SELENIUM ON FISH & SHRIMP
Selenium in Fish Nutrition
Selenium is an integral part of the enzyme glutathione peroxidase (GSH-Px) which protects cell membranes and tissues against oxidative damage. The inclusion of Se in the diet of cultured terrestrial animals has generated much interest as it has been found to have benefits for production, reproduction and product quality.
In fish, Se is required for normal growth, development and flesh quality.
Selenium plays an important role in the maintenance of fish health, in particular fish immunity. Symptoms of Se deficiency in fish include low glutathione peroxidase activity, reduced growth, impaired reproduction, anaemia, exudative diathesis, muscular dystrophy and increased mortality.
However, excessive Se can also cause a variety of toxic effects at the biochemical, cellular, organ and system levels. Vitamin E and Se function synergistically in animal tissues to form an important antioxidant defence system.
Selenium requirements of fish vary with the form of Se ingested, polyunsaturated fatty acid and vitamin E content of the diet, and the concentration of Se in the water. Interactions between Se and vitamin E have been reported in channel catfish, Atlantic salmon, rainbow trout and chinook salmon by Gatlin (1986), Wise (1993) and Thorarinsson (1994).
GSH-Px activity in the plasma and liver is used as an index of Se status in fish (NRC, 1993). In rainbow trout Se requirement was determined on the basis of optimum growth and maximum plasma GSH-Px activity which occurred at 0.38 mg/kg diet (Hilton et al., 1980); in catfish this occurred at 0.25 mg/kg diet (Gatlin and Wilson, 1984). Lovell (1998) recommended inclusion rates of 0.03, 0.10 and 0.30 mg Se/kg diet in salmond, catfish and hybrid striped bass diets, respectively. Lin and Shiau (2005) estimated the Se requirement of juvenile grouper Epinephelus malabaricus to be about 0.7 mg/kg diet.
Dietary Se levels used in some studies are markedly higher than the ones just discussed. While intracellular superoxide anion production was higher in channel catfish fed on four times (0.8 mg/kg) the recommended level of Se (Wise, 1993). Lorentzen (1994) shown that the supplementation of Se at 1 to 2 mg/kg did not appear the benefit performance in Atlantic salmon.
In an earlier study by Julshamn (1990), supplementation of Se at 0.66 or 2.6 mg/kg also did not affect growth or feed conversion efficiency in Atlantic salmon.
Although increased mortality and compromised immunity are indicative of Se deficiency in fish, there appears to be a significant interaction between Se and vitamin E in fish.
Rainbow trout fed on diets without added Se or α-tocopherol for 10 weeks showed reduced appetite, pale swollen gills, brownish-yellow livers and anaemia; those given Se or alpha-tocopherol developed normally (Oberbach and Hartfiel, 1987).
Gatlin (1986) observed that while combined deficiencies of Se and vitamin E suppressed growth and caused anaemia, severe myopathy, exudative diathesis and death in fingerling channel catfish, singular deficiencies of either Se or vitamin E did not produce any of these pathological symptoms.
Similarly, while Se deficiency reduces growth in rainbow trout (Hilton, 1990) and catfish (Gatlin, 1984).
Both Se and vitamin E are necessary to prevent muscular dystrophy in Atlantic salmon (Poston, 1976) and exudative diathesis in rainbow trout (Bell, 1985).
Atlantic salmon given Se-deficient diets (0.017 mg/kg) showed increased levels of indices of tissue peroxidation (Bell, 1987).
Although Se is an essential element in animal nutrition, toxicity can arise at concentrations only slightly greater than those required. The toxicity of Se is thought to arise from its ability to substitute for sulphur during protein synthesis. This substitution disrupts normal chemical linkages leading to improperly formed proteins and enzymes affecting subcellular, cellular, organ and system functions.
Recent studies have also shown that some forms of Se are able to generate oxidative stress.
In rainbow trout, chronic dietary Se toxicity occurred at Se 13 mg/kg dry feed, expressed as reduced growth rate, poor feed conversion efficiency and high mortality (Hilton, 1980).
In channel catfish toxicity was observed at 15 mg/kg diet (Gatlin and Wilson, 1984), with reduced growth and feed conversion efficiency.
Hicks et al. (1984) reported that rainbow trout fed on 11.4 mg/kg Se showed reduced weight, feed conversion efficiency and increased mortality; 90% of the fish also developed nephrocalcinosis.
Hilton and Hodson (1983) observed renal calcinosis and a decrease in growth and feed conversion efficiency in rainbow trout reared on high-Se and high-carbohydrate diets (10 mg/kg). Mortality increased in chinook salmon exposed for 90 days to ≥ 9.6 mg/kg Se from 2 organic sources (high Se fish meal and Se-Methionin) (Hamilton et al., 1990). Growth was reduced when chinook salmon were fed on ≥ 5.3 mg/kg Se and 18.2 mg/kg Se, from fish meal and Se-Methionin, respectively.
Se and immunity
In a study by Thorarinsson et al. (1994), groups of juvenile spring chinook salmon naturally infected with Renibacterium salmoninarum were given 2 levels of vitamin E (53 or 299 mg/kg diet) and Se (0.038 or 2.49 mg/kg diet in the form of sodium selenite) ; no mortality was observed in those those on the high vitamin E + high Se diet. Mortality was 3% in the group given the low Se + high vitamin E or high Se + low vitamin E diets, and 31% in the group given the low Se + low vitamin E diet.
In channel catfish subjected to Edwardsiella ictaluri challenge, antibody production increased as dietary Se concentration increased, with maximum survival observed at the highest concentration used (Lovell and Wang, 1997). This indicates that dietary Se is essential for optimal immune response and resistance in channel catfish infected with E. ictaluri.
More recently, Lin and Shiau (2007) noted that oxidative stress induced by high copper ingestion in the grouper, E. malabaricus, depressed its immune response. Supplementation of high dietary Se (2 times adequate) was found to reduce the oxidative stress and improve the immune response.
Se and fish quality
Organic Se supplementation is reported to improve salmon flesh texture and coloration, by decreasing astaxanthin oxidation during fish storage and display. In fact a combination of organic Se with increased vitamin E supplementation could confer pigment stability during salmon storage.
Thomas & Buchanan (2006) observed that southern bluefin tuna fed diets fortified with vitamins C and E and Se had raised levels of these antioxidants in the muscle. High levels of these antioxidants resulted in an extension of the colour shelf life of sashimi grade tuna meat.
Lyons (1998) found that flesh colour, texture and pigment deposition improved in Atlantic salmon given Se-yeast.