Perspectives on selenium nutrition in horses
Published: February 14, 2007
By: LAURIE LAWRENCE - University of Kentucky (Courtesy of Alltech Inc.)
Knowledge regarding selenium nutrition in horses lags far behind other livestock species and humans, especially in regard to health and optimal immune function. In dairy cattle, there is a well-accepted relationship between selenium status and udder health. In humans, there are active research efforts relating selenium to decreased cancer risk and enhanced immune function. In the horse, there are relatively clear data linking selenium deficiency to nutritional muscular dystrophy in foals, but information regarding optimal levels of selenium intake for optimal health status in all classes of horses is lacking. Many of the beneficial responses to selenium supplementation in humans and other animals may have application to horses.
In particular, the relationship of selenium intake to health and production responses in horses should be considered in view of the expanded understanding of the biological functions of selenium. It is of note that most of the research on selenium in horses was performed prior to 1990, when only the function of glutathione peroxidase was known. Currently, there are several selenoproteins of known function in mammals, and it has been suggested that dozens of others exist. To date, the effect of selenium nutrition on these selenoproteins and their biological role in horses has not been investigated.
Biological function of selenium
Selenium is both a toxic element and a required nutrient. In horses, the best recognized deficiency sign is muscular dystrophy, or white muscle disease, in foals. Additional deficiency signs have been identified in other species including a cardiomyopathy in humans, liver necrosis in pigs and exudative diathesis in chicks. Until the early 1970s when glutathione peroxidase (GSHPx) was identified as a selenium containing enzyme, the biological function of selenium was unknown. GSH-Px functions in the reduction of hydroperoxides, and thus is an important component of cellular antioxidant mechanisms. GSH-Px activity is observed to be low in selenium deficiency, and many of the manifestations of selenium deficiencies are related to increased oxidative damage.
After the initial research identified GSH-Px as a selenoprotein, four specific enzymes were categorized. These include GSH-Px 1 (the initial cytosolic GSH-Px); GSH-Px 2, which is present in plasma; GSH-Px 3, which is associated with the gastrointestinal tract and GSH-Px 4, which is characterized as a phospholipid-hydroperoxide glutathione peroxidase (Allan et al., 1999). GSH-Px 4 is associated with membrane-bound lipids and thus may be the mechanism through which selenium and vitamin E function synergistically. In addition, it has been suggested that this is the means through which selenium affects leukotriene synthesis (Wolfram, 1999).
Selenium has now been associated with selenoproteins that have other essential functions. Type 1 iodothyronine deiodinase (5' DI), which is responsible for the conversion of thyroxin to tri-iodothyronine is also a selenium containing enzyme. Two other deiodinases important in thyroid hormone metabolism also contain selenium. In addition, two thioredoxin reductases are now known to be selenoproteins. Other selenoproteins that are recognized, but do not have well accepted biochemical roles are selenoprotein P and selenoprotein W. Selenoprotein P is found in relatively high concentrations in plasma, and selenoprotein W is found in muscle.
EFFECT OF SELENIUM INTAKE ON SELENOPROTEINS
The effect of dietary selenium status varies with the individual selenoprotein, the specie of animal and the tissue being evaluated. It has been proposed that there is a hierarchy for selenium supply within the body and/or for different selenoproteins. When rats were fed a selenium deficient diet, selenium content was reduced by 50% in muscle and 91% in liver, compared to control animals. By comparison, the selenium content of the testes was not affected by the selenium deficiency (Behne et al., 1982). When selenium retention by deficient rats was measured, the rate of retention by the testes was much higher than in liver.
Although Yeh et al. (1997b) reported a decrease in testes selenium concentration in rats fed a deficient diet, the extent of the decrease was much less than in muscle or spleen. These authors also reported that GSH-Px activity was decreased to a much greater extent by selenium deficiency in muscle and plasma than in testes.
Marin-Guzman et al. (1997) reported that selenium deficiency decreased GSH-Px activity in the testes of growing boars, but the extent of the decrease was less than in the liver or serum. Selenium deficiency did not affect testicular weight or semen quality (volume, sperm number, etc), but fertilization rate was decreased. Decreased fertility of sperm from the deficient boars may have been related to decreased GSH-Px activity in sperm and seminal plasma. The thyroid is another tissue with a high selenium content and may be superior at retaining selenium in the face of a deficiency (Kohrle, 1999).
Brain tissue also appears to be resistant to effects of selenium deficiency (Yeh et al., 1997a; Yeh et al., 1997b). Consequently, it appears that a preferential conservation of selenium in reproductive organs and brain tissue may occur in selenium deficiency. Conversely, liver and muscle tissue are susceptible to depletion in periods of inadequate selenium supply.
