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ANIMAL NUTRITION |
* Department of Animal Sciences,
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College of Veterinary Medicine, and
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Food and Resource Economics Department, University of Florida, Gainesville 32611
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Abstract |
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 Top Abstract INTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONIMPLICATIONSLITERATURE CITED |
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Key Words: selenium • sheep • selenium tolerance • sodium selenite
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INTRODUCTION |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONIMPLICATIONSLITERATURE CITED |
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), Se toxicities are more difficult to control. In 1957, Se was established as an essential nutrient, and the benefits of Se supplementation to livestock continue to be elucidated. Current estimates put the maximum tolerable level of Se at 2 mg/kg for the major livestock species (NRC, 1980), and no differentiation exists for tolerable levels between ruminants and nonruminants.
The work of Butler and Peterson (1961) and Hidiroglou et al. (1968) suggests that inorganic Se (e.g., sodium selenite) may be reduced to insoluble selenide by microorganisms in the rumen, thus reducing the overall absorption of Se by ruminant animals. Wright and Bell (1966) reported that swine retained 77% of an oral dose of inorganic Se, which is nearly 3-fold the retention by sheep. Selenium toxicities have often been induced in ruminants using either Se injections or dietary Se (Marrow, 1968; Caravaggi et al., 1970; Shortridge et al., 1971) at levels above the maximum tolerable amount (5 to 196 mg/kg) for nonruminants (Franke and Potter, 1935; Miller and Schoening, 1938; Kim and Mahan, 2001). More recently, Cristaldi et al. (2005) demonstrated that wethers did not display signs of Se toxicosis after receiving up to 10 mg/kg of dietary Se for 1 yr.
Based on these findings, it seems that the current maximum tolerable level of Se for ruminants is underestimated. Most Se toxicity research in ruminants has been done in lambs or wethers. Controlled experiments using ewes during the stresses of production (e.g., gestation and lactation) are lacking. The objective of this long-term study was to evaluate the effects of feeding Se as sodium selenite to ewes at supranutritional levels and to determine the maximum tolerable level of Se for ewes during lamb production.
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MATERIALS AND METHODS |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONIMPLICATIONSLITERATURE CITED |
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Ewes were randomly assigned to 1 of 6 dietary treatments for the 72-wk study. The 6 dietary treatments were 0.2, 4, 8, 12, 16, or 20 mg of supplemental Se/kg (as-fed basis). The Se was fed as sodium selenite and was added to a corn and soybean meal-basal diet (Table 1). The basal diet was formulated to meet animal requirements for protein, energy as TDN, vitamins, and minerals for this class of sheep (NRC, 1985). Animal numbers per treatment were 6 for supplements of 0.2 mg of Se/kg (control) and 7 each for supplements of 4, 8, 12, 16, and 20 mg of Se/kg. Ewes were housed by treatment group in covered wooden pens (53.5 m2) with earthen floors and automatic watering cups.
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Ewe BW was recorded on d 0 and every 4 wk thereafter for the remainder of the study. For each animal, a 10-mL blood sample was collected via jugular venipuncture into a Vacutainer tube with no additive (Becton Dickinson, Franklin Lakes, NJ). The blood samples were allowed to stand for 20 min and were centrifuged at 700 x g for 25 min. The resulting serum was stored frozen at <0°C until Se analysis. Starting at wk 12, an additional 10-mL blood sample was collected into a heparinized Vacutainer tube (Becton Dickinson, Franklin Lakes, NJ). This 10-mL sample of whole blood was collected from each animal every 12 wk for the remainder of the experiment and stored frozen at <0°C until Se analysis.
The wool around the jugular of each ewe, approximately 77 cm2, was shorn initially, and regrowth was collected beginning at wk 12 and every 12 wk thereafter. The collected wool was washed with a commercial hair shampoo (Alberto VO5, Alberto-Culver Co., Melrose Park, IL) to remove oil and dirt. The wool was rinsed with deionized water, air-dried, and stored at room temperature for later Se analysis.
