Comparative effects of high dietary levels of organic and inorganic selenium on selenium toxicity of growing-finishing pigs 1,2,3

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1 Comparative effects of high dietary levels of organic and inorganic selenium on selenium toxicity of growing-finishing pigs 1,2,3 Y. Y. Kim and D. C. Mahan 4 Department of Animal Sciences, The Ohio State University and The Ohio Agricultural Research and Development Center, Columbus ABSTRACT: This experiment evaluated the effect of high dietary Se levels using organic or inorganic Se on the selenosis responses in growing-finishing swine. A 2 4 factorial arrangement of treatments in a randomized complete block design was conducted in two replicates. Sodium selenite or Se-enriched yeast was added at 5, 10, 15, or 20 ppm Se to corn-soybean meal diets. A basal diet without added Se was a ninth treatment group. Ninety crossbred barrows initially averaging 24.7 kg BW were allotted at five pigs per pen. Pigs were bled at 3-wk intervals and plasma Se, glutathione peroxidase (GSH-Px) activity, glutamic oxalacetic transaminase (PGOT), hemoglobin, packed cell volume, and blood cell Se concentration were measured. After 12 wk, pigs were killed and various tissues and bile were collected for Se analyses. Pig body weights, daily gains, and feed intakes were similar for both Se sources when provided at 5 ppm Se, but each measurement declined in a different manner for each Se source as the dietary Se level increased. The decline was more rapid when the inorganic rather than organic Se source was fed, resulting in interaction responses (P < 0.01). Hair loss (alopecia) and separation of the hoof at the coronary band site occurred at 10 ppm inorganic Se but at 15 ppm organic Se level. Plasma GSH-Px activity increased (P < 0.01) when high dietary Se levels of either Se source was fed. Plasma and blood cell Se increased at each period as dietary Se level increased (P < 0.01) and was greater when organic Se was provided (P < 0.05). Blood cell Se concentration reached a plateau when inorganic Se, but not when organic Se, was fed and increased as the experiment progressed. This resulted in a three-way interaction (P < 0.01). Plasma GOT activity at the 12-wk period was elevated when inorganic Se was provided at 15 ppm Se but not when organic Se was fed, resulting in an interaction (P < 0.05). Tissue Se concentrations increased as dietary Se level increased and when organic Se was provided, resulting in interaction responses (P < 0.05). Bile was a yellow color when the basal diet was fed but was dark brown at > 10 ppm inorganic Se and at 20 ppm when organic Se was provided. Bile Se increased as dietary Se level increased (P < 0.01). These results suggest that dietary Se from inorganic or organic sources was toxic at 5 ppm Se, but subsequent selenosis effects were more severe and occurred sooner when sodium selenite was the Se source. Key Words: Pigs, Selenium, Toxicity 2001 American Society of Animal Science. All rights reserved. J. Anim. Sci : Introduction A condition observed during the 19th century in the United States termed alkali disease or blind staggers was attributed to the consumption of plants that had a high Se content (Franke, 1934). Moxon (1937) 1 Salaries and research support provided by state and federal funds appropriated to the Ohio Agricultural Research and Development Center, The Ohio State Univ. 2 Partial financial support for this project and the Se enriched yeast source (Sel-Plex) was provided from the Alltech Biotechnology Center, Nicholasville, KY. 3 Appreciation is expressed to K. Mays for animal care and data collection and to B. Bishop for statistical analysis. 4 Correspondence: 2027 Coffey Road (phone: (614) ; fax: (614) ; mahan.3@osu.edu). Received January 24, Accepted December 6, and Miller and Schoening (1938) subsequently reported that selenosis in swine involved hair loss, cracking of hooves, and an interruption in coronary band development of the hoof. Selenosis can generally be classified into two types depending on the amount of Se ingested and the duration of its administration. Acute selenosis occurs after an extremely high dietary intake ( 20 mg/kg) or injection ( 1.65 mg/kg BW) of Se (Miller and Williams, 1940; Diehl et al., 1975; Mahan and Moxon, 1984). Acute selenosis produces respiratory distress, ataxia, diarrhea, and, often, death. Chronic selenosis occurs after consuming diets containing 5 to 20 ppm Se over a longer time period (Goehring et al., 1984a,b; Mahan and Moxon, 1984). Reduced feed intake and growth rate seemed to be the more immediate indicators of chronic 942

