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We report an outbreak of acute selenium poisoning among suckling pigs; 92 piglets were found dead or moribund without preceding symptoms. Necropsy revealed acute congestion of liver and small intestine. The source was a powdered iron supplement contaminated by sodium selenite.
Plasma selenium was determined in 92 elderly women: a marked decrease was observed from the age of 65 years. Se-status in 20 elderly women was explored by investigation of the effects of 30 days' Se-supplementation with enriched tablets (Selevit-E) 66 micrograms per day. Serial determination was performed for Se plasma, e-GSH-Px (glutathione peroxidase), MDA (malondialdehyde) and Vitamin E. Significant changes were observed in Se, e-GSH-Px and MDA.
Six primiparous Holstein cows were fed a Se-deficient diet, beginning at least 90 days before their first calving, and 6 other primiparous cows were given the same diet plus a supplement of 2 mg of Se/cow/d as sodium selenite. All cows were fed their diets for the duration of the experimental period. One uninfected quarter of each cow was injected with 25 micrograms of Escherichia coli endotoxin at postpartum week 5. Leukocytes were isolated by centrifugation from milk collected at postinjection hour 16. Isolated cells were 92 +/- 3% neutrophils and were incubated with Staphylococcus aureus or E coli in a 1:300 ratio. Phagocytosis and intracellular killing by neutrophils were assessed after 0, 30, 60, and 90 minutes by a fluorochrome assay, using acridine orange. Viability of neutrophils was assessed by use of trypan blue. Superoxide anion production and hydrogen peroxide production by neutrophils also were determined. Cows fed Se-deficient diets had significantly (P less than 0.05) lower blood Se concentration and blood glutathione peroxidase activity than cows fed Se-supplemented diets. Selenium status had no effect on the phagocytic capacity of neutrophils. Neutrophils obtained from cows fed Se-supplemented diets killed a significantly (P less than 0.05) higher percentage of ingested bacteria than did neutrophils from cows fed the Se-deficient diet. Viability was significantly (P less than 0.05) reduced by incubation with S aureus in neutrophils from both groups of cows, with neutrophils from Se-deficient cows having lower viability.(ABSTRACT TRUNCATED AT 250 WORDS)
18 factors, including possible lung cancer-causing factors and body selenium (Se) levels, were analyzed by computer-based multiple stepwise regression and main component analysis. 1. The results indicated that Se levels in blood, hair and lung had correlation with lung cancer to some extent. 2. The correlation of blood and lung Se was the most significant one, the significance of which was only second to age and smoking habits. The standardized regression and factor load coefficients showed a negative correlation with blood Se level and a positive one with lung Se level, which corresponded with the results obtained by the single factor analysis.
In cows from 15 dairy herds (n = 210), serum selenium (Se) concentrations ranged from 0.021 to 0.789 microgram/ml, whereas 0.05 to 0.40 microgram/ml is the reported range for adequate serum Se concentrations in cattle. Serum Se concentrations of dairy cattle appeared to follow a geographic distribution pattern. On the basis of herd mean serum Se concentrations, adequate serum Se concentrations were found in cattle from only 1 of 5 herds grazing forage in the geographic area classified as Se deficient for cattle. Adequate mean serum Se concentrations were found in cattle from 4 of 5 herds located in geographic areas described as having variable forage Se concentrations (Se-marginal areas). Of the 10 herds from these 2 areas, there were only 2 herds in which 95% of the cattle had serum Se concentrations in the Se-adequate range (0.05 to 0.40 microgram/ml). In 2 selected neighboring farms in the Se-deficient area, cattle in 1 herd had adequate serum Se concentrations and cattle in the other herd had less than adequate serum Se concentrations (less than 0.05 microgram/ml). Therefore, more cattle are at risk of developing Se-deficiency disease than is commonly believed and forage of neighboring farms may have different Se concentrations. Serum Se concentrations (up to 0.789 microgram/ml) correlated with glutathione peroxidase enzyme activity; this serum Se concentration (0.789 microgram/ml) is approximately 6.2 times higher than previously reported in dairy cattle. Therefore, RBC glutathione peroxidase activity may be useful in determining the diagnosis of chronic Se toxicosis.