At the termination of the experiment (wk 72), ewes were slaughtered following approved USDA procedures at the University of Florida Meats Laboratory. Immediately before slaughter, a 10-mL sample of blood was collected via jugular venipuncture into a Vacutainer and centrifuged at 700 x g for 25 min. The serum was stored frozen at 0°C until analysis of albumin and the following enzymes: alkaline phosphatase (Alk Phos), alanine transaminase (ALT), aspartate transaminase (AST), creatinine phosphokinase (CK), and gamma glutamyl transferase (GGT). Evaluation of albumin and certain enzyme activities aid in determining possible tissue breakdown resulting from Se toxicosis.
Samples of brain, diaphragm, heart, hoof tip, kidney, liver, and psoas major were collected and frozen (0°C) until analyzed for Se. Sections (1 cm3) of liver, heart, kidney, diaphragm, and psoas major muscle from all animals were placed in 10% neutral-buffered formalin for subsequent microscopic evaluation for evidence of Se toxicosis.
For histopathological evaluation, the tissue samples fixed in buffered formalin were embedded in paraffin and sectioned at 6 µm. All sections were stained with hematoxylin and eosin and examined under a light microscope (10x, 20x, and 40x). Serum albumin, Alk Phos, ALT, AST, CK, and GGT were evaluated on a Hitachi 911 analyzer (Roche Diagnostics, Indianapolis, IN) with reagents from Sigma (Sigma Chemical Co., St. Louis, MO). The Veterinary Medical Teaching Hospital at the University of Florida established these procedures.
Serum, whole blood, wool, tissue, and feed samples were analyzed for Se concentrations using a fluorometric method described by Whetter and Ullrey (1978). To help ensure the reliability of the analytical method, a certified standard (National Bureau of Standards Bovine Liver SRM-1577a; U.S. Department of Commerce, National Institute of Standards and Technology, Gaithersburg, MD) was analyzed after every 40 samples.
Statistical Analysis
Selenium data for brain, diaphragm, heart, hoof tip, kidney, liver, and psoas major were analyzed as a completely randomized design for effects of treatment using PROC GLM of SAS (SAS for Windows 8e; SAS Inst., Inc., Cary, NC). Polynomial contrast statements were used to determine the effects of treatment as described by Littell et al. (1998, 2000). The PROC MIXED procedure of SAS was used to analyze the effects of treatment, time, and the interaction of treatment x time on BW, serum Se, whole blood Se, and wool Se as repeated measures with a spatial power covariance structure with respect to day and a subplot of animal nested within treatment. Means were separated at P < 0.05, and regression analysis was used to determine the relationships between dietary Se and Se concentration of various tissues.
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RESULTS AND DISCUSSION |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONIMPLICATIONSLITERATURE CITED |
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Ewe BW was not affected by dietary Se level (P = 0.69) or dietary Se level x time interaction (P = 0.56). However, time did affect BW of all animals (P < 0.001). Initial BW was 57.4 ± 5.7 kg, and BW at the end of the experiment was 61.2 ± 15.1 kg. These findings agree with previous studies in ruminants. Supplemental Se fed up to 0.4 mg/kg, which is above the requirement but below maximum tolerable level, had no effect on rate of gain in feedlot steers (Perry et al., 1976), and BW gains in growing wether lambs fed sodium selenite up to 10 mg/kg were unaffected by dietary Se level (Cristaldi et al., 2005). Glenn et al. (1964) also reported no effect of dietary Se on BW when sodium selenate was fed to 2-yr-old ewes as a single oral dose of up to 50 mg/d. The ewes utilized by those researchers were very similar in breed type and BW to the animals used in the current study. Effect of time on ewe BW can be explained by changes in BW associated with gestation and lactation.
Ten of 41 ewes died over the course of this 72-wk study. Gross necropsies were performed on 8 ewes after death. Tissues from 2 ewes were too severely decomposed to allow for evaluation for pathological changes. Necropsy of 8 ewes cited causes of death as lymphadenitis associated with injury (2 ewes), endoparasitism (2 ewes), ketosis (3 ewes), and pneumonia (1 ewe). Pathological evidence of Se toxicosis was not found in any ewe that died before the termination of the experiment.
