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Abstracts / Comparative Biochemistry. and Physiology, Part B 126 (2000) S1-S108
ANOXIA ADAPTATIONS IN CYPRINID FISH
G6ran E. Nilsson Division of General Physiology, Department of Biology, University of Oslo, P.O.Box 1051, N-0316 Oslo, NORWAY While anoxia soon leads to brain damage and death in most vertebrates, there are some, although very few, exceptions to this rule. The best studied exceptions are freshwater turtles (genera Trachemys and Chrysemys) and cyprinid fishes of the genus Carassius (crucian carp and goldfish). Although the key to anoxic survival for these animals is to maintain brain ATP levels, they utilize contrasting strategies to achieve this. Unlike turtles, Carassius does not become comatose, but remain active during anoxia, albeit at a reduced level. During anoxia they reduce their metabolic rate by some 70 %, which is considerably less than in turtles (90-95%). This metabolic depression is probably not essential for short=term anoxic survival, but it saves on the glycogen stores and thereby prolongs anoxic survival time. Carassius shows an adenosine mediated increase in brain blood flow, but unlike turtles, this elevated blood flow is sustained throughout the anoxic period. Glycolysis is up-regulated rather than down-regulated as in turtles. The protection of brain calcium ion homeostasis is enhanced, but there is little evidence for a reduced neuronal ion permeability. The release of GABA in the anoxic Carassius brain is much smaller than in turtles. Consequently, the brain electrical activity is at least maintained to a degree which allows continued activity, although senses like vision and hearing are temporarily tuned down. As a result, Carassius is able to seek out oxygen in the water rather than having to wait for oxygen to reach it - the only option for a comatose turtle. The adaptation that allows this continued high level of glycolysis in Carassius is probably the production and excretion of ethanol as the main glycolytic end-product. Hereby, a continuous build up of lactate is avoided, and deep hypometabolism is not needed.
HEPATIC METABOLISM OF [3-13C]LACTATE IN M I C E I N F E C T E D WITH METACESTODES OF TAENIA CRASSICEPS Novak M, Corbin, I. And B.J. Blackburn Departments o f Biology and Chemistry, University of Winnipeg, Winnipeg, MB, Canada R3B 2E9 Carbon-13 decoupled proton spin-echo NMR spectroscopy was used to follow the fate of 13C label from exogenous [313C]lactate by monitoring hepatic metabolites of mice infected with metacestodes of 7aenia crassiceps. Spectral analysis revealed that two hours after intraduodenal injection of [3-13C]lactate, livers from both uninfected mice and those infected with cysticerci contained 13C label in glycogen, glucose, succinate, glutamate, alanine and lactate. Livers of infected animals had a lower percentage of 13C in glycogen, succinate, glutamate, alanine and lactate than those of uninfected controls. Infected mice had also lower concentrations of total hepatic glucose and phosphocholine, but higher concentrations of betaine, choline, acylcamitine and beta-hydroxybutyrate. Cysticerci contained 13C label in glucose, alanine and lactate. As these metacestodes are unavle to make glucose de novo from pyruvate, glucose found in cysticerci had to be synthesized by the host.