Within a tissue, certain selenoproteins appear to be affected by selenium status more than others. In rats, Arthur and coworkers (1997) reported liver 5' DI activity and GSH-Px 1 activity were reduced more than 90% by selenium deficiency but GSH-Px 4 activity was only reduced 47%. In the thyroid, there was a 25% decrease in 5' DI activity in response to selenium deficiency compared to a 45% reduction in GSH-Px 1 activity and a 75% reduction in GSH-Px 4. Vadhanavikit and Ganther (1993) reported that liver 5' DI activity in rats reached a plateau when the diet contained 0.05 ppm Se, whereas GSH-Px activity continued to increase with additional selenium supplementation. These researchers also reported that 5' DI activity in the thyroid was not affected by selenium intake, even though an effect on GSH-Px activity occurred. Because 5' DI is involved in the conversion of thyroxin (T4) to tri-iodothyronine (T3), an expected effect of selenium deficiency might be an increased level of T4 and a decreased level of T3.
Selenium deficiency appears to result in an increase in circulating T4 concentrations (Hotz et al., 1997; Ortman et al., 1999). However, a decrease in circulating T3 concentrations is not typically reported (Hotz et al., 1997; Ortman et al., 1999; Vadhanavikit and Ganther, 1993; Wu et al., 1997), although Wu et al. (1997) did find decreased myocardial T3 in deficiency.
Yeh and coworkers (1997a; 1997b) studied the effects of selenium intake on selenoprotein W concentration and GSH-Px activity of several tissues in rats. In muscle, both variables were affected by dietary selenium.
However, the relative effect of selenium concentration on GSH-Px activity was less than the effect on selenoprotein W. These researchers also found that selenoprotein W was very responsive to supplemental selenium in both sheep and rats and suggested that selenoprotein W may play a role in defending against white muscle disease.
Selenoprotein P exists in plasma and is associated with other tissues as well (Hill et al., 1996a; Hill et al., 1996b; Mork et al., 1998). There is no clear consensus regarding the biological function of selenoprotein P, but it may have transport or storage functions (Motsenbocker and Tappel, 1984) and a role in antioxidant cell defense (Mork et al., 1998). Typically, more selenium is found in selenoprotein P in plasma than in GSH-Px (Gu et al., 1998; Hill et al., 1996; Motsenbocker and Tappel, 1984). Species differences exist in the levels of selenoprotein P found in plasma, and levels appear to be responsive to dietary selenium intake. Selenoprotein P concentrations were about 10-fold higher in rats receiving 0.1 ppm Se compared to rats receiving 0.01 ppm Se (Motsenbocker and Tappel , 1984).
These authors observed a similar increase in plasma GSH-Px acitivity. Hill and coworkers (1996b) found that selenoprotein P concentrations increased in humans with increasing selenium intake within one week of initiating supplementation. It was suggested that selenoprotein P and GSH-Px were similarly predictive of dietary selenium status. Supplementation at 1 ppm did not increase selenoprotein P or GSH-Px activity in plasma beyond the levels observed at 0.1 ppm (Motsenbocker and Tappel, 1984). Yang and coworkers (1989) reported that plasma GSH-Px activity and plasma selenoprotein P concentrations decreased at similar rates when rats were given selenium deficient diets. However, when rats were repleted using various levels of selenium, selenoprotein P concentrations responded to lower intakes than either plasma GSH-Px or liver GSH-Px activity. Persson- Moschos et al. (1998) reported on increases in selenoprotein P levels in Finnish men supplemented with 0.2 mg Se per day. Basal selenium intake was approximately 0.04 mg per day.
Supplementation resulted in about a 30% increase in selenoprotein P concentrations. From previously reported data on the same subjects, the increase in plasma GSH-Px activity was 10 to 16%, depending upon the form of selenium used. However, the increase in platelet GSH-Px was between 60 and 106%, and plasma selenium increased 66 to 144% (Levander et al., 1983).
Not all selenium in plasma is present in GSH-Px or selenoprotein P. Some selenium can be incorporated in albumin and other plasma proteins as selenomethionine or selenocysteine. These selenoamino acids can also be incorporated into tissue and milk proteins. Consequently, when high levels of selenium are fed, it is possible for the activities of GSH-Px, 5' DI, etc. to plateau while levels of selenium in the tissues continue to increase. The advantage to increasing stores of selenomethionine or selenocysteine in animals has not been clearly defined.
SELENIUM IN HEALTH AND DISEASE
Many years of effort have focused on the relationship between selenium intake and cancer in human and animal models. Selenium is considered to have chemopreventive effects, although all of the mechanisms for this function are not understood (Ganther, 1999). In human medicine, selenium is also being studied for its beneficial effects during certain types of diseases.
Selenium concentrations and plasma GSH-Px activities have been reported to be reduced in certain infectious and non-infectious diseases. In addition, many disease processes involve increased production of reactive oxygen species, which could increase the need for antioxidant protection. Angstwurm and coworkers (1999) recently reported that selenium supplementation of critically ill patients improved the clinical outcome in severe systemic inflammatory response syndrome. Plasma selenium concentrations and GSH-Px activity of the patients were below normal at the time of admission but increased with selenium supplementation. Selenium status is also of great interest in regard to human immunodeficiency virus (HIV) where cellular antioxidant defenses may be compromised. Among HIV-positive children, low plasma selenium concentrations were associated with faster disease progression and increased mortality risk (Campa et al., 1999).