In the first year, 53 lambs were born over 20 d from March 9, 2002 to March 28, 2002. Fifty-two lambs were born alive and unassisted (Table 2). One lamb was very large (8 kg) and died shortly after a difficult birth. The lambs born in the first year represented a 129% lamb crop when calculated as lambs born alive per ewe exposed. In yr 2, 36 lambs were born over 34 d from January 17, 2003 to February 20, 2003 (Table 2). All lambs were born alive and unassisted. Thirty-six lambs in the second year represented a 109% lamb crop, as only 33 ewes were exposed in the second year. The number of lambs born per ewe did not affect serum Se concentration (P > 0.54) of ewes receiving any level of dietary Se.
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, who fed dietary Se up to 50 mg per ewe daily, did not observe an effect of dietary Se level on reproduction in 2-yr-old range ewes. Those researchers observed a similar number of pregnancies in each treatment group and no malformations in lambs. In contrast, Rosenfeld and Beath (1947) observed lamb deformities in a field study and attributed the anomalies to excess Se in ewe diets. However, seleniferous plants were the Se source, rather than the inorganic sources used in the present experiment. Furthermore, in a grazing situation, it is possible that lamb deformities were due to toxic elements other than Se. In both years of our study, all lambs were born free of congenital deformities, but the number of pregnancies was lowest in ewes receiving 16 mg of dietary Se/kg, but not 20 mg/kg. However, breeding soundness evaluations were not performed on ewes or rams used in this study; thus, to incriminate or exclude dietary Se level as a detriment to ewe reproduction would be observational. Blood Responses
Serum Se concentrations from wk 4, 8, and 12 were analyzed together and will be referred to throughout the remainder of this paper as late gestation yr 1. Lactation yr 1 included serum Se concentrations from wk 12, 16, 20, and 24. Week 12 was included in both late gestation and lactation for yr 1, as some ewes were lactating and some remained in late gestation when the wk 12 sampling occurred. Weeks 28, 32, 36, 40, and 48 compose the dry, rebreeding period. Late gestation in yr 2 includes serum Se measurements from wk 52, 56, and 60. Lactation in yr 2 includes wk 60, 64, 68, and 72. Similar to yr 1, one sampling date (wk 60) was common to both late gestation and lactation and was included in both periods.
During all stages of lamb production, serum Se increased linearly (P < 0.001) as dietary Se level increased (Table 3). This agrees with previous Se toxicity research, as Se concentrations in serum of growing wether lambs (Cristaldi et al., 2005) also increased linearly as dietary selenite Se was increased up to 10 mg/kg. All ewes had similar (P > 0.82) serum Se at the initiation of our experiment. Initial serum Se ranged from 90 to 120 µg/L, which is below the adequate range (120 to 180 µg/L) for adult sheep (Aitken, 2001). Serum Se increased linearly (P < 0.05) in ewes receiving 4 or 20 mg of Se/kg. Serum Se in control ewes and ewes receiving 8 or 16 mg of Se/kg responded quadratically (P < 0.05) across the stages of production, and serum Se seemed to be greater during the dry, rebreeding stage. A cubic response (P < 0.05) in serum Se was observed in ewes receiving 12 mg of dietary Se/kg, as serum Se increased from late gestation in yr 1 to lactation in yr 1, remained relatively constant through late gestation in yr 2, and seemed to increase during lactation in yr 2. An overall cubic response to treatment (P = 0.02) was observed in serum Se across the stages of production (time) from wk 4 to 72. Serum Se in ewes, in general, was greater during the dry, rebreeding stage. One plausible explanation for this is the lack of placenta, fetal tissue, and milk for deposition and excretion of Se.
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), and were at most 37% of the reported toxic level (3,700 µg/L) in swine (Aitken, 2001). Caravaggi et al. (1970) established a lethal dose at which 50% of an experimental population dies (LD50) for sheep at 455 µg/kg of BW. When our data are described on a µg/kg-of-BW basis using the 20-mg/kg concentration, highest daily intake (1,135 g/d), and average ewe BW (60 kg), these ewes were consuming, at maximum, 378 µg/kg of BW. This is 17% less than the LD50 for sheep as previously described.
The ewes in the current study were mature and maintained healthy ruminal function throughout the study. This is in contrast to the unweaned lambs used by Caravaggi et al. (1970) that received Se via i.m. injection. Administration of Se parenterally disallows the reduction of selenite Se to insoluble selenide via ruminal microorganisms as described by Whanger et al. (1968). This would suggest that the LD50 for dietary Se in sheep could be considerably greater than previously thought.
