Review: Phosphorus in Fish Nutrition

Shearer 1984), fish could require less P to increase ovary (during maturation) than to increase body weight (during
growth). The dietary P requirement, therefore, can be lower for broodfish than for young growing fish. However,
since maturing fish change their feed intake and various metabolic (hormonal) balances from the normal, it is
difficult to estimate their dietary P requirement without performing an experiment. Generally, however, the P
requirem ent for breeding animals or laying birds is similar or less compared with the requirement for young growing
ones. In humans, both P requirement and recommendation for pregnant or lactating adult women are the same as
those for the adult, but are much lower than those for the adolescent (IOM 1997). Watanabe et al. (1984a)
reported that a fish meal based diet containing 2.2% P was deficient in available P content for broodstock fish of red
seabream. Fish fed the diet for 7 months had lower fecundity, and produced eggs and larvae of much lower
hatchability and higher abnormality than those fed P-forti fied diet. However, the mineral contents of tissues
(vertebrae, liver) and eggs of the fish did not differ (Watanabe et al. 1984b). In another study of longer feeding
duration (Watanabe et al. 1984c), broodstock fish of red seabream fed P-unforti fied diet performed similar to or
better than those fed P-forti fi ed diet. Watanabe (1985, 1988) also reported that the brood fish of ayu, Plecoglossus
altivelis, fed P-unforti fied diet had lower growth and fecundity than those fed P-forti fied diet, whereas chemical
composition of the eggs (P, Ca, ash, lipids and proximate) did not differ. These experiments were not replicated.
Response criterion: Resistance to infection
Resistance to infection is a unique criterion in P nutrition. There may be some indirect effects of P-defici ency
secondary to anorexia that reduces intakes of all essential nutrients, or to increased body fat or possible changes in
phospholipids and fatty acid profiles that could affect membrane fluidity and metabolism of prostanoids. P
deficiency has been suggested to have several indirect effects on immune functions via 1,25-(OH) 2D3/VDR
-mediated pathways in extrarenal tissues (Brown, 1999; Omdahl, 2002) and via depression of leukocyte functions
associated with decreased ATP content (Knochel, 2000). However, little is known regarding the specific effects of
P deficiency on disease resistance and immune functions in any animal species. Eya & Lovell (1998) fed juvenile
channel cat fish (initial body wt 2.1 g) for 10 weeks, and estimated the dietary P requirement based on maximum
alkaline phosphatase activity, survival from Edwardsiella ictaluri challenge, and weight gain, which ranged from
0.38 to 0.42%P in diet. The authors concluded that the dietary P level influences the resistance of cat fish to the
pathogen, but the requirement for maximizing the growth is sufficient for maximizing the resistance to the pathogen.
When the fish were challenged with the pathogen, however, the fish were approximately 10 times different in size
(2.4 g in P-deficient fish and 23.1 g in P-adequate fish). If the difference in mortality was simply due to the
difference in fish size rather than to their P-status, the conclusion may be untenable even though the difference in
size was caused by P-deficiency. Also, the concentration of ascorbic acid in diets might be different due to the use
of acidic salts (NaH 2PO 4) that can reduce dietary pH, which in turn increases the stability of ascorbic acid in diets.
Jokinen et al. (2003) reported that plasma IgM concentration of whitefish fed P-deficient diets decreased
significantly compared with those fed P-siffi cient diets. Plasma lysozyme activity and the antibody response to
bovine gamma globulin did not differ between P-deficient and P-sifficient fish, while the growth of P-defici ent fish
was markedly lower. They concluded that dietary P-deficiency has only minor effects on immune functions of
whitefish, and that the dietary P level that can support normal growth of the fish is sufficient to elicit normal immune
functions.
Biochemical / Metabolic responses to P-deficiency
In 1821, Francois Magendie injected a mixture of P and oil into the circulation of a dog. Soon afterward the
animal exhaled white fum es from its nose. Magendie explained that so long as the phosphorated oil was in contact
with the blood, no reaction occurred, but as soon as it passed through the surface membrane of the lungs and came
into contact with the air a combustion took place. It seems that Magendie was aware of the role of P as a key
element in energy metabolism and lipid (beta) oxidation when little was known about P metabolism. Liebig (1843)
wrote, "The production of fat is always a consequence of a deficit supply of oxygen, for oxygen is absolutely
indispensable for the dissipation of the excess of carbon in the food (p. 85)." Liebig did not relate this to
P-deficiency; however, because P-defi ciency causes cellular hypoxia it is natural to find increased fat-deposition in
P-deficient animals. Today, we know in mammals that P deficiency and hypophosphatemia (condition of low
serum Pi) cause various disorders in terrestrial animals, including erythrocyte dys function, glucose intolerance,
necrosis of skeletal muscle, myocardial dysfunction, central nervous system dysfunction, and osteomalacia
(reviewed in Lotz et al. 1968; Knochel 1977; Kreisberg 1977; Berner & Shike 1988; Hodgson & Hurley 1993;
© 2000, 2005. Shozo H. Sugiura. All rights reserved.
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