3.1 Dietary essential fatty acid (EFA) deficiency
3.2 Dietary EFA toxicity
3.3 Toxic non-essential fatty acids
3.4 Oxidation of dietary lipids
All fish examined to date display reduced growth and poor food conversion efficiency when fed experimental diets deficient in EFA. The following additional gross anatomical deficiency signs have been reported under experimental conditions with juvenile fish fed EFA deficient diets.
1/ Scores based on comparison with the mean essential amino acid requirements of rainbow trout and carp (Ogino, 1980). Mean EAA requirement (expressed as % of total EAA) being: threonine 10.6; valine 9.5; methionine 5.4; cystine 2.7; isoleucine 7.5; leucine 13.5; phenylalanine 9.5; tyrosine 6.5; lysine 16.8; histidine 4.8; arginine 11.6; and tryptophan 1.72/ Source: 1-Kay (1979); 2-Gohl (1980); 3-Bolton and Blair (1977); 4-National Research Council (1983); 5-Tunnel AVEBE Starches Ltd., UK; 6-Cowey et al. (1971); 7-Unpublished data; 8-Cowey and Sargent (1972); 9-Connell and Howgate (1959); 10-Jackson, Kerr and Cowey (1984); 11-Tacon, Stafford and Edwards (1983); 12-Spinelli (1980)
* Limiting essential amino acids (present below 30% mean fish requirement)
|
Fish |
EFA deficiency signs1/ |
|
S. gairdneri |
Increased 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/degeneration of liver, swollen pale liver (1,2); reduced spawning efficiency (low hatching/survival rate, 3) |
|
Oncorhynchus kisutch |
Swollen pale liver, increased hepatosomatic index (fatty liver), high mortality (2) |
|
Oncorhynchus keta |
Swollen pale liver, increased hepatosomatic index (fatty liver), high mortality (2) |
|
C. carpio |
Increased mortality (4); fatty liver (5) |
|
Anguilla japonica |
Increased mortality (6) |
|
Oreochromis niloticus |
Swollen pale liver, fatty liver (7) |
|
Pagrus major |
Reduced spawning efficiency (decreased hatching rates/survival, 3) |
|
Scophthalmus maximus |
Increased mortality, reduced growth, degeneration of gill epithelium (8) |
1/ 1-Castell et al. (1972); 2-Takeuchi and Watanabe (1982); 3-Watanabe (1982); 4-Takeuchi and Watanabe (1977); 5-Farkas et al. (1977); 6-Takeuchi et al. (1980); 7-Takeuchi, Satoh and Watanabe (1983); 8-Bell et al. (1985)
Dietary EFA deficiencies generally result from poor feed formulation.
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 and Sinnhuber, 1976; Takeuchi and Watanabe, 1979; coho salmon - Yu and Sinnhuber, 1979).
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 and Sinnhuber, 1972; Hendricks et al. 1980). Other pathologies observed with trout include extreme liver damage (paleo 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 and Lee, 1973).
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 oil seed 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 major deteriorative changes which occurs in stored feedstuffs (Cockerell, Francis and Halliday, 1972; Chow, 1980).
Numerous gross anatomical pathological signs have been reported in fish fed rations containing oxidized fish/plant oils with no antioxidant (vitamin E) protection:
|
Fish |
Pathological effects of oxidized fish oil 1/ |
|
Oreochromis niloticus |
Marked congestion, with some haemorrhage, in dermal vessels around snout and at bases of pectoral/dorsal fins, lordosis, exopthalmia, abdominal swelling (oedema), cataract, orbital collapse, darkening of liver, marked distension of bile duct, steatitis of all abdominal fat bearing tissue, deposits of intra-cellular ceroid in liver, spleen, kidney and choroid, increased mortality (1) |
|
Oncorhynchus tshawytscha |
Dark body colouring, anaemia, lethargy, brown-yellow pigmented liver (ceroid deposition), abnormal kidney and evidence of gill clubbing (2) |
|
C. carpio |
Poor growth, loss of appetite, muscular dystrophy, high mortality, reduced absorption of dietary lipids (3-5) |
|
Ictalurus punctatus |
Poor growth, poor food conversion efficiency, increased mortality, exudative diathesis, muscular dystrophy, depigmentation, fatty livers (6) |
|
Seriola quinqueradiata |
Reduced growth, swollen liver, decreased lipid deposition (7); anorexia, leaning of dorsal muscle, muscular dystrophy (8) |
|
S. gairdneri |
Reduced growth (9,10); poor food conversion efficiency (9); microcytic anaemia (10,11); reduced haematocrit and haemoglobin content (9); liver lipoid degeneration (ceroid accumulation, 10,11); severe muscle damage (9); increased mentality and erythrocyte fragility (9,11,12) |
1/ 1-Soliman, Roberts and Jauncey (1983); 2-Fowler and Banks (1969); 3-Watanabe and Hashimoto (1968); 4-Hashimoto et al. (1966); 5-Hata and Kaneda (1980); 6-Murai and Andrews (1974); 7-Park (1978); 8-Sakaguchi and Hamaguchi (1969); 9-Cowey et al. (1984); 10-Smith (1979); 11-Moccia et al. (1984); 12-Hung, Cho and Slinger (1981)
With the exception of the study of Soliman, Roberts and 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 and 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, long term studies are required.
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/haemoglobin are pro-oxidants present in meat/fish meals); 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).
