MILLIKIN: NUTRIENT REQUIREMENTS OF EISHES 



1957), coho salmon (Coates and Halver 1958), 

 channel catfish (Dupree 1966), rainbow trout 

 (Kitamura et al. 1967a), Japanese eel ( Arai et al. 

 1972a), and red sea bream (Yone 1975). Most of 

 these species fed pantothenic acid-deficient diets 

 displayed mucous covered gills, anorexia, re- 

 duced weight gain, and "clubbed gills." 



Quantitative pantothenic acid requirements 

 have been determined for channel catfish fry 

 (250 mg/kg dry diet) and channel catfish finger- 

 lings (10 mg/kg dry diet) (Murai and Andrews 

 1975 and 1979, respectively) and common carp 

 fingerlings (40 mg/kg dry diet) (Ogino 1967). 

 Murai and Andrews (1975) suggested that the 

 relatively high dietary pantothenic acid require- 

 ments of channel catfish fry might be partially 

 due to higher rates of micronutrient losses in 

 small feed crumbles (high surface to volume 

 ratio) fed to fry compared with larger feed par- 

 ticles fed to fingerlings. 



Ascorbic Acid 



Ascorbic acid has several important physio- 

 logical functions in fishes and is the vitamin 

 most sensitive to processing and storage losses 

 in fish formula feeds. Therefore, extensive re- 

 search has been conducted on qualitative and 

 quantitative ascorbic acid requirements for 

 fishes. Ascorbic acid is a cofactor of an enzyme 

 which is involved in hydroxylation of proline and 

 lysine during collagen formation, thereby con- 

 tributing to bone and skin formation. Ascorbic 

 acid also has a role in iron metabolism and de- 

 toxification of organic pollutants such as toxa- 

 phene and polychlorinated biphenyls during ac- 

 cumulation in the liver. 



Qualitative dietary ascorbic acid requirements 

 have been reported for rainbow trout (McLaren 

 et al. 1947; Kitamura et al. 1965; Hilton et al. 

 1978; Sato et al. 1978; John et al. 1979), brook 

 trout (Poston 1967), coho salmon and rainbow 

 trout (Halver et al. 1969), yellowtail (Sakaguchi 

 et al. 1969), Japanese eel (Arai et al. 1972a), chan- 

 nel catfish (Lovell 1973; Wilson and Poe 1973), 

 red sea bream (Yone 1975), mrigal, Cirrhina 

 mrigala (Mahajan and Agrawal 1980a), and 

 snake head, Channa punctatus (Mahajan and 

 Agrawal 1979). Ascorbic acid deficiency symp- 

 toms in coho salmon and rainbow trout include 

 reduced growth, distorted and twisted filament 

 cartilage of the gill arches, acute lordosis and 

 scoliosis, and eventual dislocation of vertebrae 

 (Halver et al. 1969). Other physiological changes 



in ascorbic acid-deficient rainbow trout include 

 low hematocrit values (Hilton etal. 1978; John et 

 al. 1979), and high plasma levels of triglycerides 

 and cholesterol (John et al. 1979). Halver (1972b) 

 reported that the rate of repair of experimentally 

 induced wounds in salmonids is directly related 

 to the amount of ascorbic acid intake. Rainbow 

 trout fed ascorbic acid-deficient diets for 18 wk 

 displayed impaired collagen formation in the 

 skin according to an in vitro radioisotopic method 

 with labeled proline (Yoshinaka et al. 1978). 

 Brook trout fingerlings fed ascorbic acid-defi- 

 cient diets over a 34-wk period developed scoliosis 

 and/or lordosis, increased mortality rate, and in- 

 ternal hemorrhaging (Poston 1967). Scorbutic 

 channel catfish experienced lordosis, scoliosis 

 (and ultimately, broken back), hemorrhage with- 

 in the vertebral column, and brittle vertebrae 

 (Wilson and Poe 1973). Also, these investigators 

 reported reduced serum alkaline phosphatase 

 activity (65% lower), lower vertebral collagen 

 content (42% less on a dry basis), and less hydroxy- 

 proline in the collagen of scorbutic channel cat- 

 fish. Wilson and Poe (1973) speculated that re- 

 duced serum alkaline phosphatase activity may 

 indicate reduced bone formation from lower 

 osteoblastic activity. In addition to the aforemen- 

 tioned common ascorbic acid deficiency symp- 

 toms (e.g., lordosis, scoliosis, hemorrhage along 

 spinal column, and poor growth), channel catfish 

 had increased susceptibility to pathogenic bac- 

 terial infestation (Aeromonas liquefaciens) and 

 occasional formation of hemivertebrae (Lovell 

 1973). Also, Halver et al. (1975) reported hyper- 

 plasia of nuclei of eye support cartilage in salmo- 

 nids deficient in ascorbic acid. Vertebral collagen 

 percentages of 24.5% or less and liver ascorbic 

 acid concentrations of 50 /ig/g or less occurred in 

 ascorbic acid deficient channel catfish finger- 

 lings with an initial mean weight equalling 22 g 

 (Lovell and Lim 1978). In contrast, channel cat- 

 fish fingerlings fed sufficient ascorbic acid had 

 26% or greater vertebral collagen and 65 ng or 

 greater ascorbic acid/g of liver tissue. In a sepa- 

 rate study, Lim and Lovell (1978) reported the 

 following ascorbic acid deficiency symptoms in 

 smaller channel catfish fingerlings (initial mean 

 weight = 2.3 g): 1) anorexia after 9 wk, 2) scolio- 

 sis, lordosis, and darker pigmentation after 10 

 wk, and 3) lower hematocrit values after 18 wk. 

 Also, liver ascorbic acid concentrations of 30 \xgjg 

 and vertebral collagen percentages of 25% or less 

 occurred in ascorbic acid-deficient channel cat- 

 fish in this smaller size range. Snake heads with 



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