Similarly, Look and coworkers (1997) reported that low selenium concentrations were related to increased indicators of disease and inflammatory responses in HIV-positive patients. In vitro, selenium has been shown to decrease replication of the virus in T lymphocytes (Hori et al., 1997). In vivo, selenium supplementation can increase GSH-Px activity in HIV infected patients (Delmas-Beauvieux et al., 1996) and has been promoted as a supportive therapy (Hori et al., 1997; Schrauzer and Sacher, 1994).
Selenium status has been shown to affect disease resistance in several animal species (Bowers, 1997). In dairy cows, research has focused on the relationship between selenium intake and mammary health. Increased incidence of mastitis is correlated with low selenium status (Weiss et al., 1990) and under conditions of low selenium intake, somatic cell counts and resistance to mastitis may be improved with selenium supplementation (Erskine et al., 1989; Malbe et al., 1995; Morgante et al., 1999). One of the mechanisms for increased susceptibility to infection in selenium deficient animals may be impaired leukocyte function. In swine, increasing dietary selenium concentration from less than 0.1 ppm to Se 0.3 ppm Se improved microbicidal activities of blood polymorphonuclear cells (PMN) of gestating sows and also increased the microbicidal activity of PMN in colostrum. The impaired ability of PMN to kill bacteria in selenium depleted animals (Grasso et al., 1990; Wuryastuti et al., 1993), may occur because of alterations in ability to neutralize reactive oxygen species (Smith et al., 1997) or because of altered arachadonic acid metabolism (Eskew et al., 1993). In addition to affecting the microbiocidal activity of PMN, selenium status may also affect the ability of PMN to migrate to infected mammary tissue (Maddox et al., 1999).
Selenium status has also been shown to affect lymphocyte function. Selenium may influence the ratio or number of various subclasses of T lymphocytes in human patients with HIV. Selenium has been reported to influence B cell function in vitro (Stabel et al., 1991). Peplowski et al. (1980) reported a response to selenium in weanling swine when hemagglutination titers to sheep red blood cells were measured. Increased antibody responses with selenium supplementation have also been reported in weaned beef calves (Swecker et al., 1989), horses (Knight and Tyznik, 1990) and chickens (Larsen et al., 1997). In some studies, selenium supplementation has not produced consistent results. In rats fed deficient or adequate diets, IgG production was not markedly affected, but IgM concentrations were reduced in deficiency (Bauersachs et al., 1993).
Sheep vaccinated against Chlamydia psittaci had an enhanced antibody response when they received injectable sodium selenite, but not when the selenium was administered with vitamin E (Giandinis et al., 2000).
Conversely, Baalsrud and Overnes (1986) reported enhanced antibody response in hyperimmune horses to selenium and vitamin E together, but not selenium alone.
In the last several years, a number of research studies have focused on the effect of selenium nutrition on gestating females and their progeny. Passive transfer of antibodies through the colostrum is an important factor influencing neonatal disease resistance. Selenium supplementation of cows grazing selenium deficient pastures increased IgG concentrations in the colostrum and in calves (Swecker et al., 1995). Awadeh et al (1998) reported a similar response in beef cows and their calves. Although antibody levels in the colostrum were not reported, selenium supplementation increased the microbicidal activity of PMN in colostrum of sows (Wuryastuti et al., 1993), which might also be important to neonates. As the immunity conveyed by passive transfer wanes, young animals must mount their own immune response. Lacetara et al. (1999) recently reported that lymphocytes from lambs born to ewes supplemented with selenium had greater responsiveness to mitogenic stimulation than lymphocytes from lambs born to unsupplemented ewes. An enhancement of immune function in neonatal animals might be gained by enhancing selenium transfer from the dam.
Selenium can be transferred from the dam to progeny through the placenta or milk. Blood selenium levels in most livestock species appear to relatively low at birth (Stowe and Herdt, 1992) and may be below the level believed to provide optimal immune function (Pehrson et al., 1999). Selenium intake has been reported to influence milk selenium concentration in gilts (Mahan and Kim, 1996), sows (Mahan et al., 1975; Mahan, 2000) and dairy cows (Ortman and Pehrson, 1999). Selenium intake of gilts and sows can influence serum selenium concentrations of their progeny, but may not affect serum GSH-Px activity (Mahan et al., 1975; Mahan and Kim, 1996; Mahan, 2000). An important factor affecting the response of dams and their progeny to supplemental selenium appears to be the dietary form of the selenium. Currently, organic selenium appears to be more effective in raising milk selenium concentrations than inorganic selenium (Pehrson et al., 1999; Mahan, 2000).