2 Selenium for growing-finishing pigs 943 selenosis. Additional signs include hair loss, sloughing of hooves, liver cirrhosis, and anemia (Ekermans and Schneider, 1982). Few scientific experiments have reported the effects of high dietary levels of organic Se fed to swine, and most studies have used inorganic Se to establish the dietary toxicity level. Dietary organic Se from grain or selenomethionine has, however, been reported to be less toxic than inorganic Se (McAdam and Levander, 1987). Because organic Se is used as a dietary Se supplement in much of the livestock sector of the world, a comparison between both Se sources on their selenosis effects in growing-finishing pigs seems warranted. Materials and Methods An experiment was conducted to evaluate the effects of high dietary levels of organic or inorganic Se fed to growing-finishing pigs on subsequent signs of selenosis. Experimental procedures followed approved practices of the university animal care committee. The experiment conducted in two replicates was a 2 4 factorial arrangement of treatments in a randomized complete block (RCB) design with an added ninth treatment group as a negative control. Sodium selenite was the inorganic Se source and a Se-enriched yeast served as the organic Se source. The latter product contained a mixture of seleno amino acids, the principle one being selenomethionine (Kelly and Power, 1995). Each Se source was added at four dietary levels (5, 10, 15, or 20 ppm Se). A basal diet without added Se served as a negative control. A total of 90 crossbred ([Yorkshire Landrace Duroc Hampshire] Duroc) barrows initially averaging 24.7 kg BW, approximately 8 wk of age, were allotted to treatment pens on the basis of weight and litter. Treatment diets composed of corn-soybean meal mixtures formulated to contain 0.80% (total) lysine were provided during the initial 8-wk period. Corn-soybean meal diets containing 0.70% (total) lysine were fed during the last 4 wk of the experiment. Both Se sources were premixed in finely ground corn to contain 200 ppm Se and added to the diets at the appropriate amount at the expense of corn. Both premixes and final diets were subsequently analyzed to confirm their Se levels. Other dietary nutrients met or exceeded NRC (1988) standards. The composition of the basal diets provided during the experiment is presented in Table 1. Pigs were housed in complete confinement facilities with partially slotted (34%) concrete floors in groups of five pigs per pen. Treatment diets were provided for ad libitum consumption throughout the experiment, and feed wastage was collected daily, weighed, and subtracted from that offered. Performance data (weight gain and feed intake) were evaluated for the 12-wk experimental period. Hair loss (alopecia), disconnection of the coronary band in the hoof, and gait (staggers) were subjectively evaluated on each animal at 3-wk intervals. Table 1. Composition of experimental diets (as-fed basis) Ingredient Growing, % a Finishing, % b Corn Soybean meal (44% CP) L-Lysine HCl Dicalcium phosphate Limestone Trace mineral premix c Salt Se premix d + + Vitamin mix e Antibiotic f a Formulated to contain 0.80% (total) lysine, 0.65% Ca, and 0.55% (total) P. The diet analyzed 0.07 ppm Se. Both are expressed on an as-fed basis. b Formulated to contain 0.70% (total) lysine, 0.55% Ca, and 0.50% (total) P. The diet analyzed 0.06 ppm Se. Both are expressed on an as-fed basis. c Supplied per kilogram of diet: 10 mg of Cu (copper oxide), 100 mg of Fe (ferrous sulfate), 0.2 mg of I (calcium iodate), 40 mg of Mn (manganese oxide), and 120 mg of Zn (zinc oxide). d Inorganic or organic Se was premixed in ground corn at 200 ppm Se and added to the diets at the expense of corn. e Supplied per kilogram of diet: 1,750 IU of vitamin A (palmitate), 200 IU of vitamin D 3 (acetate), 11 IU of vitamin E (acetate), 0.5 mg of vitamin K (menadione), 3.0 mg of riboflavin, 10 mg of pantothenic acid, 13 mg of niacin, 0.3 mg of folacin, 0.05 mg of biotin, 15 g of vitamin B 12, 0.4 g of choline, and 66 mg of butylated hydroxytoluene (BHT) as an antioxidant. f Tylan was added at 10 mg per kilogram of diet for the growing and at 5 mg for the finishing diets, respectively. Blood samples were collected initially from the anterior vena cava from a total of five randomly selected pigs in each of the two replicates. All pigs were bled in a similar manner at 3-wk intervals for the 12-wk experimental period. Upon collection, the blood was separated into two vials and immediately placed on ice for delivery to the laboratory. Hemoglobin and packed cell volume were measured in individual whole blood samples to which citrate had been added to prevent clotting. The second blood sample was centrifuged at 2,200 g at 4 C, and blood cells and plasma were separated, frozen, and analyzed for their Se concentrations. The plasma was analyzed for glutathionine peroxidase (GSH-Px) activity and glutamic oxalacetic transaminase (PGOT) activity. At 12 wk, the pigs were stunned by electric shock and killed by exsanguination, and samples of liver, loin, lung, pancreas, spleen, heart, and kidney were collected, frozen, and analyzed for Se. The gall bladder was excised from each liver and the bile was removed, sealed in test tubes using parafilm to prevent moisture loss, stored (4 C), and individually analyzed for its Se and other mineral concentrations. Plasma, blood cells, premixes, diets, bile, and tissues were wet-ashed with perchloric and nitric acid, and Se analyses were conducted according to the fluorometric method of AOAC (1995). Hemoglobin was determined colorimetrically (Sigma, 1994) using cyanmethemoglobin and Drabkin s solution. Packed cell volume was determined using a microcapillary centrifuge (Interna-

