Selenium as an Essential Nutrient

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Nonruminants played the key role in obtaining the first evidence that selenium was important in nutrition. These animals have been used to demonstrate that selenium is indeed an essential nutrient—one that must be included in the diet for supporting life. In independent discoveries in 1957, selenium was identified as the third factor (vitamin E and cystine had already been identified) active in preventing degeneration of the liver in rats (Schwarz and Foltz, 1957) and was shown to prevent exudative diathesis in chicks fed a torula yeast diet low in vitamin E (Patterson et al., 1957). These discoveries led to investigations with other species of animals. All the early work with selenium was done with diets containing some selenium and substantial unsaturated fat, and most of the studies revealed a relationship between vitamin E and selenium. Recently the use of synthetic amino acid diets extremely low in selenium with Japanese quail and chicks has shown that severe deficiency signs and death occur even in the presence of very high die tary levels of vitamin E (Thompson and Scott, 1969). Adding small quantities of selenium prevented all signs of deficiency.


A deficiency of selenium in the diets of rats results in necrotic liver degeneration. To produce this condition, Schwarz (1951) used a semi-purified diet containing torula yeast as the major source of protein. The diet contained a very low level of vitamin E and was deficient in amino acids containing sulfur. Adding either vitamin E or cystine to this diet prevented liver necrosis, as did selenium, referred to by Schwarz as Factor 3. Subsequent work suggested that the effectiveness of cystine may have been related to its incidental selenium content (Schwarz et al., 1959). In necrotic liver degeneration, no macroscopic changes in the liver are evident during the first 3 to 6 weeks that the rats are on a deficient diet. The time required for symptoms to occur depends on the strain used and probably on the initial content of selenium and vitamin E in the tissues of the rats (Schwarz, 1958). Before gross signs of liver necrosis appear, however, changes in the cytoplasm and mitochondria can be detected by electron microscopy. Death results in a few days after the microscopic appearance of liver necrosis. Although either vitamin E or selenium prevents liver necrosis in rats, supplementing the diet with selenium does not prevent other symptoms of vitamin E deficiency, such as peroxidation and discoloration of body fat, brown discoloration of uterus, depigmentation of incisors, in vitro hemolysis of erythrocytes, and impaired reproductive capacity of females (Christensen et al., 1958; Harris et al., 1958). However, McCoy and Weswig (1969) observed effects of selenium deficiency that were independent of vitamin E in the offspring of rats. Rats fed a low selenium ration containing torula yeast supplemented with 60 mg of ¿-a-tocopheryl acetate per kg grew and reproduced normally. Their offspring were almost hairless, grew more slowly, and failed to reproduce; but adding 0.1 ppm of selenium restored haircoat, growth, and reproductive ability. Selenium also appeared to be necessary for preventing eye discoloration.

Hurt, Cary, and Visek (1971) have further confirmed the essentiality of selenium for growth of rats. They depleted rats of selenium in one of two ways: by feeding a basal purified diet containing amino acids as the only nitrogen source; or by feeding females through pregnancy on a torula yeast diet, containing 0.012 ppm Se, and using their


FIGURE 2 Litter mate rats from females fed a diet containing 0.012 ppm of Se throughout pregnancy. The upper animal was fed the basal diet and the lower animal the same diet plus 0.5 ppm Se as selenomethionine for 25 days post-weaning at which time they weighed 82 g and 124 g, respectively. (Courtesy of W. J. Visek, Department of Animal Science, Cornell University, Ithaca, N.Y.)

young as experimental subjects. In either case, supplementation stimulated growth of the young rats (Figure 2).


Multiple necrotic degeneration of tissue is observed in mice fed a tor-ula yeast diet similar to that used for rats (DeWitt and Schwarz, 1958). Liver and kidney necrosis are evident, and there may be pancreatic dystrophy, degeneration of the skeletal muscle, and pronounced degeneration of the heart muscle. All these conditions induced by feeding a torula yeast diet can be prevented by either vitamin E or selenium.

In rabbits and guinea pigs, myopathy produced by feeding diets low in vitamin E and high in polyunsaturated fatty acids cannot be prevented by selenium. Rabbits fed a diet deficient in vitamin E develop a progressive muscular weakness that leads to death in 4 to 6 weeks.