Most studies evaluating PMN or antibody responses have compared deficient diets (usually less than 0.09 ppm selenium) with one or two levels of supplementation. Diets that have enhanced PMN responses have contained from 0.14 ppm selenium (Erskine et al., 1989) to 0.35 ppm selenium (Wuryastuti et al., 1993). Diets that have enhanced antibody responses have contained from 0.2 ppm (Bauersachs et al., 1993) to 0.45 ppm (Larsen et al., 1997). The current NRC (1998) recommendation for gestating swine is 0.15 ppm diet dry matter. The recommendation for lactating dairy cows is 0.3 ppm of diet dry matter. By comparison, the recommended level of dietary selenium for horses is 0.1 ppm (NRC, 1989). It is unknown whether this level of dietary selenium is adequate for optimal immune response in horses.
Dietary selenium supplementation of broodmares
The relationship between selenium status and immunity is of interest in management of the broodmare and neonatal foal. Risk of septicemia, a 188 leading cause of death in foals, is reduced by ensuring adequate passive transfer of antibodies. The primary source of antibodies for neonatal foals is colostrum. Any management strategy that enhances colostral antibody transfer has potential to improve foal health.
Appropriate rates of selenium supplementation of mares in late gestation may be one such strategy. In addition, increasing milk selenium concentration, and thus selenium consumption by foals, may enhance the selenium status of the foal. The current NRC (1989) recommendation for selenium intake is 0.1 ppm in diet dry matter for horses of all physiological classes. For a 600 kg mare consuming 12 kg of dry matter per day this concentration of selenium would result in a daily intake of 1.2 mg. Although this level of dietary selenium appears adequate to prevent classical signs of selenium deficiency, it is not known whether it is adequate for optimal immune function. Lewis (1995) suggests a selenium concentration of 0.2 ppm in the total diet for pregnant and lactating mares (at least 2.4 mg/day). Based on the information in other species, it seems likely that the broodmare requires more than the 1.2 mg selenium recommended by the current NRC (1989).
In 1999, a study was initiated at the University of Kentucky to evaluate the effect of dietary selenium intake on broodmares and their foals (Janicki et al, 2000). Fifteen pregnant mares were blocked by expected foaling date and then randomly assigned to one of three treatment programs. The three treatment programs were: 1 mg selenium as sodium selenite; 3 mg selenium as sodium selenite and 3 mg selenium as selenium yeast (Sel-Plex, Alltech, Inc., Nicholasville KY). Treatments were initiated approximately 55 days prior to foaling and all mares were fed a diet consisting of hay, pasture and a mixed grain concentrate without supplemental selenium.
Treatments were individually topdressed on the concentrate feed of each mare once a day.
Treatments were continued for 8 weeks post foaling. As has been reported in other studies, selenium intake did not influence birth weight of foals or average daily gain. Placental weight and time for placental expulsion were not affected by treatment. Serum IgG concentrations were measured in mares and foals, with foal IgG concentrations responding to treatment. Thus far, the data from this study are consistent with those from Knight and Tyznik (1990) that demonstrated an effect of dietary selenium intake on antibody responses in horses. With supporting data on levels of selenium and GSH-Px in the mares and foals, these results may support a suggestion that optimal dietary selenium concentrations for broodmares may be greater than 0.1 ppm of diet dry matter.
Other roles for selenium in equine nutrition
Based on information in other species, it appears that muscle tissue has a relatively low priority for selenium in times of marginal or deficient intakes.
This may have particular importance in the management of performance horses. During exercise, the opportunity for oxidative stress is increased and thus the selenium requirement for optimal GSH-Px activity could be elevated. Furthermore, increased urinary excretion of selenium may occur in exercising horses (Pagan et al., 1999). Changes in concentrations of blood and plasma selenium are known to occur in exercising horses, but effects of exercise on specific selenoproteins have not been described. Training may increase GSH-Px activity in plasma and erythrocytes in humans (Tessier et al., 1995), and presumably could have the same effect in horses.
Avellini et al. (1999) have recently suggested a beneficial effect of vitamin E and selenium supplementation in exercising horses. Yeh and coworkers (1997a) have suggested that selenoprotein W could be an important determinant in susceptibility of muscle to nutritional muscular dystrophy. This selenoprotein appears to be more sensitive to changes in dietary selenium than GSH-Px, and thus could be of interest to study in exercising horses.
In addition to potential effects on muscle, selenium status may have implications for horses with lung related problems. Exercise has been noted to increase free radical generation in lung tissue in vitamin E and selenium deficient rats (Reddy et al., 1998). It is possible to speculate that selenium status could be of importance in the incidence or severity of exercise induced pulmonary hemorrhage. Selenium has been linked to bone and cartilage development and may be of interest in the prevention or treatment of osteoarthritis and osteochondrosis in horses (Jeffcott, 2000). Perhaps the most interesting potential for selenium in equine management relates to the relationship between selenium status and disease. Low selenium concentrations have been reported in severely ill human patients, and may increase the rate of progress of certain diseases.
The effect of disease on serum selenium concentrations does not appear to have been evaluated in horses.
