| The amount of phosphorus (P) in fish feeds must be carefully balanced to prevent deficiency signs as well as to minimize the urinary and fecal P excretions. A comprehensive study was undertaken to measure the quantitative dietary P requirement, bone mineralization, and the urinary and fecal P excretions, as well as to characterize bone deformities associated with dietary P deficiency or excess levels in haddock (Melanogrammus aeglefinus L.). The nutritional status of P was assessed in terms of growth, vertebrae ash and P concentration in plasma and tissue. According to the dose-response study using growth and bone mineralization as the requirement indicator, juvenile haddock require 0.96% P or 0.34 g digestible P per MJ energy of diet. Growth, feed conversion ratio, vertebrae and opercula ash content and urinary P excretion were all positively correlated with dietary P levels. Approximately 43.2% of organic P in feed was digestible for haddock, whereas the digestibility of inorganic P was 99%. Haddock fed a commercial diet had a higher P concentration in the urine than in Atlantic salmon, however, a higher volume of urine was excreted by Atlantic salmon.; Bone deformities associated with P deficiency or an excess amount of dietary P was characterized using radiography, histology, histomorphometry, or enzyme histochemistry. Juvenile haddock were fed experimental diets containing low (0.42%), optimum (1.02%) and excess (1.42%) levels of P for 20 weeks. Ash (total minerals) content of vertebrae, opercula, preopercula and ventral pharyngeal bone have indicated that the excess dietary P affects only vertebrae, though deficient P affects all bone equally. Tartrate resistant acid phosphatase (TRAP) staining employed for osteoclasts detection in vertebrae revealed that bone resorption occurs at the endosteal surfaces of the neural arches. Histomorphometrical examinations showed that the dietary P affects in bone formation, mineralization and resorption. Haddock juvenile diet deficient in P causes for the delay in bone mineralization. In contrast, excess amount of P in diet increased matrix deposition and an accelerated mineralization. Osteoclasts could be involved in P homeostatic balance. Observations of the number of osteoclasts and osteoclasts, and the amounts of mineralized bone and osteoid suggest that P deficiency in haddock bone initially increases bone resorption and subsequently decreases bone mineralization followed by a decrease in bone formation. It appears that skeletal tissue metabolism of haddock like other vertebrates is directly affected by the dietary phosphorus (P) intake. These findings will be useful in characterizing P deficiency and toxicity as well as to improve the health of farmed haddock. |