Selenium is completely ineffective in preventing or retarding this nutritional disease (Draper, 1957; Hove et al., 1958). Whether rabbits might develop other deficiency signs as a result of selenium deprivation has not been established. In the studies in which myopathy was produced in rabbits, the level of selenium in the natural ingredients of the diets was high enough to prevent necrotic liver degeneration in rats. In guinea pigs, myopathy produced by feeding a diet low in vitamin E was not prevented by supplementing the diet with selenium (Seidel and Harper, 1960; Bonetti and Stirpe, 1963). The basal diets used in these studies probably contained selenium; so that the role of selenium in this species is not yet conclusively established.


Swine are also affected by a combined deficiency of vitamin E and selenium. When semipurified diets containing torula yeast and adequate levels of sulfur amino acids were fed to weanling pigs, the animals developed liver necrosis or hepatosis diaetetica and eventually died unless the diet was supplemented with vitamin E or selenium (Eggert et al., 1957). In other studies, liver necrosis and degeneration of cardiac muscle (Mulberry heart) and skeletal muscle were observed in pigs fed a torula yeast diet that was deficient in vitamin E (Pellegrini, 1958). These deficiency signs were prevented by supplementing the diet with vitamin E or selenium, but not with cystine. Grant and Thafvelin (1958) fed newly weaned pigs a hepa-tonecrogenic diet based on soybean meal and observed the effect of supplementing this diet with sodium selenite. All pigs fed the basal diet died between the twenty-second and forty-fifth days of the experiment. The pigs had liver necrosis, massive transudations, degeneration of skeletal and heart muscle, and deposits of ceroid pigment in the adipose tissue. Those supplemented with sodium selenite survived and had normal livers. However, degeneration of skeletal muscle and deposits of ceroid in the fat tissue occurred. Similar symptoms occurred in pigs fed a torula yeast diet deficient both in selenium and vitamin E (Ewan et al., 1969). Supplementing the diet with 0.5 ppm of selenium (selenite) or 100 ppm cf-a-tocopherol, or both, significantly reduced the incidence of mortality. Nutritional muscular dystrophy was also studied in pigs fed a diet of oats, barley, and cottonseed oil, all treated to reduce the vitamin E content (Orstadius et al., 1963). The presence of disease was determined by an elevated glutamic-oxaloacetic transaminase content of the plasma.

Either vitamin E or selenium inhibited elevation of this enzyme, but the best results were obtained with a combination of both nutrients, which suggested that vitamin E and selenium were acting synergisti-cally.

Field cases of hepatosis diaetetica observed in Michigan and Washington suggest that the diets used in these areas are low in selenium. Outbreaks of a disease in pigs, believed to be due to a selenium deficiency, have been observed in New Zealand (Hartley and Grant, 1961). Necropsy showed degeneration of the liver. Other conditions observed were generalized subcutaneous edema, pale skeletal musculature, accumulation of straw-colored fluid in the body cavity, and degeneration of the myocardium (Mulberry heart). Losses have been controlled by administering selenium.


Although there are no clear-cut experimental results with horses, field observations in New Zealand suggest that a selenium deficiency may lead to myopathy in this species (Dodd et al., 1960; Hartley and Grant, 1961). White muscle disease has been endemic in foals in New Zealand, and severely affected animals usually die. Upon autopsy, thick, firm layers of yellow-brown fat and many small hemorrhages are observed. The degenerated skeletal muscle has a watery appearance and is chalky white. The animals also lose hair. Although no control was maintained, no evidence of muscular dystrophy was observed in 65 foals injected with sodium selenate at birth and 10 days of age, whereas considerable dystrophy had been observed in the same area in previous years. Serum selenium levels for horses have been reported by Stowe (1967).