However, a number of disease conditions exist where horses may be critically ill for an extended period. Some of these diseases, such as laminitis, involve significant inflammatory responses, where a beneficial role for selenium could be envisioned. Future research should examine the potential role of selenium as a preventive or supportive therapy in critically ill horses.
References
In particular, the relationship of selenium intake to health and production responses in horses should be considered in view of the expanded understanding of the biological functions of selenium. It is of note that most of the research on selenium in horses was performed prior to 1990, when only the function of glutathione peroxidase was known. Currently, there are several selenoproteins of known function in mammals, and it has been suggested that dozens of others exist. To date, the effect of selenium nutrition on these selenoproteins and their biological role in horses has not been investigated.
Biological function of selenium
Selenium is both a toxic element and a required nutrient. In horses, the best recognized deficiency sign is muscular dystrophy, or white muscle disease, in foals. Additional deficiency signs have been identified in other species including a cardiomyopathy in humans, liver necrosis in pigs and exudative diathesis in chicks. Until the early 1970s when glutathione peroxidase (GSHPx) was identified as a selenium containing enzyme, the biological function of selenium was unknown. GSH-Px functions in the reduction of hydroperoxides, and thus is an important component of cellular antioxidant mechanisms. GSH-Px activity is observed to be low in selenium deficiency, and many of the manifestations of selenium deficiencies are related to increased oxidative damage.
After the initial research identified GSH-Px as a selenoprotein, four specific enzymes were categorized. These include GSH-Px 1 (the initial cytosolic GSH-Px); GSH-Px 2, which is present in plasma; GSH-Px 3, which is associated with the gastrointestinal tract and GSH-Px 4, which is characterized as a phospholipid-hydroperoxide glutathione peroxidase (Allan et al., 1999). GSH-Px 4 is associated with membrane-bound lipids and thus may be the mechanism through which selenium and vitamin E function synergistically. In addition, it has been suggested that this is the means through which selenium affects leukotriene synthesis (Wolfram, 1999).
Selenium has now been associated with selenoproteins that have other essential functions. Type 1 iodothyronine deiodinase (5' DI), which is responsible for the conversion of thyroxin to tri-iodothyronine is also a selenium containing enzyme. Two other deiodinases important in thyroid hormone metabolism also contain selenium. In addition, two thioredoxin reductases are now known to be selenoproteins. Other selenoproteins that are recognized, but do not have well accepted biochemical roles are selenoprotein P and selenoprotein W. Selenoprotein P is found in relatively high concentrations in plasma, and selenoprotein W is found in muscle.
EFFECT OF SELENIUM INTAKE ON SELENOPROTEINS
The effect of dietary selenium status varies with the individual selenoprotein, the specie of animal and the tissue being evaluated. It has been proposed that there is a hierarchy for selenium supply within the body and/or for different selenoproteins. When rats were fed a selenium deficient diet, selenium content was reduced by 50% in muscle and 91% in liver, compared to control animals. By comparison, the selenium content of the testes was not affected by the selenium deficiency (Behne et al., 1982). When selenium retention by deficient rats was measured, the rate of retention by the testes was much higher than in liver.
Although Yeh et al. (1997b) reported a decrease in testes selenium concentration in rats fed a deficient diet, the extent of the decrease was much less than in muscle or spleen. These authors also reported that GSH-Px activity was decreased to a much greater extent by selenium deficiency in muscle and plasma than in testes.
Marin-Guzman et al. (1997) reported that selenium deficiency decreased GSH-Px activity in the testes of growing boars, but the extent of the decrease was less than in the liver or serum. Selenium deficiency did not affect testicular weight or semen quality (volume, sperm number, etc), but fertilization rate was decreased. Decreased fertility of sperm from the deficient boars may have been related to decreased GSH-Px activity in sperm and seminal plasma. The thyroid is another tissue with a high selenium content and may be superior at retaining selenium in the face of a deficiency (Kohrle, 1999).
Brain tissue also appears to be resistant to effects of selenium deficiency (Yeh et al., 1997a; Yeh et al., 1997b). Consequently, it appears that a preferential conservation of selenium in reproductive organs and brain tissue may occur in selenium deficiency. Conversely, liver and muscle tissue are susceptible to depletion in periods of inadequate selenium supply.
Within a tissue, certain selenoproteins appear to be affected by selenium status more than others. In rats, Arthur and coworkers (1997) reported liver 5' DI activity and GSH-Px 1 activity were reduced more than 90% by selenium deficiency but GSH-Px 4 activity was only reduced 47%. In the thyroid, there was a 25% decrease in 5' DI activity in response to selenium deficiency compared to a 45% reduction in GSH-Px 1 activity and a 75% reduction in GSH-Px 4. Vadhanavikit and Ganther (1993) reported that liver 5' DI activity in rats reached a plateau when the diet contained 0.05 ppm Se, whereas GSH-Px activity continued to increase with additional selenium supplementation. These researchers also reported that 5' DI activity in the thyroid was not affected by selenium intake, even though an effect on GSH-Px activity occurred. Because 5' DI is involved in the conversion of thyroxin (T4) to tri-iodothyronine (T3), an expected effect of selenium deficiency might be an increased level of T4 and a decreased level of T3.