3 944 Kim and Mahan tional Equipment, Boston, MA) and values were expressed as a percentage of packed blood cells in whole blood. Plasma GSH-Px activities were determined by the coupled method of Lawrence and Burk (1976). Plasma GOT activities values are expressed as Sigma- Frankel (SF) units by the method outlined by Sigma Chemical Co. (1990). Except for Se, the macro- and microminerals in the bile were analyzed by the inductively coupled plasma method (ICP; AOAC, 1995). Statistical analyses of the data used the GLM procedure of SAS (SAS Inst. Inc., Cary, NC) following the RCB design outlined by Steel and Torrie (1980). Pen averages for all measurements were considered the experimental unit. Selenium source responses for each measurement period were contrasted by single df contrasts. Each Se source was analyzed by linear regression and the basal diet was included in the regression contrasts for each Se source. In addition, repeated measures analyses of the various blood measurements were conducted by placing day of collection into the statistical model and contrasting treatment means by polynomial regression. Treatment means are presented in the tables. Results and Discussion Performance Responses. During the experiment it was observed that pigs with a predominance of red or black hair that consumed the higher dietary Se levels were heavier in body weight than white-haired pigs (Figure 1). Because of the unequal distribution and absence of these hair colors in the various treatment pens, subsequent partitioning of performance responses of these pig groups could not be conducted. Figure 1. Pigs with red (left), black (middle), and white (right) hair color after 12 wk of being fed a 10 ppm Se (sodium selenite) diet. Pig BW at the time of the photograph were 101, 103, and 74 kg, respectively. Liver Se contents of these three pigs were 4.32, 4.41, and 5.35 ppm Se, respectively. Performance responses of growing-finishing pigs fed organic and inorganic Se sources at the various dietary Se levels are presented in Table 2. Final body weights were similar when either Se source was fed from 0 to 5 ppm Se. Body weights declined curvilinearly and in a different manner for each Se source as the dietary Se level increased, resulting in a Se source Se level interaction (P < 0.05). Body weights of pigs fed inorganic Se declined more rapidly and quadratically (P < 0.01) as dietary Se level increased, whereas body weight declined in a slower but linear (P < 0.05) manner when the organic Se source was provided. Consequently, at the end of the 12-wk trial pigs that were fed the organic Se source at 20 ppm were approximately 30 kg heavier in body weight than their treatment counterparts fed inorganic Se. Daily gain, feed intake, and gain:feed ratio responses each declined differently, but in a curvilinear manner for both Se sources as the dietary level of Se increased, resulting in Se source Se level interactions (P < 0.01). When the dietary Se level was > 5 ppm, daily gains declined more rapidly when the inorganic rather than the organic Se source was fed, resulting in an interaction (P < 0.01). For the overall 12-wk period, daily gains of pigs fed 20 ppm organic Se were approximately sevenfold greater than those of pigs fed 20 ppm inorganic Se. Daily feed intake declined as the dietary Se level increased for both Se sources, but the decrease seemed to be more gradual, and differences between Se sources lower, than daily gain. There was, however, an interaction (P < 0.01) between dietary Se level and Se source; feed intake declined more when the inorganic Se source was fed at higher dietary Se levels. There was an approximately twofold difference in overall daily feed intake for the 12-wk period when the two Se sources were compared. Feed refusal and wastage were prevalent during the first and every week thereafter in the trial, particularly when diets contained > 10 ppm Se. Reduction of feed intake has occurred when diets fed to growing pigs contained 20 ppm Se (Harrison et al., 1983; Goehring et al., 1984a,b; Mahan and Moxon, 1984) or 50 ppm Se (Wilson et al., 1982). Our pig performance responses indicated that toxic levels of dietary Se can be recognized relatively early by these criteria. Mahan and Moxon (1984) and Wahlstrom et al. (1984) also demonstrated reduced pig growth and feed intakes when dietary Se exceeded 5 to 7 ppm. A general body weakness and(or) staggering gait were observed within 3 to 6 wk of the start of the experiment, particularly noticeable in the forelegs when animals were fed 20 ppm Se from either Se source. The weakened and staggering condition may be at least partially attributed to their lower feed and energy intakes when the high Se-containing diets were provided. Hair loss (alopecia) occurred within 3 wk of the start of the trial when 10 ppm inorganic Se or 15 ppm organic Se were fed. This response was more noticeable in white-haired than in red- or black-haired pigs. Hoof

