Vitamin E nutrition and pancreas disease in farmed Atlantic salmon (Salmo salar L.)

Tissue vitamin E in farmed Atlantic salmon (Salmo salar L.) fed commercial diets, were measured by high-performance liquid chromatography. In healthy fish, fed diets containing about 20 mg lOO g*‘supplementary all-rac-a-tocopheryl acetate, vitamin E (a-tocopherol) accummulated in the liver and plasm...

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Bibliographic Details
Main Author: Roy, William J.
Format: Doctoral or Postdoctoral Thesis
Language:English
Published: University of Stirling 1991
Subjects:
Online Access:http://hdl.handle.net/1893/29431
http://dspace.stir.ac.uk/bitstream/1893/29431/1/Roy.pdf
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Summary:Tissue vitamin E in farmed Atlantic salmon (Salmo salar L.) fed commercial diets, were measured by high-performance liquid chromatography. In healthy fish, fed diets containing about 20 mg lOO g*‘supplementary all-rac-a-tocopheryl acetate, vitamin E (a-tocopherol) accummulated in the liver and plasma. Over a 20 month period, beginning four months prior to seawater transfer, mean a-tocopherol concentrations ranged between 51 and 754 |tg g*' in liver and 7 and 68 pg nl*‘ in plasma. Sharp increases in the a-tocopherol content of these tissues were related to a rise in the proportion of lipid as polyunsaturated fatty acid in response to transfer to seawater. There was no marked difference between tissue vitamin E concentrations in farmed and wild salmon. In contrast, vitamin E depletion was found to be a consistent feature of pancreas disease (PD) in farmed salmon. The degree of depletion was found to vary from case to case. A serial study indicated that the onset of vitamin E depletion occurred early in the course of the outbreak. Soma information was collected with regard to the cause and possible pathological effects of vitamin E depletion in PD, but definitive studies are still required. Parental administration of all-rac-a-tocopherol in molten cocoa-butter reduced plasma pyruvate kinase activity in affected fish from one outbreak of PD, suggesting that muscle degeneration in PD may respond to treatment with vitamin E. However, no effects on the histological signs of PD were noted. In a second outbreak, supplementation of the diet with 100 mg all-rac-a-tocopherol 100 g'* produced no statistically significant elevation of plasma vitamin E or reduction in plasma pyruvate kinase activity. In a third case, dietary supplementation with a water-miscible preparation of all-rac-a-tocopheryl acetate produced no significant rise in plasma vitamin E concentrations and no histological evidence of any therapeutic effect was obtained. Relationships between husbandry practices and vitamin E status were examined experimentally. ...