Selenium deficiency appears to result in an increase in circulating T4 concentrations (Hotz et al., 1997; Ortman et al., 1999). However, a decrease in circulating T3 concentrations is not typically reported (Hotz et al., 1997; Ortman et al., 1999; Vadhanavikit and Ganther, 1993; Wu et al., 1997), although Wu et al. (1997) did find decreased myocardial T3 in deficiency.
Yeh and coworkers (1997a; 1997b) studied the effects of selenium intake on selenoprotein W concentration and GSH-Px activity of several tissues in rats. In muscle, both variables were affected by dietary selenium.
However, the relative effect of selenium concentration on GSH-Px activity was less than the effect on selenoprotein W. These researchers also found that selenoprotein W was very responsive to supplemental selenium in both sheep and rats and suggested that selenoprotein W may play a role in defending against white muscle disease.
Selenoprotein P exists in plasma and is associated with other tissues as well (Hill et al., 1996a; Hill et al., 1996b; Mork et al., 1998). There is no clear consensus regarding the biological function of selenoprotein P, but it may have transport or storage functions (Motsenbocker and Tappel, 1984) and a role in antioxidant cell defense (Mork et al., 1998). Typically, more selenium is found in selenoprotein P in plasma than in GSH-Px (Gu et al., 1998; Hill et al., 1996; Motsenbocker and Tappel, 1984). Species differences exist in the levels of selenoprotein P found in plasma, and levels appear to be responsive to dietary selenium intake. Selenoprotein P concentrations were about 10-fold higher in rats receiving 0.1 ppm Se compared to rats receiving 0.01 ppm Se (Motsenbocker and Tappel , 1984).
These authors observed a similar increase in plasma GSH-Px acitivity. Hill and coworkers (1996b) found that selenoprotein P concentrations increased in humans with increasing selenium intake within one week of initiating supplementation. It was suggested that selenoprotein P and GSH-Px were similarly predictive of dietary selenium status. Supplementation at 1 ppm did not increase selenoprotein P or GSH-Px activity in plasma beyond the levels observed at 0.1 ppm (Motsenbocker and Tappel, 1984). Yang and coworkers (1989) reported that plasma GSH-Px activity and plasma selenoprotein P concentrations decreased at similar rates when rats were given selenium deficient diets. However, when rats were repleted using various levels of selenium, selenoprotein P concentrations responded to lower intakes than either plasma GSH-Px or liver GSH-Px activity. Persson- Moschos et al. (1998) reported on increases in selenoprotein P levels in Finnish men supplemented with 0.2 mg Se per day. Basal selenium intake was approximately 0.04 mg per day.
Supplementation resulted in about a 30% increase in selenoprotein P concentrations. From previously reported data on the same subjects, the increase in plasma GSH-Px activity was 10 to 16%, depending upon the form of selenium used. However, the increase in platelet GSH-Px was between 60 and 106%, and plasma selenium increased 66 to 144% (Levander et al., 1983).
Not all selenium in plasma is present in GSH-Px or selenoprotein P. Some selenium can be incorporated in albumin and other plasma proteins as selenomethionine or selenocysteine. These selenoamino acids can also be incorporated into tissue and milk proteins. Consequently, when high levels of selenium are fed, it is possible for the activities of GSH-Px, 5' DI, etc. to plateau while levels of selenium in the tissues continue to increase. The advantage to increasing stores of selenomethionine or selenocysteine in animals has not been clearly defined.
SELENIUM IN HEALTH AND DISEASE
Many years of effort have focused on the relationship between selenium intake and cancer in human and animal models. Selenium is considered to have chemopreventive effects, although all of the mechanisms for this function are not understood (Ganther, 1999). In human medicine, selenium is also being studied for its beneficial effects during certain types of diseases.
Selenium concentrations and plasma GSH-Px activities have been reported to be reduced in certain infectious and non-infectious diseases. In addition, many disease processes involve increased production of reactive oxygen species, which could increase the need for antioxidant protection. Angstwurm and coworkers (1999) recently reported that selenium supplementation of critically ill patients improved the clinical outcome in severe systemic inflammatory response syndrome. Plasma selenium concentrations and GSH-Px activity of the patients were below normal at the time of admission but increased with selenium supplementation. Selenium status is also of great interest in regard to human immunodeficiency virus (HIV) where cellular antioxidant defenses may be compromised. Among HIV-positive children, low plasma selenium concentrations were associated with faster disease progression and increased mortality risk (Campa et al., 1999).
