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Energy levels and anaerobic endproducts in the brains of two species of teleost fish at death in anoxic waterDiAngelo, Constance Rose 14 November 2012 (has links)
The brain of fish, as in other vertebrates, is responsible for many functions basic to life and is also thought to be an anoxia-sensitive tissue. Therefore, during anoxia, the maintenance of energy within the brain is of paramount importance to the survival of the animal. Studies concerning energy levels and storage and the use of anaerobic metabolism in fish brains following exposure to anoxia are lacking.
Rainbow trout (<u>Salmo gairdneri</u>) and brown bullhead catfish (<u>Ictalurus nebulosus</u>) occupy ecologically distinct habitats. Their tolerance of anoxia is different; trout survived l2 minutes while bullhead survived 62 minutes in anoxic water. Brains from control and anoxiaâ exposed trout and bullheads were analyzed using enzymatic assays and high pressure liquid chromatography (HPLC).
Control bullhead brains had higher concentrations of glycogen, ATP, CrP, and glucose than control trout. With anoxia, bullheads showed a significant decrease in ATP, CrP, and glycogen with no change noted for glucose, ketone bodies (betaâ hydroxybutyrate and acetoacetate), or alternative anaerobic endproducts (succinate, alanine, propionate, isobutyrate, isovalerate, and ethanol). Lactic acid increased two-fold with anoxia. The bullhead was able to generate ATP by depleting its CrP stores and through classical anaerobic glycolysis. Death was most likely due to an inability to maintain ATP levels. Catfish may survive anoxia longer than trout in part due to greater fuel stores.
Rainbow trout brain stored approximately one sixth the amount of glycogen as bullheads. With anoxia, these stores were depleted but there was no significant decrease in ATP, CrP, or glucose; the alternative endproducts also did not change. There was a l00% increase in lactic acid, suggesting that anaerobic glycolysis helped maintain ATP levels. Death may be due to factors other than ATP depletion such as lactic acid injury and increased intracellular free calcium. / Master of Science
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