Glenn et al. (1964) fed sodium selenate at high levels to range ewes that were similar in BW to ewes on the current study. Those researchers did not induce any deaths with daily oral doses of <25 mg of Se per ewe. Of the 17 deaths reported in their experiment, only 1 was induced with a daily dose of 25 mg of Se per ewe, 8 deaths were induced with a daily dose of 37.5 mg of Se per ewe, and 8 deaths were induced with a daily dose of 50 mg of Se per ewe. The ewe deaths reported were not caused by acute Se toxicosis. The ewes received experimental Se doses for at least 80 d before death was induced. In the same experiment, Glenn et al. (1964) further suggested an average minimum toxic level of Se for 2-yr-old ewes to be 0.825 mg/kg of BW when fed for 100 d. Using this estimate, the minimum toxic level of Se for ewes of the size used in our study would be 50.3 mg/d. Selenium consumption, at the highest dietary level of 20 mg/kg, never reached even 50% of that level throughout our study.
Blodgett and Bevill (1987) reported an LD50 for sheep using sodium selenite via i.m. injection at 0.7 mg/kg of BW. Other researchers (Rosenfeld and Beath, 1946) reported death in mature sheep with less Se (30 mg/d); however, the Se maximum intake level used in our study was approximately 25% less. It is important to note that we used sodium selenite as the source of supplemental Se, whereas previous research (Rosenfeld and Beath, 1946; Caravaggi et al., 1970) used sodium selenate as the source of additional Se. Henry et al. (1988) reported a lower relative bioavailability for selenite than selenate. This suggests the possibility of a greater tolerance for sodium selenite vs. sodium selenate.
Whole blood Se was measured in addition to serum Se because use of whole blood eliminates the possibility of falsely high Se readings in serum caused by hemolysis (Maas et al., 1992). Whole blood Se was measured at wk 12, 24, 36, 48, 60, and 72 (Table 4). Dietary Se level, time, and dietary Se level x time affected (P < 0.05) ewe whole blood Se. Whole blood Se increased linearly (P < 0.001) as dietary Se increased. The response of whole blood Se across treatments over time was cubic (P < 0.01), which agrees with the time response of serum Se.
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reported a strong correlation (0.88) for whole blood Se and serum Se. Our data support this relationship because serum Se and whole blood Se responded to dietary Se level in a similar fashion. The cubic response of whole blood Se over time may be attributed to ewes having no fetal tissue and producing no milk to use as a route of excretion during the dry, rebreeding period, which encompassed the midpoint of this study. Each dietary Se level was evaluated individually over time, and Se in whole blood of control ewes and of ewes supplemented with 8 mg of Se/kg neither increased nor decreased with time (P > 0.20). Whole blood Se from ewes receiving 4 mg of Se/kg responded cubically (P = 0.019), and that of ewes receiving 16 mg of dietary Se/kg tended (P = 0.07) to respond cubically. Whole blood Se concentrations changed more sporadically over time in ewes receiving 12 or 20 mg of dietary Se/kg, and each treatment produced a fifth degree polynomial (P < 0.05).
Cristaldi et al. (2005) also reported a linear increase in whole blood Se as dietary Se was increased. Similarly, Cristaldi et al. (2005) noted differences in treatment means compared with controls as dietary Se levels were increased up to 10 mg/kg. Increased whole blood Se concentrations were reported in dairy cows as their salt-based mineral mixtures were increased from 20 to 120 mg of sodium selenite/kg (Awadeh et al., 1998). Whole blood Se increased linearly in young swine as dietary Se was fed up to 20 mg/kg (Goehring et al., 1984).
Wool
Selenium concentrations in new growth wool were measured at wk 12, 24, 36, 48, 60, and 72 (Table 5). Dietary Se level, time, and dietary Se level x time affected (P < 0.001) wool Se. Wool Se increased linearly (P < 0.001) as dietary Se increased. Wool Se concentrations increased quadratically over time (P < 0.001), and time response for each dietary Se level was evaluated individually. Wool Se from controls and ewes receiving 8, 12, and 16 mg of dietary Se/kg responded quadratically (P < 0.03) from wk 12 to 72. Wool Se from ewes receiving 4 mg of Se/kg responded cubically (P < 0.05), and that of ewes receiving 20 mg of Se/kg increased linearly (P< 0.01) across time.