A combined deficiency of selenium and vitamin E in chicks results in exudative diathesis (Figure 3). This disease can be prevented by supplementing the diets with vitamin E or selenium. If amino acid diets very low in selenium are used, chicks show poor growth, poor feathering, and fibrotic degeneration of the pancreas (Thompson and Scott, 1970). Death usually occurs following markedly decreased absorption of lipids, including vitamin E. The pancreatic degeneration results in a decrease in pancreatic and intestinal lipase, which causes a failure to digest fat. Under these conditions, bile flow dim-

Bile Salt Fat Absorption
FIGURE 3 Exudative diathesis, a selenium-responsive disease, in the chick. (Courtesy M. L. Scott, Department of Poultry Science, Cornell University, Ithaca, New York.)

inishes markedly. In the absence of bile and of monoglycerides in the intestinal lumen, there is a failure of lipid-bile salt micelle formation, which in turn impairs the absorption of vitamin E. Thompson and Scott showed that the addition to the basal diet of free fatty acids, monoglycerides, and bile salts improved the absorption of vitamin E and survival during the experimental period of 4 weeks. It prevented exudative diathesis, but it did not prevent the degenerative changes of the pancreas. The selenium requirement for prevention of pancreatic degeneration was found to depend on the vitamin E level in the diet. With very high dietary vitamin E levels (> 100 IU per kg), as little as 0.01 mg of selenium-as sodium selenite-per kg of diet prevented pancreatic degeneration. However, when the vitamin E content of the diet was at nearer normal levels (10-15 IU per kg), 0.02-0.04 mg of selenium per kg of diet was required.

It was observed in these experiments that exudative diathesis did not occur as long as some vitamin E was being absorbed. Thus, either vitamin E or selenium in the diet will prevent exudative diathesis, but a good blood level of vitamin E also helps to preserve the selenium in the body tissues, thereby reducing the dietary level of selenium required to protect the pancreas. Vitamin E spares the selenium requirement, and, conversely, selenium enhances absorption of a-tocopherol, thereby reducing the dietary requirement for vitamin E.

Exudative diathesis is characterized by an escape of fluids from capillaries, particularly under the skin on the breast and abdomen. Small hemorrhages are evident in the tissues near the edematous areas, and because of degeneration of the hemoglobin, the abdominal wall and other regions of the bird take on a greenish-blue appearance. In addition to edema and hemorrhage, hematological changes are evident in the chick. Anemia occurs, as well as a reduced concentration of serum protein. The level of albumin is greatly reduced, and globulins tend to increase, resulting in a markedly lowered albumin-globulin ratio (Goldstein and Scott, 1956; Walter et al, 1963). Signs of this disease will appear from 2 to 3 weeks after chicks are placed on a diet deficient in both vitamin E and selenium (Scott et al, 1955). The disease invariably leads to death if the use of such a diet is continued.

A diet low in sulfur amino acids and selenium results in myopathy (Calvert et al, 1962). White striations are observed in the breast muscle. Adding, methionine, cystine, or vitamin E prevents myopathy in chicks, but selenium is only partly effective (Nesheim and Scott, 1961). The effectiveness of methionine or cystine is not due to selenium contamination. Vitamin E and selenium appear to act synergistically in preventing this disease (Calvert et al., 1962). Combined low levels of these two nutrients prevent the condition, but the same level of either one will not prevent the disease.

Encephalomalacia, another disease caused by deficiency of vitamin E, can be produced in chicks by feeding a diet high in polyunsaturated fatty acids. This condition is prevented by supplementing the diet with vitamin E or a synthetic antioxidant; neither selenium nor sulfur amino acids (Dam et al, 1957) are effective against it, although some evidence has been obtained that selenium delays the onset of the disease (Century and Horwitt, 1964; Jenkins et al., 1965).

It appears that between 0.05 and 0.08 mg of selenium, as sodium selenite, is needed per kg of diet to prevent exudative diathesis in chicks. The amount depends on the type of diet used and the vitamin E level. Using a semipurified diet containing torula yeast, Nesheim and Scott (1958) observed that adding 0.08 mg of selenium per kg of diet prevented exudative diathesis in White Leghorn chicks. They also observed a growth response to selenium in the presence of a high level of vitamin E, providing the first evidence that selenium is required for maximum growth rate in chicks independent of vitamin E.

