Each rainbow trout egg, weighing 80–85 mg, contained 5–6 ng
of vitamin D activity as determined by chick toe–ash bioassay. No
25(OH)D was detected by competitive protein binding analysis in
the trout egg lipid extract. It was, therefore, assumed that each
fish
at hatching, contained up to 6 ng cholecalciferol. HPLC analysis of
lipid extracts of the
fish diet was unable to detect any
cholecalciferol or 25(OH)D. The absence of detectable 25(OH)D
or 1,25(OH)2D in blood plasma as the
fish grew, suggested also that
these
fish were vitamin D deficient and that they were not making
vitamin D by a metabolic process. There was a significant decrease
(p < 0.05) in total Ca in blood plasma (1.6
0.48 mmol/l, mean
SD, n = 15) of the vitamin D-deficient trout compared to that from
non-deficient commercial trout of 2.70
0.06 mmol/l. There was
also a significant decrease (p < 0.05) in plasma protein concentration
from 35.00
0.27 mg/ml in commercial trout to
22.80
0.46 mg/ml in the deficient trout. No differences were
found in plasma phosphorus concentration or in bone calcium or
bone phosphorus content between the vitamin D-deficient trout
and non-deficient commercial trout. There were no behavioural or
other visible signs of abnormality demonstrated by these trout
Each rainbow trout egg, weighing 80–85 mg, contained 5–6 ngof vitamin D activity as determined by chick toe–ash bioassay. No25(OH)D was detected by competitive protein binding analysis inthe trout egg lipid extract. It was, therefore, assumed that eachfishat hatching, contained up to 6 ng cholecalciferol. HPLC analysis oflipid extracts of thefish diet was unable to detect anycholecalciferol or 25(OH)D. The absence of detectable 25(OH)Dor 1,25(OH)2D in blood plasma as thefish grew, suggested also thatthesefish were vitamin D deficient and that they were not makingvitamin D by a metabolic process. There was a significant decrease(p < 0.05) in total Ca in blood plasma (1.60.48 mmol/l, meanSD, n = 15) of the vitamin D-deficient trout compared to that fromnon-deficient commercial trout of 2.700.06 mmol/l. There wasalso a significant decrease (p < 0.05) in plasma protein concentrationfrom 35.000.27 mg/ml in commercial trout to22.800.46 mg/ml in the deficient trout. No differences werefound in plasma phosphorus concentration or in bone calcium orbone phosphorus content between the vitamin D-deficient troutand non-deficient commercial trout. There were no behavioural orother visible signs of abnormality demonstrated by these trout
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Each rainbow trout egg, weighing 80–85 mg, contained 5–6 ng
of vitamin D activity as determined by chick toe–ash bioassay. No
25(OH)D was detected by competitive protein binding analysis in
the trout egg lipid extract. It was, therefore, assumed that each
fish
at hatching, contained up to 6 ng cholecalciferol. HPLC analysis of
lipid extracts of the
fish diet was unable to detect any
cholecalciferol or 25(OH)D. The absence of detectable 25(OH)D
or 1,25(OH)2D in blood plasma as the
fish grew, suggested also that
these
fish were vitamin D deficient and that they were not making
vitamin D by a metabolic process. There was a significant decrease
(p < 0.05) in total Ca in blood plasma (1.6
0.48 mmol/l, mean
SD, n = 15) of the vitamin D-deficient trout compared to that from
non-deficient commercial trout of 2.70
0.06 mmol/l. There was
also a significant decrease (p < 0.05) in plasma protein concentration
from 35.00
0.27 mg/ml in commercial trout to
22.80
0.46 mg/ml in the deficient trout. No differences were
found in plasma phosphorus concentration or in bone calcium or
bone phosphorus content between the vitamin D-deficient trout
and non-deficient commercial trout. There were no behavioural or
other visible signs of abnormality demonstrated by these trout
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