4 Selenium for growing-finishing pigs 945 Table 2. Effect of dietary Se source and level on growth performance responses of growing-finising pigs a Se source: Inorganic Organic Item Added Se, mg/kg: SEM Final weight, kg bcde Daily gain, kg bcf Daily feed intake, kg bcf Gain:feed ratio, kg/kg bcf a Each treatment mean represents 10 pigs with an initial body weight of 24.7 kg. b Dietary Se source response (P < 0.01). c Dietary inorganic Se level quadratic response (P < 0.01). d Dietary Se level linear response (P < 0.01). e Dietary Se level Se source interaction (P < 0.05). f Dietary Se level Se source interaction (P < 0.01). separation was present at the juncture of the coronary band of the hoof. This latter response was observed when 5 ppm inorganic Se was fed for the 12-wk experimental period but was not observed until 10 ppm of organic Se had been fed. The severity of hoof separation and alopecia was more extensive as the dietary Se level increased for both Se sources, particularly with whitehaired pigs. Goehring et al. (1984a,b), Mahan and Moxon (1984), and Wahlstrom et al. (1984) also reported hair loss and hoof separations after pigs were fed high Se-containing diets. Blood Measurements. At each 3-wk measurement period, plasma Se concentrations increased as the dietary Se level increased (P < 0.01) and when the organic Se source was provided (P < 0.05; Table 3). The interaction, however, between these two variables was not significant (P > 0.15). The repeated measures analysis demonstrated that each Se source had plasma Se concentrations that increased linearly (P < 0.01) over time, but there was no interaction between the day of collection and the two Se variables (P > 0.15). Blood cell Se content was approximately three to five times greater than plasma Se concentration and was affected by both dietary Se source and Se level. At each 3-wk period blood cell Se concentration increased as the dietary Se level increased (P < 0.01). A three-way time Se source Se level interaction (P < 0.01) occurred in blood cell Se concentration for the 12-wk period. When sodium selenite was fed, blood cell Se concentration increased as the dietary inorganic Se level increased and as the experiment progressed but seemed to reach a maximum concentration at approximately 5.5 ppm Se, and plateaued. When organic Se was provided, blood cell Se concentration continued to increase during the experiment, reaching cellular concentrations of > 10 ppm Se as the dietary level of organic Se increased. These results suggest that when excess Se was consumed, the blood cell not only retained substantial quantities of Se, but it also increased more than plasma Se concentrations. These results indicate that the erythrocyte may retain increasing amounts of Se when high dietary Se levels are consumed. This effect may reduce the impact of toxic dietary levels of the element, particularly when Se is provided in the organic form. Neither hemoglobin nor packed cell volume was affected (P > 0.15) by dietary Se source or Se level at the dietary levels evaluated, nor was it affected over the duration of the experiment. This suggests that when toxic dietary Se levels are consumed these blood components maintained their normal production and blood cell integrity. Plasma GSH-Px activity increased (P < 0.01) within each measurement period as dietary Se level increased and was greater when inorganic Se was the Se source (P < 0.05), but the Se source Se level interaction was significant (P < 0.05) only at wk 12. The results imply that there may be an increase in or perhaps overproduction and(or) activity of the enzyme at high dietary Se levels. Plasma GSH-Px activity increased numerically for each measurement period even when the basal diet was fed. This suggests that the activity of this enzyme increased with age, a response also noted by Mahan et al. (1999). Plasma GSH-Px values generally declined from the 9- to the 12-wk period when high dietary Se levels were fed, but pigs on those treatment groups also consumed less daily feed during this time period. Plasma GOT activities at 12 wk were influenced by dietary Se source (P < 0.05) and Se level (P < 0.01), resulting in an interaction (P < 0.05). Plasma GOT values were similar for both Se sources up to the 10 ppm dietary Se level, whereupon higher PGOT values occurred when pigs were fed inorganic Se. This suggests the possibility of cellular tissue damage from feeding 20 ppm dietary inorganic Se, but it also seems that membrane integrity was not affected at 20 ppm Se when the organic source was fed. Elevated plasma GOT activities generally reflect cellular damage, because this cytosolic enzyme is released into the circulatory fluid when cell membrane integrity is damaged. Tissue Measurements. When the basal non-se-fortified diet was fed, the soft tissues having the highest Se concentrations were, in descending order, kidney cortex, pancreas, liver, spleen, heart, lung, and loin (Table 4).

