Metabolic and ionoregulatory responses of the Amazonian cichlid, Astronotus ocellatus, to severe hypoxia.
We examined the metabolic and ionoregulatory responses of the Amazonian cichlid, Astronotus ocellatus, to 20 h exposure to severe hypoxia (0.37 +/- 0.19 mg O(2)/l; 4.6% air saturation) or 8 h severe hypoxia followed by 12 h recovery in normoxic water. During 20 h exposure to hypoxia, white muscle [ATP] was maintained at normoxic levels primarily through a 20% decrease in [creatine phosphate] (CrP) and an activation of glycolysis yielding lactate accumulation. Muscle lactate accumulation maintained cytoplasmic redox state ([NAD(+)]/[NADH]) and was associated with an inactivation of the mitochondrial enzyme pyruvate dehydrogenase (PDH). The inactivation of PDH was not associated with significant changes in cytoplasmic allosteric modulators ([ADP(free)], redox state, or [pyruvate]). Hypoxia exposure caused an approximately 65% decrease in gill Na(+)/K(+) ATPase activity, which was not matched by changes in Na(+)/K(+) ATPase alpha-subunit protein abundance indicating post-translational modification of Na(+)/K(+) ATPase was responsible for the decrease in activity. Despite decreases in gill Na(+)/K(+) ATPase activity, plasma [Na(+)] increased, but this increase was possibly due to a significant hemoconcentration and fluid shift out of the extracellular space. Hypoxia caused an increase in Na(+)/K(+) ATPase alpha-subunit mRNA abundance pointing to either reduced mRNA degradation during exposure to hypoxia or enhanced expression of Na(+)/K(+) ATPase alpha-subunit relative to other genes.
Richards
J G
JG
Department of Zoology, The University of British Columbia, 6270 University Blvd, Vancouver, BC, Canada V6T 1Z4. jrichard@zoology.ubc.ca
Wang
Y S
YS
Brauner
C J
CJ
Gonzalez
R J
RJ
Patrick
M L
ML
Schulte
P M
PM
Choppari-Gomes
A R
AR
Almeida-Val
V M
VM
Val
A L
AL
D000222:Adaptation, Physiological / Q000502:physiology*; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D023681:Cichlids / Q000378:metabolism / Q000502:physiology*; D003401:Creatine / Q000378:metabolism; D004909:Erythrocyte Indices; D005880:Gills / Q000201:enzymology; D006003:Glycogen / Q000378:metabolism; D006400:Hematocrit; D006454:Hemoglobins / Q000032:analysis / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000503:physiopathology*; D007477:Ions / Q000097:blood; D007668:Kidney / Q000201:enzymology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D019344:Lactic Acid / Q000097:blood / Q000378:metabolism; D008099:Liver / Q000201:enzymology / Q000378:metabolism; D018656:Muscle Fibers, Fast-Twitch / Q000201:enzymology / Q000378:metabolism; D010100:Oxygen / Q000097:blood / Q000378:metabolism; D010725:Phosphocreatine / Q000378:metabolism; D011768:Pyruvate Dehydrogenase Complex / Q000378:metabolism; D019289:Pyruvic Acid / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000235:genetics / Q000378:metabolism
D001786:Blood Glucose; D006454:Hemoglobins; D007477:Ions; D011768:Pyruvate Dehydrogenase Complex; D012333:RNA, Messenger; D010725:Phosphocreatine; D019344:Lactic Acid; D019289:Pyruvic Acid; D000255:Adenosine Triphosphate; D006003:Glycogen; D007770:L-Lactate Dehydrogenase; D000254:Sodium-Potassium-Exchanging ATPase; D003401:Creatine; D010100:Oxygen