A 75Se-labeled hydrogenase was purified to near homogeneity from extracts of Methanococcus vannielii cells grown in the presence of [75Se]selenite. The molecular weight of the enzyme was estimated as 340,000 by gel filtration. The enzyme tends to aggregate and occurs also as a larger protein species (Mr = 1.3 x 10(6)). The same phenomenon was observed on native gel electrophoretic analysis. Hydrogenase activity exhibited by these two protein bands was proportional to protein and 75Se content. Both molecular species reduce the natural cofactor, 8-hydroxy-5-deazaflavin, and tetrazolium dyes with molecular hydrogen. Sodium dodecyl sulfate-gel electrophoresis of 75Se-labeled enzyme showed that 75Se is present exclusively in an Mr = 42,000 subunit. A value of 3.8 g atoms of selenium/mol of enzyme (Mr = 340,000) was determined by atomic absorption analysis. The chemical form of selenium in the enzyme was shown to be selenocysteine. This was identified as the [75Se]carboxymethyl and [75Se]carboxyethyl derivatives in acid hydrolysates of alkylated 75Se-labeled protein. The hydrogenase is extremely oxygen-sensitive but can be reactivated by incubation with molecular hydrogen and dithiothreitol.
In 3 experiments, 684 newly hatched White Pekin ducklings were fed (for 15 to 28 days) a commercial starter mash that was adequate in selenium and vitamin E (Se-E) content, either alone or with supplements of Ag (3,000 mg/kg of feed, as acetate), Cu (1,500 mg/kg, as sulfate), Co (200 or 500 mg/kg, as chloride), Te (500 mg/kg, as tetrachloride), Cd (100 or 500 mg/kg, as sulfate), Zn (3,000 or 6,000 mg/kg, as sulfate), or V (100 mg/kg, as vanadate). The ducklings fed Ag, Cu, Co, Te, Cd, and Zn frequently developed lesions characteristic of Se-E deficiency, such as necrosis of skeletal and cardiac muscle and of smooth muscle of the gizzard and intestine. Complete protection from the muscle lesions produced by Cu, Co, Te, Cd, and Zn supplements was provided by vitamin E (200 IU of alpha-tocopherol acetate/kg) and Se (2 mg/kg, as selenite). Ducklings fed Ag were protected by supplements of vitamin E and partial protection was achieved by Se addition. The birds fed excessive Zn developed pancreatic necrosis and fibrosis that was not prevented by supplements of Se or vitamin E. Terminally, blood glutathione peroxidase activity was low and hepatic Se concentration was increased in the ducklings fed Ag. However, neither blood glutathione peroxidase activity nor hepatic Se concentrations was consistently abnormal in ducklings fed other trace elements, although lesions of Se-E deficiency were often present in these animals.
Growing pigs were fed diets containing 5 or 10% white sweet clover, and 0, 3.5 or 7.0 ppm selenium (Se) supplied as sodium selenite (Na2SeO3) or occurring naturally in white sweet clover harvested from a coal fly ash dump. Ground carcasses of these pigs were included in corn meal diets at 23% and fed back to pigs. Compared to the pigs fed the high Se, fly ash-grown clover diets, the pigs fed Na2SeO3 diets had higher blood Se levels but lower Se concentrations in kidney, liver and skeletal muscle. Tissues of the pigs which were fed carcasses of the high Se clover-fed pigs had higher Se concentrations than those of the pigs fed carcasses of the Na2SeO3 - fed pigs.
