Abstract

Rainbow trout (Salmo gairdneri), initially averaging 125 g, were fed a complete or a pyridoxine-deficient diet for 14 wk. Vitamin B6 status was evaluated biweekly by direct measurement of liver pyridoxine and pyridoxal levels by HPLC and by determining pyridoxal-5′-phosphate-enhanced liver aspartate aminotransferase (ASAT) activity. By 14 wk, mortality had severely reduced the number of fish remaining in the pyridoxine-deficient group. At 14 wk, no significant differences in liver pyridoxine and pyridoxal levels were detected between the trout fed the complete or pyridoxine-deficient diet. Significant differences between dietary groups are found in ASAT activity in liver and percent stimulation of liver ASAT by the addition of pyridoxal-5′-phosphate after 8 wk. Clinical signs of vitamin B6 deficiency including anorexia, listlessness, frantic and erratic swimming, and ataxia were observed after 11 wk of feeding a pyridoxine-deficient diet. This study shows that vitamin B6 deficiency in rainbow trout can be readily determined weeks before signs of clinical deficiency are apparent by measuring pyridoxine-enhanced liver ASAT activity. However, liver levels of pyridoxine and pyridoxal are not sensitive indicators of vitamin B6 status.

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