Field cases of exudative diathesis and myopathy in chicks have been seen in the United States. Several outbreaks of typical exudative diathesis have been observed in flocks in New Zealand (Hartley and Grant, 1961), and necropsy showed degeneration of the breast and, occasionally, degeneration of the gizzard musculature. White muscle disease in pullets 4 to 6 months old has also been observed in New Zealand, in spite of widespread use of wheat-germ meal and synthetic vitamin E (Salisbury et al., 1962). These conditions have been prevented and controlled, however, by adding selenium to the drinking water.

Although a vitamin E deficiency in chicken breeder hens can readily be developed, as evidenced by reduced hatchability of fertile eggs, no evidence has been obtained that selenium can substitute for vitamin E as a means of remedying the deficiency. Hens were fed semipurified diets containing torula yeast for several weeks; no increase in rate of egg production, fertility, or hatchability of fertile eggs was obtained by adding 1 mg of selenium per kg of diet (Jensen and McGinnis, 1960). The hens used in these studies were fed regular stock rations during the growing period, and considerable selenium may have accumulated in their tissues before they were placed on the dietary treatments. In New Zealand, congenital white muscle disease has been observed in newly hatched chicks (Salisbury et al., 1962).


Manifestations of a combined vitamin E and selenium deficiency in turkey poults differ somewhat from those in chicks. Although a mild form of exudative diathesis has been reported in turkey poults (Creech et al., 1957; Rahman et al., 1960), the condition is not nearly as severe as that observed in chicks. Excess pericardial fluid is observed in some poults, but in many poults exhibiting other evidence of a selenium deficiency, little or no edema is observed (Walter and Jensen, 1963). Hemorrhaging, also, is not as extensive in turkey poults as in chicks with a selenium deficiency. Some hemorrhaging, varying in severity, was observed, particularly on the thighs, in about 25 percent of the turkeys fed a low-selenium diet (Walter and Jensen, 1963). The most characteristic sign of selenium deficiency in poults is a degeneration of the gizzard musculature. White striation in the breast musculature is also observed, but only 25-50 percent of the poults will have myopathy in this area, whereas almost 100 percent have degeneration of the gizzard. Degeneration of heart muscle is also observed in turkey poults (Scott et al, 1967). In addition to myopathy, anemia accompanied by a change in the serum proteins occurs in turkey poults fed a low-selenium diet (Walter and Jensen, 1963). The albumin level is reduced and globulins increase, resulting in a marked lowering of the albumin-globulin ratio. Serum glutamic-oxalacetic transaminase levels are elevated in the blood of selenium-deficient poults.

In contrast to the chicken, myopathy observed in the gizzard, heart, and breast of turkey poults is not influenced by the level of methionine or cystine in the diet, and these myopathies are prevented by selenium. Field outbreaks of selenium deficiency in turkey poults have been observed in the United States (Scott et al, 1967). Poults grew poorly, had a high mortality rate, and showed severe hyaline degeneration of the gizzard musculature. Myopathy in turkeys appears to be primarily a selenium-responsive disease, since degeneration of the gizzard is observed even in the presence of supplemental vitamin E. Poults fed a semipurified diet containing torula yeast had a 13 percent incidence of gizzard myopathy even when supplemented with 20 IU of vitamin E per kg of diet (Walter and Jensen, 1964).

Although vitamin E deficiency can readily be produced in turkey breeder hens, no evidence has been obtained that selenium can substitute for the function of vitamin E in reproduction (Jensen, 1968a).


In Japanese quail (Coturnix coturnix), the sign of selenium deficiency appears to be a wasting of the entire body, as evidenced by an extremely thin breast (Scott and Thompson, 1968). Poor feathering also occurs. Impaired reproduction was demonstrated in quail that had been fed a diet low in both selenium and vitamin E from 1 day of age to maturity (Jensen, 1968b). Rates of egg production and fertility were not affected by the deficiency, but hatchability of fertile eggs was markedly reduced, and viability of both the adult females and the newly hatched quail was reduced. Either selenium or vitamin E prevented the impaired reproduction. Quail hatched from eggs of hens fed the basal diet were extremely weak, and most of the quail were prostrate in the hatching trays. Most of the newly hatched quail had a peculiar posture, in which the legs were extended posteriorly, and many of them had the legs extended upward to give a "rocking chair" appearance. A high incidence of gizzard myopathy was observed in the young quail.

