa PCO
<sub>2</sub>
) for 48 h exhibited incomplete pH compensation in blood and red blood cells. Despite pHe depression, intracellular pH (pHi) of white muscle, heart, brain, and liver did not decrease during a transient (6 h of 1.5 kPa PCO
<sub>2</sub>
) or prolonged (48 h at 3 and 6 kPa PCO
<sub>2</sub>
) blood acidosis. This pHi protection was not due to high intrinsic buffering in tissues. Such tight active cellular regulation of pHi in the absence of pHe compensation represents a unique pattern for non-air-breathing fishes, and we hypothesize that it is the basis for the exceptional CO
<sub>2</sub>
tolerance of white sturgeon and, likely, other CO
<sub>2</sub>
tolerant fishes. Further research to elucidate the specific mechanisms responsible for this tremendous pH regulatory capacity in tissues of white sturgeon is warranted.</s0>
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<s0>Protection</s0>
<s5>03</s5>
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<s0>Protección</s0>
<s5>03</s5>
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<s0>Extracellulaire</s0>
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<s5>04</s5>
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<s5>04</s5>
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<s0>Tolérance</s0>
<s5>05</s5>
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<s5>05</s5>
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<s5>06</s5>
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<s0>Pisces</s0>
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<s5>06</s5>
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<s5>07</s5>
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<s5>07</s5>
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<s5>08</s5>
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<s5>08</s5>
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<s0>Sangre</s0>
<s5>08</s5>
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<s0>Plasma</s0>
<s5>10</s5>
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<s0>Plasma</s0>
<s5>10</s5>
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<s0>Plasma</s0>
<s5>10</s5>
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<s0>Hydrogénocarbonate</s0>
<s2>NA</s2>
<s5>11</s5>
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<s0>Hydrogencarbonates</s0>
<s2>NA</s2>
<s5>11</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Hidrógenocarbonato</s0>
<s2>NA</s2>
<s5>11</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE">
<s0>Chlorure</s0>
<s2>NA</s2>
<s5>13</s5>
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<s2>NA</s2>
<s5>13</s5>
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<s0>Cloruro</s0>
<s2>NA</s2>
<s5>13</s5>
</fC03>
<fC03 i1="12" i2="X" l="FRE">
<s0>Branchie</s0>
<s5>14</s5>
</fC03>
<fC03 i1="12" i2="X" l="ENG">
<s0>Gill</s0>
<s5>14</s5>
</fC03>
<fC03 i1="12" i2="X" l="SPA">
<s0>Branquia</s0>
<s5>14</s5>
</fC03>
<fC03 i1="13" i2="X" l="FRE">
<s0>Dioxyde de carbone</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>69</s5>
</fC03>
<fC03 i1="13" i2="X" l="ENG">
<s0>Carbon dioxide</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>69</s5>
</fC03>
<fC03 i1="13" i2="X" l="SPA">
<s0>Carbono dióxido</s0>
<s2>NK</s2>
<s2>FX</s2>
<s5>69</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Appareil circulatoire</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Circulatory system</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Aparato circulatorio</s0>
<s5>20</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Système nerveux central</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Central nervous system</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Sistema nervioso central</s0>
<s5>21</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Appareil digestif</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Digestive system</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Aparato digestivo</s0>
<s5>22</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Trouble de l'équilibre acidobasique</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Acid base balance disorder</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Trastorno equilibrio acidobásico</s0>
<s5>23</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Trouble métabolique</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Metabolic disorder</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Trastorno metabolismo</s0>
<s5>24</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Pathologie de l'appareil respiratoire</s0>
<s5>25</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Respiratory disease</s0>
<s5>25</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Aparato respiratorio patología</s0>
<s5>25</s5>
</fC07>
<fN21>
<s1>187</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
<affiliations>
<list>
<country>
<li>Canada</li>
<li>Portugal</li>
<li>États-Unis</li>
</country>
<region>
<li>Californie</li>
</region>
</list>
<tree>
<country name="Canada">
<noRegion>
<name sortKey="Baker, D W" sort="Baker, D W" uniqKey="Baker D" first="D. W." last="Baker">D. W. Baker</name>
</noRegion>
<name sortKey="Brauner, C J" sort="Brauner, C J" uniqKey="Brauner C" first="C. J." last="Brauner">C. J. Brauner</name>
<name sortKey="Huynh, K T" sort="Huynh, K T" uniqKey="Huynh K" first="K. T." last="Huynh">K. T. Huynh</name>
<name sortKey="Morgan, J D" sort="Morgan, J D" uniqKey="Morgan J" first="J. D." last="Morgan">J. D. Morgan</name>
</country>
<country name="États-Unis">
<region name="Californie">
<name sortKey="Matey, V" sort="Matey, V" uniqKey="Matey V" first="V." last="Matey">V. Matey</name>
</region>
</country>
<country name="Portugal">
<noRegion>
<name sortKey="Wilson, J M" sort="Wilson, J M" uniqKey="Wilson J" first="J. M." last="Wilson">J. M. Wilson</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>

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