5 946 Kim and Mahan Table 3. Effect of dietary Se source and level on blood measurements of growing-finishing pigs a Se source: Basal Inorganic Organic Item Added Se, ppm: SEM Plasma Se, ppm Initial wk ef 6 wk fg 9 wk fg 12 wk fg Blood cell Se, ppm Initial wk f 6 wk efh 9 wk fgh 12 wk fgi Hemoglobin, g/dl Initial wk wk wk wk PCV, % b Initial wk wk wk wk GSH-Px, units/ml c Initial wk f 6 wk f 9 wk f 12 wk fh PGOT, SF units/ml d 12 wk efi a Each mean is the mean of 10 pigs. b PCV = packed cell volume. c One unit of glutathione peroxidase (GSH-Px) activity equals 1 mol of NADPH oxidized per minute per milliliter of serum. d One Sigma-Frankel (SF) unit of plasma glutamic transaminase (PGOT) represents the formation of mol glutamic acid/min at ph 7.5 and 25 C. e Dietary Se source (P < 0.05). f Dietary Se level linear response (P < 0.01). g Dietary Se source (P < 0.01). h Dietary Se level Se source interaction (P < 0.05). i Time dietary Se level Se source interaction (P < 0.01). Table 4. Effect of dietary Se source and level on tissue Se content of growing-finishing pigs Se source: Basal Inorganic Organic Tissue Se, ppm a Added Se, ppm: SEM Kidney bcd Liver bcd Pancreas bcd Spleen bcd Lung bcd Heart bcd Loin bcd Hoof bcd a Each mean represents eight pigs with tissue Se concentrations expressed on a wet-tissue basis. b Dietary Se source (P < 0.01). c Dietary Se linear response (P < 0.01). d Dietary Se level Se source interaction (P < 0.01).

6 Selenium for growing-finishing pigs 947 Table 5. Effect of dietary Se source and level on bile mineral composition Se source Added Se, ppm Item Inorganic Organic SEM SEM No. of pigs Bile minerals, g/g Se 1,389 1, a 11 1,080 1,863 1,284 1, b Ca P Na 4,865 5,143 1,347 6,681 4,831 5,224 5,235 4, K Mg Mn Fe Zn Cu Al a c a Dietary Se source (P < 0.01). b Dietary Se level linear response (P < 0.01). c Dietary Se level linear response (P < 0.05). As the dietary level of both Se sources increased, the Se content in these soft tissues increased (P < 0.01), but to a greater extent when the organic Se source was provided (P < 0.01). This resulted in Se source Se level interactions (P < 0.01) for the various soft tissues. Although all tissues had greater Se concentrations as the dietary Se level increased, the liver had the greater increase. The retention of Se by the liver when high levels of Se were provided to pigs has been demonstrated previously (Diehl et al., 1975; Mahan and Moxon, 1984). The loin and heart muscle Se contents were approximately 50- to 60-fold greater when the organic Se source was fed compared with pigs fed the basal diet, whereas when inorganic Se was provided the increase in Se content in these two muscles was only two- to fourfold greater. The higher loin muscle tissue Se concentration that occurred when the organic Se source was fed probably represents the replacement of methionine with selenomethionine in soft tissues, which was at a high level in the organic Se source (Kelly and Power, 1995). When the basal diet was fed, the keratin tissue of the hoof had a higher Se concentration than other soft tissues, except the kidney. Hoof Se concentration increased as dietary Se level increased (P < 0.01) but increased more when the organic (P < 0.01) rather than the inorganic Se source was fed. This resulted in a Se source Se level interaction (P < 0.01). Hoof Se concentration was, however, lower when 20 ppm Se levels from either Se source was fed. Because hoof separation around the coronary band site occurred prior to the end of the experiment, the Se in this tissue in those pigs fed the higher dietary Se levels may not have continued to accumulate Se because hoof separation was in an advanced stage. Hoof separation at the coronary band site also seemed to be more prevalent and occurred sooner in white-haired than in the red- or blackhaired pigs. Bile Minerals. Bile collected from pigs consuming the basal diet was yellow in color. When inorganic Se was fed at 10 ppm Se or at the 