Scott and Thompson (1968) demonstrated that selenium is an essential element for this species. They formulated a purified diet containing amino acids as the only source of nitrogen, which contained 0.002-0.005 mg of selenium per kg of diet. This value is considerably lower than that which can be obtained by using intact protein such as torula yeast. To further ensure the development of a selenium deficiency, Scott and Thompson (1968) fed purified diets low in selenium to the breeding quail. When the diet was fed to quail chicks, none of the quail survived to 25 days of age unless the diet was supplemented with selenium. Even in the presence of 100 mg of d-a-tocopheryl acetate per kg of diet, all the quail died in the absence of dietary selenium. Fairly good viability was obtained when the diet was supplemented with selenium, and there were no signs of disease. The results of this study established selenium as an essential element for life.



Soon after evidence was provided that selenium, at extremely low dietary levels, performed a useful function in nutrition, it was used successfully in treating white muscle disease (WMD), a myopathy that occurs in young ruminants (Muthef al., 1958;Hogue, 1958).

The etiology and pathologic changes of WMD have been described in detail by Muth (1955, 1963). Briefly stated, this disorder most commonly occurs in young calves or lambs born to dams fed a ration that is extremely low in its selenium content-about 0.02 ppm in the dry matter (Oldfield et al., 1963). Such dietary levels of selenium may result from a simple deficiency of the element in the soil on which feed forages are grown (see "Distribution of Selenium," p. 30), or they may result from the inefficiency with which certain forage plants draw selenium from the soil (Hamilton and Beath, 1963). A reason for the prevalence of WMD among cattle and sheep may be that these, more than any other domestic species, are likely to consume such native forages as virtually their entire diet. Moreover, as pointed out by Cousins and Cairney (1961), reduction of selenium to less readily available forms takes place in ruminants through the action of rumen microflora. In some cases, selenium deficiency in animals may be mediated through some interference in selenium uptake by plants, perhaps through application of gypsum as a soil amendment (Schubert et al, 1961; Hartley and Grant, 1961). The disease gets its common name from a lightening in the color of affected muscles (Figure 4), which may vary considerably from a slight bleaching to a distinct calcification often appearing as stria-tions in skeletal muscle. Both skeletal and heart muscles are commonly affected. White muscle disease or a similar symptomatology has been reported in numerous countries other than the United States, including Australia (Gardiner, 1962), Bulgaria (Natscheff etal., 1963), Canada (Schofield, 1953), Finland (Oksanen, 1965), Italy (Chiatti, 1964), Japan (Goto and Fujimoto, 1961), New Zealand (Drake etal., 1959), Norway (Ribe, 1963), Russia (Naumow, 1955), Scotland (Sharman et al, 1959), South Africa (Tustin, 1959), and Sweden (Lilleengen, 1944). Thus, it appears that the condition is widespread and well-recognized and that it is found in the major livestock-producing countries of the world.

FIGURE 4 Leg of lamb showing typical lesions of white muscle disease, a prominent selenium-responsive condition in young ruminants. Damage to skeletal muscles, as shown, may severely impair locomotion; similar damage in heart muscle may cause death. (Courtesy O. H. Muth, Department of Veterinary Medicine, Oregon State University, Corvallis.)

