Resumé
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Journal of Comparative Physiology. B, Biochemical, Systemic, and Environmental Physiology |
| Vol/bind | 178 |
| Sider (fra-til) | 909-915 |
| ISSN | 0174-1578 |
| Status | Udgivet - 2008 |
Fingeraftryk
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Physiological response in the European flounder (Platichthys flesus) to variable salinity and oxygen conditions. / Lundgreen, Kim; Kiilerich, Pia; Tipsmark, Christian Kølbæk; Madsen, Steffen; Jensen, Frank Bo.
I: Journal of Comparative Physiology. B, Biochemical, Systemic, and Environmental Physiology, Bind 178, 2008, s. 909-915.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
TY - JOUR
T1 - Physiological response in the European flounder (Platichthys flesus) to variable salinity and oxygen conditions
AU - Lundgreen, Kim
AU - Kiilerich, Pia
AU - Tipsmark, Christian Kølbæk
AU - Madsen, Steffen
AU - Jensen, Frank Bo
PY - 2008
Y1 - 2008
N2 - Physiological mechanisms involved in acclimation to variable salinity and oxygen levels and their interaction were studied in European flounder. The fish were acclimated for two weeks to freshwater (1 ‰ salinity), brackish water (11 ‰) or full strength seawater (35 ‰) 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.
AB - Physiological mechanisms involved in acclimation to variable salinity and oxygen levels and their interaction were studied in European flounder. The fish were acclimated for two weeks to freshwater (1 ‰ salinity), brackish water (11 ‰) or full strength seawater (35 ‰) 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.
M3 - Journal article
VL - 178
SP - 909
EP - 915
JO - Journal of Comparative Physiology B: Biochemical, Systems, and Environmental Physiology
JF - Journal of Comparative Physiology B: Biochemical, Systems, and Environmental Physiology
SN - 0174-1578
ER -