5.2 Essential Minerals for Finfish
5.2.9. Selenium 1. Functions and Metabolism
The essentiality of dietary selenium for several animal species and its close metabolic relations have been well recognized. The biochemical role
of Se puzzled workers until the discovery that Se is an integral part of glu- tathione peroxidase (Rostrucket al.,1973). Glutathione peroxidase activity in erythrocytes, plasma, and other tissues decreases in direct proportion to the reduction in Se intake and is believed to account for the manifestation of Se deficiency in terrestrial animals. Glutathione peroxidase destroys hydro- gen peroxide and hydroperoxides by using reducing equivalents from glu- tathione, thereby protecting cells and membranes against oxidative damage.
The exact physiological role of this enzyme is not clear because catalase and non-Se-dependent glutathione peroxidase also remove hydroperoxides. Se- lenium also has other biochemical roles (Shamberger, 1984). The protective effects of Se and Se compounds against the toxicity of heavy metals such as cadmium and mercury are widely recognized.
Prior to the discovery of the essential role of Se, its toxic properties were well recognized. Certain geographic areas are seleniferous and produce plants with a high Se content. Animals grazing on these alkali pastures show several toxicity syndromes such as blind staggers. The signs of Se toxic- ity are extensively described by Underwood (1977). High levels of Se exert their toxic effects in animals probably through competition with sulfur com- pounds or a strong affinity for sulfur in the formation of sulfur–selenium complexes. However, the precise biochemical mechanism involved in Se toxicity remains to be established. Diets high in sulfur or protein provide some protection against Se toxicity. A review by Shamberger (1984) provides a detailed account of developments in Se metabolism.
The absorption, distribution, and excretion of dietary and waterborne Se in salmonids have been investigated. Low concentrations of Se are found extensively in aquatic ecosystems. The uptake of Se as selenite across gills is very efficient at low waterborne concentrations (Hodsonet al.,1980). The toxicity of both dietary and waterborne Se has been experimentally pro- duced (Hodson and Hilton, 1983). Liver and kidneys play important roles in the excretory process of Se in trout, in which the major excretory routes appear to be the gills and urine. A correlation between liver Se and Cu has been observed in rainbow trout and Atlantic salmon (reviewed by Hilton, 1989). Selenium and Cu interactions reduce the metabolically active form of these elements by the formation of Se–Cu complexes.
5.2.9.2. Deficiency
Selenium deficiency causes growth depression in rainbow trout (Hilton et al., 1980), carp (Satoh et al., 1983b), and catfish (Gatlin and Wilson, 1984c), but the Se deprivation alone does not produce any pathological sign in these fish. Both Se and vitamin E are required to prevent muscular dystrophy in Atlantic salmon (Postonet al.,1976) and exudative diathesis in rainbow trout (Bellet al.,1985). Glutathione peroxidase activity in plasma
and liver decreases during Se deficiency (Postonet al.,1976; Hiltonet al., 1980; Bellet al.,1985; Gatlin and Wilson, 1986c).
Selenium toxicity occurs in rainbow trout and catfish when the dietary Se exceeds 13 and 15 mg/kg dry feed, respectively (Hilton et al., 1980;
Gatlin and Wilson, 1984c). Reduced growth, poor feed efficiency, and high mortality are the major effects of Se toxicity. Trout reared on high-Se diets (10 mg/kg) also show renal calcinosis (Hilton and Hodson, 1983).
5.2.9.3. Requirement
The minimum selenium requirement of fish varies with the form of Se ingested, availability of Se in the diet, vitamin E content of the diet, and con- centration of waterborne Se. The Se requirement determined on the basis of optimum growth and maximal plasma glutathione peroxidase activity is estimated to be 0.15 to 0.38 mg Se/kg diet for rainbow trout and 0.25 mg Se/kg diet for channel catfish (Hiltonet al.,1980; Gatlin and Wilson, 1984c).
The Se requirements of other finfish are not known, but coho salmon reared on diets containing 5–8 mg/kg selenium had better seawater survival than those fed only 1 mg/kg in the dry diet (Feltonet al.,1996).
5.2.9.4. Sources
Selenium is widely distributed at low concentrations in freshwater (0.2–
10μg/liter) and seawater (approximately 0.09μg/liter) (National Research Council, 1976). It also occurs naturally in foods and feedstuffs in organic complexes, primarily in the form of selenomethionine, selenium–methyl- selenomethionine, selenocystine, and selenocysteine. The selenium content of feedstuffs of plant origin varies according to the level and biological availability of Se in the soil at the various geographical locations. A detailed list of the Se content of food and feedstuffs is summarized by Lo and Sandi (1980) and Scott (1973). Fish meals and marine by-products represent the best natural sources of Se among the common feedstuffs for fish. However, certain fish meals, e.g., tuna may have a poor biological availability because of heavy metal complexing of Se. Selenium present in fish meal has a low digestibility, whereas selenomethionine is highly digestible (Bell and Cowey, 1989).
