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3.1 Dietary essential fatty acid deficiency

All fish examined to date display reduced growth and poor feed efficiency when fed experimental diets deficient in essential fatty acids (EFA). Table 3 shows the additional gross anatomical deficiency signs which have been reported with juvenile fish fed EFA deficient diets. In general dietary EFA deficiencies result from poor feed formulation or from the use of EFA deficient live food organisms.

Table 3. Report essential fatty acid (EFA) deficiency signs in fish
Fish speciesDeficiency signs1
O. mykissIncreased mortality, elevated muscle water content, increased susceptibility to caudal fin erosion by Flexebacterium sp., fainting or shock syndrome, decreased haemoglobin and red blood cell volume (1), fatty infiltration and degeneration of liver, swollen pale liver (1,2), reduced spawning efficiency (low hatching and larval survival rate, 3)
Oncorhynchus kisutchSwollen pale liver, increased hepatosamtic index (fatty liver), high mortality (2)
Oncorhynchus ketaSwollen pale liver, increased hepatosamtic index (fatty liver), high mortality (2)
C. carpioIncreased mortality (4), fatty liver (7)
Anguilla japonicaIncreased mortality (6)
Oreochromis niloticusSwollen pale liver, fatty liver (7)
Pagrus majorReduced spawning efficiency (decreased hatching and survival rates (3), reduced appetite and growth, increased liver lipid content, high mortality (12)
Lates calcariferReduced growth and feed efficiency, reddening of fins (8)
Scophthalmus maximusIncreased mortality, reduced growth, degeneration of gill epithelium (9)
Ctenopharyngodon idellaReduced growth and feed efficiency, swollen pale liver, increased mortality, lordosis, shock syndrome (10)
Pseudocaranx dentexReduced appetite and swimming activity, reduced growth and feed efficiency, high mortality (11)
Coregonus lavaretusReduced growth, feed efficiency and survival rate, swollen pale liver (13,14)

1 1-Castell et al. (1972),
2-Takeuchi & Watanabe (1982),
3-Watanabe (1982),
4-Takeuchi &Watanabe (1977),
5-Farkas et al. (1977),
6-Takeuchi et al. (1980),
7-Takeuchi, Satoh & Watanabe(1983),
8-Wanakowat et al. (1991),
9-Bell et al. (1985),
10-Takeuchi et al. (1991),
11-Watanabeet al. (1989),
12-Takeuchi et al. (1990),
13-Watanabe et al. (1989a),
14-Thongrod et al. (1989)

3.2 Dietary essential fatty acid toxicity

Under laboratory conditions it has been found that a dietary excess of EFA may exert a negative effect on fish growth and feed efficiency (rainbow trout - Yu & Sinnhuber, 1976; Takeuchi & Watanabe, 1979; coho salmon - Yu & Sinnhuber, 1979).

3.3 Toxic non-essential fatty acids

Cyclopropenoic acid is a toxic fatty acid found in the lipid fraction of cottonseed products. Experimentally, cyclopropenoic acid has been shown to reduce growth rate in rainbow trout and to act as a potent synergist for the carcinogenity of aflatoxins (Lee & Sinnhuber, 1972; Hendricks et al. 1980). Other pathologies observed with trout include extreme liver damage (liver is pale in colour) with increased glycogen deposition and decreased protein content, and a decrease in activity of several key enzymes (Roehm et al. 1970, Taylor, Montgomery & Lee, 1973).

3.4 Oxidation of dietary lipids

In the absence of suitable antioxidant protection lipids rich in polyunsaturated fatty acids (PUFA, including EFA) are highly prone to auto-oxidation on exposure to atmospheric oxygen. Under these conditions, the nutritional benefit of EFA in fact becomes deleterious to the health of the fish. Feedstuffs rich in PUFA which are particularly susceptible to lipid oxidative damage (oxidative rancidity) include fish oils, fish meal, rice bran and expeller oilseed cakes containing little or no natural antioxidant activity. During the process of lipid auto-oxidation chemical degradation products are formed, including free radicals, peroxides, hydroperoxides, aldehydes and ketones, which in turn react with other dietary ingredients (vitamins, proteins and other lipids) reducing their biological value and availability during digestion. At present oxidative rancidity is believed to be one of the most deteriorative changes which occurs in stored feedstuffs (Cockerell, Francis & Halliday, 1972; Chow, 1980). Table 4 summarizes the major anatomical pathological signs which have been reported in fish fed rations containing oxidized fish/plant oils with no antioxidant (vitamin E) protection.