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observed a linear increase of Se in the hair of pigs as Se in their diet was increased. Goehring et al. (1984) reported a quadratic response in the hair of swine as dietary Se (sodium selenite) was increased up to 20 mg/kg. Similarly, Perry et al. (1976) reported increased Se in the hair of feedlot steers as dietary selenite was increased. Cristaldi et al. (2005) reported a linear increase in the wool of growing sheep as dietary Se was increased and also observed differences in wool Se of wethers receiving 6, 8, or 10 mg of Se/kg vs. controls.
The previous researchers did not report a significant treatment x time interaction. However, wool Se in the current study was affected by time and the interaction of treatment x time, as wool Se increased and then seemed to reach a plateau around wk 48. Kim and Mahan (2001) and Cristaldi et al. (2005) used 10 mg of Se/kg as the highest dietary level and reported linear responses in hair and wool. However, with 20 mg/kg as the highest dietary level, the quadratic responses observed by Goehring et al. (1984) and in our study suggest that Se in wool and hair does not continue to increase linearly as dietary Se is increased to >10 mg/kg. During this experiment, some wool loss was observed in 2 ewes receiving 20 mg of dietary Se/kg during lactation in yr 1. However, after lambs were weaned and lactation had ceased, both ewes regrew a full fleece.
Tissues
Selenium concentrations in all tissues were affected (P < 0.001) by dietary Se level. Selenium concentrations in brain ranged from 1.90 to 6.45 mg/kg of DM and increased linearly (P < 0.05) as dietary Se increased (Figure 1). Regressing brain Se (mg/kg of DM) on dietary Se concentrations (mg/kg) produced the following relationship:
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Diaphragm Se ranged from 1.27 to 4.01 mg/kg of DM and increased (P < 0.05) in a linear manner as dietary Se was increased (Figure 1
). Regressing diaphragm Se (mg/kg of DM) on dietary Se concentrations (mg/kg) produced the following relationship:
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Heart tissue Se (Figure 1) ranged from 1.83 to 6.24 mg/kg of DM and increased in a linear fashion with increasing dietary Se (P < 0.001). Regressing heart Se (mg/kg of DM) on dietary Se concentrations (mg/kg) produced the following relationship:
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Selenium concentrations in hoof ranged from 0.93 to 7.68 mg/kg of DM and increased cubically as dietary Se increased (Figure 2). Regressing hoof Se (mg/kg of DM) on dietary Se concentrations (mg/kg) produced the following relationship:
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Selenium concentrations in psoas major (i.e., tenderloin), a muscle commonly consumed by humans, ranged from 0.60 to 3.66 mg/kg of DM and increased linearly as dietary Se increased (Figure 2). Regressing psoas major Se (mg/kg of DM) on dietary Se concentrations (mg/kg) produced the following relationship:
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Kidney Se ranged from 5.18 to 31.61 mg/kg of DM and responded to increased dietary Se in a cubic fashion (Figure 2). Regressing kidney Se (mg/kg of DM) on dietary Se concentrations (mg/kg) produced the following relationship:
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Liver Se concentrations ranged from 4.20 to 230.36 mg/kg of DM and responded quadratically as dietary Se level increased (Figure 3.) Regressing liver Se (mg/kg of DM) on dietary Se concentrations (mg/kg) produced the following relationship:
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Linear increases in the Se concentrations of loin, liver, kidney, and hoof were reported in swine (Kim and Mahan, 2001) and sheep (Cristaldi et al., 2005). Similarly, Echevarria et al. (1988) reported linear responses of sheep liver, kidney, heart, and muscle to dietary Se as sodium selenite. In our study, loin, diaphragm, heart, and brain responded linearly; kidney and hoof responded cubically; and liver responded quadratically. These higher degree polynomials may be due to changes in metabolism of Se as dietary Se concentrations approach 20 mg/kg. Most previous research used 10 mg of Se/kg as the highest dietary concentration.