The efficiency of selenium in preventing or curing WMD in lambs and calves is well documented. In Oregon, 0.1 ppm selenium, as Na2Se03, in low-selenium diets of pregnant ewes consistently prevented WMD in their lambs (Muth et al., 1961). Supplementing the maternal ration with vitamin E was ineffectual. The diet consisted of Ladino clover or alfalfa hays grown on selenium-deficient soils. It was fed with small amounts of ground oats, which served as a carrier for the diet supplements. Similar studies at the University of Nevada, which also involved "natural" diet ingredients, confirmed the prenatal protective effect of selenium-supplemented ewes' diets (Kuttler and Marble, 1960). Cornell workers (Hintz and Hogue, 1964) reported that adding 0.17 ppm selenium, as Na2 Se03, to myo-pathogenic diets fed to lactating ewes had no significant effect on clinical incidence of nutritional myopathy but did reduce the number of lambs showing high levels of serum glutamate-oxalacetate transaminase (SG-OT), which are indicative of muscle damage (Blincoe and Dye, 1958). In New Zealand, ewes were given single oral doses of 5 mg of selenium as sodium selenate (Drake et al., 1960). As a result, incidence of WMD in the lambs was significantly reduced. In this work, as in the Oregon studies, supplementation with vitamin E was ineffective in reducing incidence of WMD. In a number of other experiments, the incidence of WMD in lambs was reduced by administering low levels of selenium, orally or parenterally, to pregnant ewes (Oksanen, 1965; Young et al., 1961; Setchell, 1962; Setchell et al., 1962; Hamdy et al., 1963). Selenium has also been given prophylactically to lambs born to ewes fed a WMD-causative diet, with considerable success. Lagace (1961), for example, obtained highly satisfactory results with 1 mg of Na2 Se03 given sub-cutaneously to 8-week old lambs.

Evidence relating selenium to prevention of myopathy of cattle is less plentiful, although similarities in the pathology of WM D in cattle and sheep imply a like response. Field trials conducted by Hartley and Grant (1961) in New Zealand showed that dairy and beef calves raised on pumice soil pastures responded favorably to subcutaneous injection of 20 mg of selenium given at 4-month intervals. Canadian experiments showed that selenium treatment of pregnant cows fed low-selenium hay prevented WMD in their calves only when it was given concurrently with vitamin E (Nelson et al, 1964). The dosage of selenium used in this work (0.05 mg per kg of body weight) was lower, however, than that usually given successfully to sheep. The level of c?-a-tocopheryl acetate used was equivalent to 2.3 IU per kg of body weight. White muscle disease in Califor-

nia calves was prevented by injecting vitamin E plus selenium after vitamin E alone had proved ineffective (Schultz, 1960). Oksanen (1965) has reported on field trials conducted in the Seinájoki district of Finland, where oral administration of 100 mg of Na2 Se03 per 30 kg of body weight to pregnant cows prevented WMD in their calves, as measured both by absence of clinical signs and by low levels of SG-OT (<200 Sigma-Fraenkel units).

In cattle and sheep, both the incidence of WMD and the responses to administration of selenium may have been influenced by extraneous factors, especially in the field trials reported. Such factors include metabolic stresses imposed by low environmental temperatures (Gardiner, 1962), by parasitism, and by muscular activity (Young and Keeler, 1962); interference by selenium-antagonists in the forages involved (Hogue et al., 1962; Cartan and Swingle, 1959); and loss of appetite, perhaps induced by cobalt deficiency. Implications of these factors are discussed in a review article by Allaway and Hodgson (1964).


A logical extension of the study of the effects of selenium on myopathy was an inquiry into its effects on growth per se. It is, of course, difficult in many cases to separate completely these two kinds of effects. A review of some of the Oregon data suggested that prepartum administration of selenium to ewes increased the weight gains of their lambs (Oldfleld et al., 1960). Similar experiences have been reported from New Zealand, where McLean, et al. (1959) listed growth responses of 12-40 percent over controls by lambs receiving 1.0 mg of selenium every 10 days, and Jolly (1960) indicated an optimum dosage of 2.5-5.0 mg of selenium per lamb, once monthly. In Australia, experiences varied. Skerman (1962), in Victoria, reported a significant weight response to 5.0 mg of selenium given orally in aqueous solution at 1- to 2-week intervals and observed that muscular dystrophy had not been diagnosed in the flocks concerned. In New South Wales, on the other hand, Setchell et al. (1962) noted "significant but slight" growth response to selenium in lambs and subsequently variations ranging from significant growth increases to one significant decrease (Setchell, 1962); weight gains of lambs were not significantly increased by oral dosage of 5.0 mg of selenium per head monthly during the pasture season. Montana investigators found that weights of lambs were not increased by either prepartum administration of selenium to the gestating ewes or postpartum administration to the lambs themselves; however, they did observe increases in lambs with WMD (Young and Hawkins, 1962). It is unfortunate that precise evaluation of the selenium status of the feeds and the animals is unavailable in some of these reports. There is some reason to presume that growth responses to selenium occur when animals are fed a selenium-deficient diet or are born into selenium-deficiency situations and that the responses are lacking when dietary selenium is adequate. This concept is strengthened by field trials in Scotland conducted under Blaxter's (1962) direction, which involved 4,448 lambs on 76 farms. Half of the lambs were given 3.0 mg of selenium, as selenate, by subcutaneous injection at 4-week intervals; the other half were untreated controls. Overall response showed that selenium-treated lambs gained an average of 0.81 lb more than controls over a 3- to 4-month period. However, the positive growth response averaged 1.72 ± 0.32 lb on 31 farms, where the selenium content of the diet was presumed to be low, and 0.16 ± 0.34 lb on 27 farms, where it was presumed to be high. Wright (1956b) examined tissues from fast- and slow-growing lambs having a common dietary history, following injection of 75 Se. The fast-growing lambs accumulated much more radioselenium in the kidney and pituitary than the slow-growing lambs, but not in the muscle, pancreas, abomasum, or liver.