With the exception of the study of soliman, Roberts & Jauncey (1983) with Oreochromis niloticus, the pathological effects of oxidized lipids have been shown to be prevented by dietary supplementation with dl-alpha tocopherol acetate (vitamin E). During the six weeks feeding trial of Soliman, Roberts & Jauncey (1983) the dietary supplementation of vitamin E to an oxidized fish oil diet only prevented the occurrence of lordosis. Although no vitamin E analyses were performed on diet or fish tissue at the end of the experiment, in contrast to previous studies with fast growing tropical fish these authors also reported no pathological deficiency signs in fish fed diets containing fresh lipid with no dietary vitamin E supplementation. Clearly, longer term studies will be required to confirm these findings.

In the absence of suitable antioxidant protection the rate of lipid auto-oxidation in stored feedstuffs has been found to increase in the presence of lipoxidase (present in raw soybeans), haeme compounds (myoglobin and haemoglobin are pro-oxidants present in meat meals and fishmeals), peroxides (product of lipid auto-oxidation), light (UV - formation of singlet oxygen/free radicals), increased temperature (reaction rate), and trace elements (Fe and Cu have been found to accelerate lipid oxidation by direct electron transfer in redox reactions, whereas Zn induces the breakdown of hydro-peroxides to free radicals (ADCP, 1983).

Table 4. Reported pathological effects of oxidized fish oil in fish
Fish speciesPathological effects 1
O. niloticusMarked congestion, with some haemorrhage, in dermal vessels around snout and at bases of pectoral/dorsal fins, lordosis, exophthalmia, abdominal swelling (oedema), cataract, orbital collapse, darkening of liver, marked distension of bile duct, steatitis of all abdominal fat bearing tissue, deposits of intracellular ceroid in liver, spleen, kidney and choroid, increased mortality (1)
C. carpioPoor growth, loss of appetite, muscular dystrophy, high mortality, reduced absorption of dietary lipids (3–5)
lctalurus punctatusPoor growth, poor feed efficiency, increased mortality, exudative diathesis (increased permeability of blood capillaries), muscular dystrophy, depigmentation, fatty liver (6)
Seriola quinqueradiataReduced growth, swollen liver, decreased lipid deposition (7), anorexia (loss of appetite), leaning of dorsal muscle, muscular dystrophy (8)
Oncorhynchus tshawytschaDark body colouring, anaemia, lethargy, brown-yellow pigmented liver (ceroid deposition), abnormal kidney and evidence of gill clubbing (2)
O. mykissReduced growth (9,10), poor feed efficiency (9), microcytic anaemia (10,11), reduced haematocrit and haemoglobin content, liver lipoid degeneration (ceroid accumulation; 10–11,13), severe muscle damage (9), increased mortality and erythrocyte fragility (9,11,12)
Salmo salarReduced growth, increased mortality (14)
O. kisutchReduced growth (14,15), increased mortality (14), reduced feed efficiency (15)

1 1-Soliman, Roberts & Jauncey (1983),
2-Fowler & Banks (1969),
3-Watanabe & Hashimoto(1968),
4-Hashimoto et al. (1966),
5-Hata & Kaneda (1980),
6-Murai & Andrews (1974),
7-Park (1978),
8-Sakaguchi & Hamaguchi (1969),
9-Cowey et al. (1984),
10-Smith (1979),
11-Moccia et al. (1984),
12-Hung, Cho & Slinger (1981),
13-Rehulka (1990),
14-Ketola, Smith &Kindschi (1989),
15-Forster et al. (1988)

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