FISHERY BULLETIN: VOL. 80, NO. 4 



ascorbic acid deficiency had an elevated liver 

 cholesterol content after 150 d, in addition to the 

 occurrence of scoliosis, lordosis, and decreased 

 ascorbic acid concentrations in blood and kidney 

 (Mahajan and Agrawal 1979). Ascorbic acid de- 

 ficiency in fish from the same study resulted in 

 normochromic, normocytic anemia after 120 d 

 and normochromic, macrocytic anemia between 

 180 and 210 d (Agrawal and Mahajan 1980). 

 Using 45 Ca as a tracer, snake heads had reduced 

 absorption of calcium from surrounding water 

 by gills and skin and lower muscle and bone cal- 

 cium content when fed an ascorbic acid-deficient 

 diet for 210 d (Mahajan and Agrawal 1980b). 

 Since distortion of gill filaments from cartilage 

 malformation often occurs in ascorbic acid-defi- 

 cent fish, decreased calcium absorption through 

 the gills may have resulted from the ascorbic 

 acid deficiency (Mahajan and Agrawal 1980b). 

 Channel catfish (initial weight slightly >5 g), fed 

 either 670 or 5,000 mg of ascorbic acid/kg dry 

 diet, did not receive any additional advantages in 

 weight gain or backbone collagen concentration 

 (Mayer et al. 1978). However, channel catfish ex- 

 posed to increasingly higher concentrations of 

 toxaphene were at least partially protected from 

 growth retardation, vertebral development 

 anomalies, and skin integrity problems, when 

 higher dietary ascorbic acid concentrations were 

 consumed. For instance, the no-effect toxaphene 

 concentration on skin integrity (e.g., mucous cell 

 numbers and epidermal thickness) was <37 ng/1 

 for channel catfish fed 63 or 670 mg ascorbic 

 acid/kg dry diet, while the no-effect toxaphene 

 concentration was between 68 and 108 ng/1 for 

 fish fed 5,000 mg ascorbic acid/kg dry diet 

 (Mayer et al. 1978). Methods to measure rupture 

 (the force level causing specimen failure) and 

 elastic limit (the force level above which perma- 

 nent structural damage occurs in a test speci- 

 men) according to Hamilton et al. (1981a) were 

 used to evaluate effects of ascorbic acid deficiency 

 on bone strength of channel catfish (Hamilton et 

 al. 1981b). Channel catfish fingerlings (initial 

 weight = 4 to 5 g) fed diets containing no ascorbic 

 acid had significant reductions in length and 

 weight after 150 d. Also, after 150 d, fish fed no 

 supplemental ascorbic acid had reductions of 

 10% in backbone collagen and 16% in hydroxy- 

 proline concentration in collagen. Additionally, 

 in channel catfish fed no supplemental ascorbic 

 acid, 24% less force was required to cause perma- 

 nent damage of vertebral centra (elastic limit) 

 and failure of vertebral centra (rupture) occurred 



at 16% less force than in individuals fed 500 mg 

 ascorbic acid/kg dry diet. 



Quantitative ascorbic acid requirements have 

 been determined for several fish species. Rain- 

 bow trout (initial mean weight = 0.3 g) require 

 100 mg ascorbic acid/kg dry diet and coho salm- 

 on (initial mean weight = 0.4 g) require about 

 50 mg ascorbic acid/kg dry diet based upon blood 

 and anterior kidney ascorbic acid concentrations 

 and growth rate (Halver et al. 1969). The mini- 

 mal level of ascorbic acid in the blood of coho 

 salmon and rainbow trout accompanying normal 

 growth and survival rate is 35 Mg ascorbic acid/g 

 blood. Hilton et al. ( 1978) reported a lower ascor- 

 bic acid requirement (40 mg/kg dry diet) for 

 larger rainbow trout (initial mean weight = 6.7 

 g), based upon growth, feed conversion, survival 

 rate, and serum iron levels. Andrews and Murai 

 (1975) estimated that channel catfish fingerlings 

 (initial mean weight = 2.3 g) require 50 mg ascor- 

 bic acid/kg dry diet over a 28-wk period based on 

 growth, feed conversion, and absence of ascorbic 

 acid deficiency symptoms. Channel catfish fin- 

 gerlings (initial mean weight = 2.3 g) required 

 30 mg ascorbic acid/kg dry diet over a 22-wk 

 period for maximal growth, whereas 60 mg 

 ascorbic acid/kg (the next highest experimental 

 concentration) was sufficient to prevent distor- 

 tion of gill filament cartilage and promote re- 

 generation of skin and muscle in experimentally 

 inflicted wounds after 10 d (Lim and Lovell 1978). 

 Mahajan and Agrawal (1980a) concluded that 

 mrigal fry and fingerlings require about 700 mg 

 ascorbic acid/kg dry diet based upon growth, 

 survival rates, and percentage occurrence of 

 skeletal deformities. 



Several sources of dietary ascorbic acid have 

 been evaluated for relative nutritional value for 

 channel catfish and rainbow trout. Channel cat- 

 fish fingerlings (initial mean weight = 7.9 g) fed 

 equimolar concentrations of 25 mg i.-ascorbic 

 acid (uncoated or ethylcellulose coated) or dipo- 

 tassium L-ascorbate 2-sulfate dihydrate (AS) per 

 kg dry diet over a 20-wk period did not show sco- 

 liosis, whereas 42% of the fingerlings fed a diet 

 containing <5 mg ascorbic acid/kg dry diet had 

 scoliosis (Murai et al. 1978). Maximal weight 

 gains and feed efficiency of channel catfish var- 

 ied with dietary ascorbic acid sources. Only 50 

 mg of ethylcellulose coated or uncoated L-ascor- 

 bic acid were required for maximal growth and 

 feed efficiency, while 200 mg of L-ascorbate-2- 

 sulfate dihydrate were required for similar in- 

 crements of weight gain. Generally, growth 



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