Again, reports on cattle are less plentiful. Burroughs et al. (1963), in Iowa, studied responses of feeder cattle to additions of 0.05-0.10 ppm of selenium, as Na2 Se03, to high-concentrate rations. Cattle fed supplemental selenium gained significantly more than untreated controls over a 141-day period. In New Zealand, Hartley's (1961) laboratory recorded that growth of Aberdeen Angus calves treated with selenium increased 50 percent over controls.

Specific effects of selenium on growth of wool and hair have been investigated by Hartley and Grant (1961) and by Slen et al (1961), who noted that supplementing diets of sheep with subtoxic amounts of selenium increased total weight of the fleece and thickness of the wool fiber. Wool fibers that had been weakened by reduction of cystine cross-linkages to cystine residues were restrengthened when treated in vitro with selenious acid, apparently because of selenium-containing cross-linkages (Holker and Speakman, 1958).


Hartley et al (1960) first drew attention to beneficial effects of selenium in correcting certain cases of poor reproductive performance, expressed as low lambing percentages, in sheep. They noted that numbers of barren ewes were higher on properties where WMD had been observed than on those where it had not. Subsequently, half the ewes on three properties that had experienced abnormally low lambing percentages, as well as severe selenium-responsive unthrifti-ness, were treated orally with 5 mg of selenium, as Na2 Se03, at monthly intervals, and their productivity was compared with that of the untreated ewes (Hartley and Grant, 1961). In addition to completely controlling WMD, the selenium treatment increased lambing percentages from about 62 percent to about 94 percent. Continued investigation showed that oral dosing of ewes once, prior to mating, with 5 mg of selenium, as selenite, was sufficient to substantially increase lambing percentages. Hill et al. (1969) have suggested that fertility, as measured by incidence of barrenness in 2-year-old ewes, was unaffected by selenium therapy, but that fecundity, as measured by twinning, was significantly increased. They speculated that the increased twinning was a secondary response to the increased weight of selenium-treated animals, rather than a direct physiological response to selenium. Evidence that selenium deficiency impairs testicular function in rats has been provided by Wu et al. (1969). Data are unavailable on effects of selenium on fertility in cattle.


Although most of the biological benefits contributed to ruminants by administering appropriate, low levels of selenium can be interpreted as effects on growth or reproduction, certain other effects appear to merit identification. One of these, a therapeutic effect on diarrhea following selenium treatment in lambs and calves, has been reviewed by Wolf et al. (1963). In California trials, Kendall (1960) successfully treated cattle with selenium for scours that had not responded to antibiotics or anthelmintics. Moreover, a dosage similar to that used by Kendall (44 Mg of selenium per kg in a mixed preparation of selenium and vitamin E) was reported to be effective in clearing up a persistent diarrhea in cattle, and improved growth resulted (Smithcors, 1962). Hartley and Grant (1961) mentioned a beneficial response to selenium by beef and dairy calves in New Zealand that had exhibited severe and rapidly progressive unthriftiness associated with profuse diarrhea. The same authors and others have noted virtual elimination of periodontal disease in sheep (characterized by loosening and shedding permanent premolars and molars and sometimes incisors) by treatment with selenium

(Hartley and Grant, 1961; McLean et al., 1959; MacKinnon, 1959).