20 ppm organic Se level, bile was dark brown. The dark color of the bile was probably attributable to hepatic tissue damage that occurred when the toxic dietary Se level was fed. Because organic Se seemed to express fewer toxicity signs at comparable dietary Se levels in our experiment, liver damage and the dark bile probably may not have occurred until the extremely high dietary Se levels were fed. The Se concentration in bile increased linearly (P < 0.01) as dietary Se increased (Table 5). Although bile is considered to have a minor role in normal Se excretion (Levander and Bauman, 1966), our experiment implies that bile contributes to the Se excretion pathway. The other minerals in bile were generally not affected by dietary Se level (P > 0.15). There was, however, a lower Al content (P < 0.05) in the bile when dietary Se increased. The reason that this specific element declined as Se level increased is unknown. There was a numerical increase in the Fe content in the bile as dietary Se increased, but the response was not significant (P > 0.15). Although there was no effect of Se level on the other biliary mineral contents, there was a reduced feed intake and thus a lower mineral consumption when the higher dietary Se levels were provided. There was a tendency for Ca, P, Na, K, Mg, Mn, Fe, Cu, and Zn concentrations to be somewhat greater when organic Se was fed, but this was attributed to the higher feed intake and subsequently higher mineral consumption when pigs were fed this Se source (Table 2). Conclusions Clearly, feeding pigs the organic Se source resulted in different responses to the selenosis conditions com-

7 948 Kim and Mahan pared with feeding inorganic sodium selenite. As dietary Se levels increased in excess of 5 ppm selenosis was worse when inorganic Se was fed, as reflected by pigs reduced weight gains and reduced feed intakes and a greater occurrence of alopecia, staggering gait, coronary band separation, and elevated PGOT activity. The same general responses occurred when organic Se was fed, but the severity of these responses was not as great until the higher dietary Se levels were fed. These signs are considered classic responses to high dietary Se levels (Moxon, 1937; Miller and Schoening, 1938). The higher retention of organic Se in the various tissues and blood cells may effectively reduce the available Se used to precipitate the selenosis response. This may be the reason for the slower onset of selenosis when the organic Se source was fed. Retaining more Se in the various soft and hard tissues and erythrocytes, particularly muscle, can effectively reduce the amount of Se available to damage the membrane integrity of other tissues. This was suggested by the darkened color of the bile when inorganic Se was fed at 10 ppm, whereas this effect was not observed until 20 ppm organic Se had been provided. The elevated PGOT level when high levels of inorganic Se were fed was consistent with that observation. White-haired pigs were more sensitive to the onset of selenosis than pigs that had red or black hair within the same treatment group. It was also of interest that when red or black and white hair colors were present on the same pig, alopecia always occurred in the whitehaired body areas of the pigs prior to the loss of darkcolored hair. Olson et al. (1954) had previously demonstrated that alopecia occurred when dietary Se concentrations were > 10 ppm. The results of our experiment suggest that Se retention in hair may differ by color and thus could affect the onset of selenosis. Wahlstrom et al. (1984), however, demonstrated that black and white pigs were less affected by Se toxicosis than redhaired pigs. Implications Feeding a diet containing > 5 ppm Se of inorganic (sodium selenite) or organic Se (Se-enriched yeast) produced selenosis signs in growing pigs. Selenosis was more severe and occurred sooner when inorganic rather than organic Se was fed. The greater retention of Se by various body tissues when the organic Se source was fed may reduce the availability of Se for precipitating selenosis and may explain why the organic Se source seemed to induce fewer selenosis signs than the inorganic form of the element. Pigs with red or black hair seemed to be less vulnerable to Se toxicosis than pigs with white hair. Literature Cited AOAC Official Methods of Analysis. 