Common Se supplements include selenite, selenate, selenomethionine, selenium–methylselenomethionine, selenocystine, and selenocysteine. Mo- nogastric animal nutrition studies have demonstrated the following relative availability of Se in pure compounds: selenite>selenate>selenomethio- nine>selenide>elemental selenium. In several countries there are regu- lations to limit Se supplementation in fish and animal feeds, and generally the limit is about 0.1 mg Se/kg in aquatic animal feeds.
5.2.10. Cobalt, Chromium, and Other Trace Elements 5.2.10.1. Cobalt
The biological function of cobalt relates to its role as a component of vitamin B12. Approximately 4.5% of the molecular weight of B12(cyano- cobalamin) is contributed by elemental cobalt. Cobalt is of particular sig- nificance in ruminant nutrition, where it is used solely in the synthesis of the vitamin B12 molecule by rumen microflora. Most animals depend on microorganisms for their supply of vitamin B12. Certain algae also contain Co (reviewed by Castellet al.,1986). The marine rotiferBranchionus plicatilis is reported to have a definite requirement for vitamin B12(Scott, 1981).
Extensive Russian studies on pond culture of carp have demonstrated that the addition of cobalt chloride and/or cobalt nitrate to the feed or cobalt chloride to the water of fish ponds enhances growth and hemoglobin formation in carp (reviewed by Castellet al.,1986). Kashiwadaet al.(1970) isolated bacteria from the intestinal tract of carp that produced vitamin B12 in vitro. Removal of Co from the diet of catfish significantly reduces intestinal synthesis of vitamin B12(Limsuwan and Lovell, 1981). Most of the Co detected in maturing Atlantic salmon ovaries is present as part of vitamin B12( Julshamn and Braekkan, 1975). Some uptake of Co occurs in rainbow trout eggs during embryonic development (Kuenzeet al.,1978).
5.2.10.2. Chromium
Chromium is an essential element for animals and humans. It exists com- monly in the oxidation states Cr(II), Cr(III), and Cr(VI). Chromium(III) is required for normal carbohydrate and lipid metabolism. The ability of Cr to form coordination compounds and chelates is an important chemical characteristic that makes this essential metal available to living organisms.
Chromium is found in foods as inorganic Cr(III) and as part of a biolog- ically active molecule. Although the exact structure of the biologically ac- tive form(s) is not fully characterized, the active molecule appears to be a dinicotinatochromium(III) complex, stabilized with glutathione or its con- stituent amino acids (Toepferet al.,1977).
The biological function of Cr is closely related to that of insulin. Most chromium-potentiated reactions are also insulin dependent. In humans, Cr potentiates the action of insulinin vitroandin vivo; maximalin vitroactivity requires a chemical form termed the glucose tolerance factor and tenta- tively identified as a Cr–nicotinic acid complex (Mertz, 1993). Chromium supplementation in carp diet improved the glucose utilization, probably by modulation of endogenous insulin activity (Hertzet al.,1989), however, glucose utilization was not affected by dietary Cr in channel catfish (Ng and Wilson, 1997). Supplementation of the tilapia diet containing glucose
with chromic oxide improved growth, energy retention, and liver glycogen depostion (Shiau and Chen, 1993).
To date, the only study with fish on the effects of dietary Cr(III) did not show any deficiency signs or a change in tissue distribution of rainbow trout fed a low-chromium purified diet (Tacon and Beveridge, 1982). No attempts have been made to demonstrate the dietary toxicity of Cr(III).
Toxicological effects of Cr(VI) in brook trout have been observed (Benoit, 1976). Common sources of Cr feed supplements include chromic chloride, high-Cr-yeast, Cr nicotinate, and Cr picolinate.
5.2.10.3. Other Trace Elements
Information on the dietary requirement of other trace elements is lim- ited. Pageet al.(1978) found that sulfate failed to promote growth or provide the requirements of sulfur amino acids in rainbow trout. George (1970) in- dicated that boron and/or molybdenum supplementation of the carp diet improved growth and survival. Increased dietary intake of fluoride enhances fluoride accumulation in the vertebrae of rainbow trout (Tiewset al.,1982).
There is minimal evidence that boron is essential to organisms other than vascular plants. A role of boron in embryonic growth of rainbow trout has been demonstrated (Eckhert, 1998). Deficiency signs and requirements of these elements remain to be established.
5.3