Similarly, Look and coworkers (1997) reported that low selenium concentrations were related to increased indicators of disease and inflammatory responses in HIV-positive patients. In vitro, selenium has been shown to decrease replication of the virus in T lymphocytes (Hori et al., 1997). In vivo, selenium supplementation can increase GSH-Px activity in HIV infected patients (Delmas-Beauvieux et al., 1996) and has been promoted as a supportive therapy (Hori et al., 1997; Schrauzer and Sacher, 1994).
Selenium status has been shown to affect disease resistance in several animal species (Bowers, 1997). In dairy cows, research has focused on the relationship between selenium intake and mammary health. Increased incidence of mastitis is correlated with low selenium status (Weiss et al., 1990) and under conditions of low selenium intake, somatic cell counts and resistance to mastitis may be improved with selenium supplementation (Erskine et al., 1989; Malbe et al., 1995; Morgante et al., 1999). One of the mechanisms for increased susceptibility to infection in selenium deficient animals may be impaired leukocyte function. In swine, increasing dietary selenium concentration from less than 0.1 ppm to Se 0.3 ppm Se improved microbicidal activities of blood polymorphonuclear cells (PMN) of gestating sows and also increased the microbicidal activity of PMN in colostrum. The impaired ability of PMN to kill bacteria in selenium depleted animals (Grasso et al., 1990; Wuryastuti et al., 1993), may occur because of alterations in ability to neutralize reactive oxygen species (Smith et al., 1997) or because of altered arachadonic acid metabolism (Eskew et al., 1993). In addition to affecting the microbiocidal activity of PMN, selenium status may also affect the ability of PMN to migrate to infected mammary tissue (Maddox et al., 1999).
Selenium status has also been shown to affect lymphocyte function. Selenium may influence the ratio or number of various subclasses of T lymphocytes in human patients with HIV. Selenium has been reported to influence B cell function in vitro (Stabel et al., 1991). Peplowski et al. (1980) reported a response to selenium in weanling swine when hemagglutination titers to sheep red blood cells were measured. Increased antibody responses with selenium supplementation have also been reported in weaned beef calves (Swecker et al., 1989), horses (Knight and Tyznik, 1990) and chickens (Larsen et al., 1997). In some studies, selenium supplementation has not produced consistent results. In rats fed deficient or adequate diets, IgG production was not markedly affected, but IgM concentrations were reduced in deficiency (Bauersachs et al., 1993).
Sheep vaccinated against Chlamydia psittaci had an enhanced antibody response when they received injectable sodium selenite, but not when the selenium was administered with vitamin E (Giandinis et al., 2000).
Conversely, Baalsrud and Overnes (1986) reported enhanced antibody response in hyperimmune horses to selenium and vitamin E together, but not selenium alone.
In the last several years, a number of research studies have focused on the effect of selenium nutrition on gestating females and their progeny. Passive transfer of antibodies through the colostrum is an important factor influencing neonatal disease resistance. Selenium supplementation of cows grazing selenium deficient pastures increased IgG concentrations in the colostrum and in calves (Swecker et al., 1995). Awadeh et al (1998) reported a similar response in beef cows and their calves. Although antibody levels in the colostrum were not reported, selenium supplementation increased the microbicidal activity of PMN in colostrum of sows (Wuryastuti et al., 1993), which might also be important to neonates. As the immunity conveyed by passive transfer wanes, young animals must mount their own immune response. Lacetara et al. (1999) recently reported that lymphocytes from lambs born to ewes supplemented with selenium had greater responsiveness to mitogenic stimulation than lymphocytes from lambs born to unsupplemented ewes. An enhancement of immune function in neonatal animals might be gained by enhancing selenium transfer from the dam.
Selenium can be transferred from the dam to progeny through the placenta or milk. Blood selenium levels in most livestock species appear to relatively low at birth (Stowe and Herdt, 1992) and may be below the level believed to provide optimal immune function (Pehrson et al., 1999). Selenium intake has been reported to influence milk selenium concentration in gilts (Mahan and Kim, 1996), sows (Mahan et al., 1975; Mahan, 2000) and dairy cows (Ortman and Pehrson, 1999). Selenium intake of gilts and sows can influence serum selenium concentrations of their progeny, but may not affect serum GSH-Px activity (Mahan et al., 1975; Mahan and Kim, 1996; Mahan, 2000). An important factor affecting the response of dams and their progeny to supplemental selenium appears to be the dietary form of the selenium. Currently, organic selenium appears to be more effective in raising milk selenium concentrations than inorganic selenium (Pehrson et al., 1999; Mahan, 2000).
Most studies evaluating PMN or antibody responses have compared deficient diets (usually less than 0.09 ppm selenium) with one or two levels of supplementation. Diets that have enhanced PMN responses have contained from 0.14 ppm selenium (Erskine et al., 1989) to 0.35 ppm selenium (Wuryastuti et al., 1993). Diets that have enhanced antibody responses have contained from 0.2 ppm (Bauersachs et al., 1993) to 0.45 ppm (Larsen et al., 1997). The current NRC (1998) recommendation for gestating swine is 0.15 ppm diet dry matter. The recommendation for lactating dairy cows is 0.3 ppm of diet dry matter. By comparison, the recommended level of dietary selenium for horses is 0.1 ppm (NRC, 1989). It is unknown whether this level of dietary selenium is adequate for optimal immune response in horses.