16th ed. Association of Official Analytical Chemists, Arlington, VA. Diehl, D. S., D. C. Mahan, and A. L. Moxon Effects of single intramuscular injections of selenium at various levels to young swine. J. Anim. Sci. 40: Ekermans, L. G., and J. V. Schneider Selenium in livestock production: A review. J. South Afr. Vet. Assoc. 53: Franke, K. W A new toxicant occurring naturally in certain samples of plant foodstuffs. I. Results obtained in preliminary feeding trial. J. Nutr. 8: Goehring T. B., I. S. Palmer, O. E. Olson, G. W. Libal, and R. C. Wahlstrom. 1984a. Effects of seleniferous grains and inorganic selenium on tissue and blood composition and growth performance of rats and swine. J. Anim. Sci. 59: Goehring T. B., I. S. Palmer, O. E. Olson, G. W. Libal, and R. C. Wahlstrom. 1984b. Toxic effects of selenium on growing swine fed corn-soybean meal diets. J. Anim. Sci. 59: Harrison, L. H., B. M. Colvin, B. P. Stuart, L. T. Sangester, E. J. Gorgacz, and H. S. Gosser Paralysis in swine due to focal symmetrical poliomalacia: Possible selenium toxicosis. Vet. Pathol. 20:265 B 273. Kelly, M. P., and R. F. Power Fractionation and identification of the major selenium compounds in selenized yeast. J. Dairy Sci. 78(Suppl. 1):237 (Abstr.). Lawrence, R. A., and R. F. Burk Glutathione peroxidase activity in selenium-deficient rat liver. Biochem. Biophys. Res. Commun. 71: Levander, O. A., and C. A. Bauman Selenium metabolism VI. Effect of arsenic on the excretion of selenium in the bile. Toxicol. Appl. Pharmacol. 9: Mahan, D. C., T. R. Cline, and B. Richert Effects of dietary levels of selenium-enriched yeast and sodium selenite as selenium sources fed to growing-finishing pigs on performance, tissue selenium, serum glutathione peroxidase activity, carcass characteristics and loin quality. J. Anim. Sci. 77: Mahan, D. C., and A. L. Moxon Effect of inorganic selenium supplementation on selenosis in postweaning swine. J. Anim. Sci. 58: McAdam, P. A., and O. A. Levander Chronic toxicity and retention of dietary selenium fed to rats and D- or L-selenomethionine, selenite or selenate. Nutr. Res. 7: Miller, W. T., and H. W. Schoening Toxicity of selenium fed to swine in the form of sodium selenite. J. Agric. Res. (Wash DC) 56: Miller, W. T., and K. T. Williams Minimum lethal dose of selenium, as sodium selenite, for horses, mules, cattle and swine. J. Agric. Res. 60: Moxon, A. L Alkali disease or selenium poisoning. In: Agric. Exp. Sta. Bull. 311, South Dakota State College of Agriculture and Mechanic Arts, Brookings. pp NRC Nutrient Requirements of Swine. 9th ed. National Academy Press, Washington, DC. Olson, O. E., C. A. Dinkel, and L. D. Kamstra A new aid in diagnosing selenium poisoning. S. D. Farm Home Res. 6:12. Sigma Transaminases (ALT/GPT and ASP/GOT). Quantitative, colorimetric determination in serum, plasma or cerebrospinal fluid (procedure no. 505). Sigma Chemical Co., St. Louis, MO. Sigma Total hemoglobin: Procedure No Sigma Chemical Co., St. Louis, MO. Steel, R. G. D., and J. H. Torrie Principles and Procedures of Statistics: A Biometrical Approach. (2nd ed.) McGraw-Hill Publishing Co., New York. Wahlstrom, R. C., T. B. Goehring, D. D. Johnson, G. W. Libel, O. E. Olson, I. S. Palmer, and R. C. Thaler The relationship of hair color to selenium content of hair and selenosis in swine. Nutr. Rep. Int. 29: Wilson, T. M., R. Scholz, and T. Drake Porcine focal symmetrical poliomyelomalacia and selenium toxicity: Description of a field outbreak and preliminary observations on experimental reproduction. In: Proc. 25th Annu. Mtg. Am. Assoc. Vet. Lab. Diagn., Nashville, TN. pp