Enzymes and Histopathology
Serum for evaluation of albumin and enzyme activities was collected at wk 72 along with samples of brain, diaphragm, heart, hoof tip, kidney, psoas major, and liver for histopathological evaluation. Concentrations of albumin and activities of Alk phos, ALT, AST, and CK in serum were at or below the normal range for adult sheep (Table 6). Gamma glutamyl transferase activity was only slightly elevated. In instances of Se toxicosis, the activities of these enzymes should have been increased because of tissue necrosis. The majority of our observations agree with those reported by Cristaldi et al. (2005), as albumin and enzyme activities in wether sheep receiving up to 10 mg of Se/kg were in the normal ranges.
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Hepatic lipidosis was diagnosed in 4 ewes. Two cases (1 severe; 1 moderate) were diagnosed in ewes receiving 16 mg of dietary Se/kg. In the moderate case, there was also evidence of bile retention. Neither of these ewes lambed in either year. This would indicate that the hepatic lipidosis could be treatment related rather than attributable to metabolic changes associated with gestation, parturition, and lactation. One ewe receiving 12 mg of Se/kg and 1 ewe receiving 4 mg/kg were diagnosed with mild hepatic lipidosis; however, both ewes lambed in both years. Thus, the hepatic lipidosis was likely due to metabolic changes associated with lamb production.
No evidence of significant pathological changes was observed in ewes receiving 20 mg of dietary Se/kg, which was the greatest Se level used in this study. Cristaldi et al. (2005) found no abnormalities after microscopic evaluation of heart, liver, kidney, diaphragm, and muscle from wethers consuming up 10 mg of Se/kg for 1 yr. Similarly, only one instance of abnormal pathology was observed in ewes consuming <10 mg of Se/kg on our study. Furthermore, our study was approximately 40% longer in duration, utilized treatments of up to 100% more Se, and introduced stresses of production, all of which should have contributed to the development of Se toxicosis and, thus, abnormal organ pathology. However, abnormal pathological findings were few and did not follow a pattern with respect to dietary level, which would be indicative of Se toxicosis.
No clinical signs of Se toxicosis, such as abnormal hoof growth or loss of wool, were observed in ewes receiving >16 mg of Se/kg. However, some excessive hoof growth was observed after approximately 1 yr in ewes receiving 16 and 20 mg of Se/kg, and wool loss was observed during lactation in 2 ewes receiving 20 mg of Se/kg. Livestock suffering from alkali disease were reported to have hair Se concentrations of up to 45 mg/kg and whole blood Se of 4.1 mg/L; hooves, liver, and kidney of the affected animals contained 
10 mg of Se/kg (NAS, 1983).
At no time during our study did wool Se reach even 10 mg/kg, and whole blood Se remained <50% of the aforementioned 4.1-mg/L concentration. Also, hoof Se remained <8 mg/kg for all treatments during the course of our study. Liver and kidney Se concentrations from our study were greater than the 10 mg/kg previously reported. The elevated concentrations of Se in the liver and kidney of ewes consuming 16 and 20 mg/kg, and the observation of some clinical signs of Se toxicosis and limited pathological abnormalities in ewes consuming these Se levels may indicate that some ewes were beginning to suffer from Se toxicosis. However, definitive evidence was not observed. Therefore, either dietary Se concentrations or duration of the experiment would need to be increased to induce a definitive Se toxicosis using inorganic Se.
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IMPLICATIONS |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONIMPLICATIONSLITERATURE CITED |
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Footnotes |
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2 Use of brand names is necessary to accurately report these data; however, the University of Florida does not guarantee or warrant any said products. Furthermore, the use of the name does not imply approval or exclusion of other products that may also be suitable.
3 Special thanks go to D. Bernis and D. Glicco for feed mixing and animal care; to E. Y. Matsuda-Fugisaki for assistance in analysis of plasma and tissues; and to D. J. Davis for assistance with the design of equipment to aid in this research.
4 Corresponding author: mcdowell{at}animal.ufl.edu
Received for publication October 20, 2004. Accepted for publication November 7, 2005.
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LITERATURE CITED |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONIMPLICATIONSLITERATURE CITED |
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