Dietary selenium supplementation of broodmares
The relationship between selenium status and immunity is of interest in management of the broodmare and neonatal foal. Risk of septicemia, a 188 leading cause of death in foals, is reduced by ensuring adequate passive transfer of antibodies. The primary source of antibodies for neonatal foals is colostrum. Any management strategy that enhances colostral antibody transfer has potential to improve foal health.
Appropriate rates of selenium supplementation of mares in late gestation may be one such strategy. In addition, increasing milk selenium concentration, and thus selenium consumption by foals, may enhance the selenium status of the foal. The current NRC (1989) recommendation for selenium intake is 0.1 ppm in diet dry matter for horses of all physiological classes. For a 600 kg mare consuming 12 kg of dry matter per day this concentration of selenium would result in a daily intake of 1.2 mg. Although this level of dietary selenium appears adequate to prevent classical signs of selenium deficiency, it is not known whether it is adequate for optimal immune function. Lewis (1995) suggests a selenium concentration of 0.2 ppm in the total diet for pregnant and lactating mares (at least 2.4 mg/day). Based on the information in other species, it seems likely that the broodmare requires more than the 1.2 mg selenium recommended by the current NRC (1989).
In 1999, a study was initiated at the University of Kentucky to evaluate the effect of dietary selenium intake on broodmares and their foals (Janicki et al, 2000). Fifteen pregnant mares were blocked by expected foaling date and then randomly assigned to one of three treatment programs. The three treatment programs were: 1 mg selenium as sodium selenite; 3 mg selenium as sodium selenite and 3 mg selenium as selenium yeast (Sel-Plex, Alltech, Inc., Nicholasville KY). Treatments were initiated approximately 55 days prior to foaling and all mares were fed a diet consisting of hay, pasture and a mixed grain concentrate without supplemental selenium.
Treatments were individually topdressed on the concentrate feed of each mare once a day.
Treatments were continued for 8 weeks post foaling. As has been reported in other studies, selenium intake did not influence birth weight of foals or average daily gain. Placental weight and time for placental expulsion were not affected by treatment. Serum IgG concentrations were measured in mares and foals, with foal IgG concentrations responding to treatment. Thus far, the data from this study are consistent with those from Knight and Tyznik (1990) that demonstrated an effect of dietary selenium intake on antibody responses in horses. With supporting data on levels of selenium and GSH-Px in the mares and foals, these results may support a suggestion that optimal dietary selenium concentrations for broodmares may be greater than 0.1 ppm of diet dry matter.
Other roles for selenium in equine nutrition
Based on information in other species, it appears that muscle tissue has a relatively low priority for selenium in times of marginal or deficient intakes.
This may have particular importance in the management of performance horses. During exercise, the opportunity for oxidative stress is increased and thus the selenium requirement for optimal GSH-Px activity could be elevated. Furthermore, increased urinary excretion of selenium may occur in exercising horses (Pagan et al., 1999). Changes in concentrations of blood and plasma selenium are known to occur in exercising horses, but effects of exercise on specific selenoproteins have not been described. Training may increase GSH-Px activity in plasma and erythrocytes in humans (Tessier et al., 1995), and presumably could have the same effect in horses.
Avellini et al. (1999) have recently suggested a beneficial effect of vitamin E and selenium supplementation in exercising horses. Yeh and coworkers (1997a) have suggested that selenoprotein W could be an important determinant in susceptibility of muscle to nutritional muscular dystrophy. This selenoprotein appears to be more sensitive to changes in dietary selenium than GSH-Px, and thus could be of interest to study in exercising horses.
In addition to potential effects on muscle, selenium status may have implications for horses with lung related problems. Exercise has been noted to increase free radical generation in lung tissue in vitamin E and selenium deficient rats (Reddy et al., 1998). It is possible to speculate that selenium status could be of importance in the incidence or severity of exercise induced pulmonary hemorrhage. Selenium has been linked to bone and cartilage development and may be of interest in the prevention or treatment of osteoarthritis and osteochondrosis in horses (Jeffcott, 2000). Perhaps the most interesting potential for selenium in equine management relates to the relationship between selenium status and disease. Low selenium concentrations have been reported in severely ill human patients, and may increase the rate of progress of certain diseases.
The effect of disease on serum selenium concentrations does not appear to have been evaluated in horses.
However, a number of disease conditions exist where horses may be critically ill for an extended period. Some of these diseases, such as laminitis, involve significant inflammatory responses, where a beneficial role for selenium could be envisioned. Future research should examine the potential role of selenium as a preventive or supportive therapy in critically ill horses.
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Author: LAURIE LAWRENCE
University of Kentucky, Lexington, Kentucky, USA
University of Kentucky, Lexington, Kentucky, USA
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