English workers (Trinder et al.y 1969) investigated the effects of selenium therapy, in a low-selenium diet situation, on the incidence of retained placenta. They found that parenteral administration of vitamin E and potassium selenate 1 month prepartum greatly reduced retention of the placentas in a dairy herd, but that potassium selenate was less effective when given alone.

Consideration of the data cited, which by no means exhausts the literature on the subject, suggests an extensive and important biochemical involvement for selenium in ruminant metabolism.


Schwarz (1965b) reported that administration of selenium to two children with kwashiorkor stimulated growth. This was the first such exploratory work in humans. Similar preliminary results were reported by Majaj and Hopkins (1966) after selenium as sodium selenite was administered to three infants with kwashiorkor. The latter work also related selenium to response of reticulocytes.

Studies by Burk et al. (1967) with children in Guatemala indicated that in active kwashiorkor the blood of children contained only about half as much selenium as did that of children who had been treated by diet and recovered from kwashiorkor. The levels of selenium in the blood of untreated and treated children averaged 0.08 and 0.14 ppm, respectively—in good agreement with Allaway et al. ( 1968).

Majaj and Hopkins (1966) reported that typical American diets analyzed by neutron activation procedures had less than 0.1 ppm of selenium. One finds selenium in all foods and in all animal tissues analyzed (Muth et al., 1967a). Well-balanced rations for animals, for example, frequently contain 0.1-0.5 ppm of selenium. Food processing would be expected to cause some loss of selenium, chiefly by volatilization. Thus, the report of less than 0.1 ppm of selenium in complete human diets is surprising and calls for more analyses of complete diets.

There are many unknowns regarding the role that selenium may play in human health and disease. The first to resolve is the level and range of selenium intake by humans. Generally, meat and fish products appear to be the most consistently reliable sources, and grain products appear to be more variable.

Liebscher and Smith ( 1968) reported average concentrations of selenium in vacuum-dried human liver of 2.34 ppm and heart of 1.17 ppm.

Within limits, levels of selenium in tissues, milk, eggs, and hair of animals directly reflect levels of selenium in the ration. Thus, dried skim milk from cows on diets low and high in selenium contained 0.06 and 0.28 ppm of selenium, respectively (Mathias et al., 1967). Similarly, eggs from hens on a diet low in selenium, a diet with 2 ppm of selenium added, and a diet with 8 ppm of selenium added contained, respectively, 0.12, 0.74, and 1.04 ppm of selenium (Thapar et al., 1969).

In seleniferous areas, considerable ranges have been reported in the selenium content of various foods (Table 1) (see "Selenium in Animal Tissues in Relation to Feed Composition," p. 39). A narrower range of variation occurred in wheat from nonseleniferous areas (Robinson, 1936), whereas in low-selenium areas, low selenium content in cow's milk (Ludwig and Bibby, 1969; Hadjimarkos and Bonhorst, 1961) and in human blood (Allaway et al., 1968) reflects the ambient shortage of the element.

The values as given in Table 1 may be reasonably representative of an area that is not recognized as either high or low in selenium.

Selenium has been found in all human tissues analyzed to date. The levels found are comparable to levels of selenium in tissues of wild and domestic animals, with kidney highest.

TABLE 1 Average Values of Selenium in Various Dried Foods*


Selenium (ppm)


0.07-1.01 0.22-0.31 0.30-0.58 0.47-0.88 0.19-0.35 0.31-0.35 3.53-3.97

Meat (beef, pork) Liver (beef, pork) Heart (beef, pork) Lungs (beef, pork) Spleen (beef, pork) Kidney (beef, pork) Whole milk

Whole egg

Fish (freshwater) Fish (marine)

"Study conducted in Germany (Oelschaeger and Menke, 1969).

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