Effects of selenium (Se) deficiency and supplementation on production of colostral immunoglobulins by beef cows and transfer of antigen-specific and nonspecific immunoglobulins to their calves were examined. Eight beef cows, with marginal to deficient Se status (blood Se concentration, 50 micrograms/L), were allotted by breed and age to 1 of 4 Se treatment groups (n = 20/group): no supplemental Se; parenteral administration of 0.1 mg of Se and 1 mg of vitamin E/kg of body weight; ad libitum consumption of 120 mg of Se/kg of salt-mineral mix (SMM); and parenteral administration of 0.1 mg of Se and 1 mg of vitamin E/kg plus ad libitum consumption of 120 mg of Se/kg of SMM. All cows were inoculated IM with lysozyme. Cows consumed Se-deficient pastures or hay (21 to 62 micrograms/kg) during the study that began at mid-gestation and ended at postpartum hour 24. Although the concentration of specific lysozyme antibodies was not affected, cows given 120 mg of Se/kg of SMM (treatments 3 and 4) had higher colostral IgG concentration (P < 0.002) than did Se-deficient cows (treatments 1 and 2). Calves from cows in treatments 3 and 4 had higher postsuckle serum concentrations of IgG (P < 0.01) than did calves from cows in treatments 1 and 2. Colostral IgM and calf serum IgM concentrations did not differ among treatments.
The effect of an increased intake of wheat selenium (Se) on platelet Se, serum Se, whole-blood Se, and glutathione peroxidase (GSH-Px) levels was investigated in 14 healthy Norwegian females (age 21-53 years). The intake of 60 micrograms Se per day as wheat Se, for six weeks, significantly increased the platelet Se (mean +/- SEM) from 9.1 +/- 1.1 mumol/L to 11.4 +/- 0.9 mumol/L, the serum Se from 1.43 +/- 0.18 mumol/L to 1.63 +/- 0.25 mumol/L, and the whole blood Se from 1.77 +/- 0.18 mumol/L to 2.01 +/- 0.18 mumol/L. The increase in percent of initial Se values was twice as high for platelets as for serum and whole blood. The GSH-Px levels were not altered during the experiment. Platelet Se was not significantly correlated to the Se intake initially. At the end of the experimental period, the Se in platelets reflected the total Se intake, but not with a simple linear correlation. No significant correlation between the total Se intake and the Se concentration in whole blood or serum was found.
The aim of this work was to determine the effect of selenium (Se) deficiency on the porcine liver oxidative stability and to investigate Se content and oxidative status in porcine liver after dietary supplementation with vitamin E (vit E), sodium selenite, and selenized yeast. Experimental animals were fed a basal corn meal, low in Se and vit E, for a 4-week depletion period before being given the experimental diets containing different levels of Se and/or vit E for 5 months. Dietary treatments were the basal diet with no additions (control); the basal diet supplemented with 25 mg of vit E/kg of feed (group I); basal diet + 0.3 mg selenite-Se/kg (group II); basal diet + 0.3 mg selenized yeast-Se/kg (group III); basal diet + 0.1 mg selenite-Se + 10 mg vit E/kg (group IV); and basal diet + 0.3 mg selenite-Se + 25 mg vit E/kg (group V). The Se content in pig liver samples was 33 to 192% lower in the control group than in all the other groups. Dietary Se from selenized yeast had a more pronounced effect on Se level than dietary sodium selenite. The highest Se content was found in liver samples from the Se + vit E supplemented group (group V). All the dietary supplementation schemes significantly improved the oxidative status of porcine liver compared with the control group samples. The best results were obtained by simultaneous dietary supplementation with Se + vit E (groups IV and V) > group III > group II > group I.
We studied the activity of erythrocyte selenium (Se)-dependent, Se-non-dependent glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) in uremic patients (UP) in clinically healthy members from families affected with Balkan nephropathy (HMF/BEN) and in healthy volunteers from endemic settlements (control group). The SOD activity was not significantly different in the groups studied and the Se-non-dependent GSH-Px activity in HMF/BEN and UP was not different from the control group. However, the activity of Se-dependent GSH-Px in UP was lower compared with the control group, whereas the mean value of the Se-dependent GSH-Px activity in HMF/BEN was not significantly different when compared with the other two investigated groups.
The influence of selenium (Se) restriction on disposition in plasma and urine fractions of infused (74)Se (selenite) was studied when adult males (Enshi City, Hubei Province, PRC) whose habitual daily Se intake is approximately 480 microg per day were transferred to Lichuan County, where the daily intake is approximately 30 microg. The subjects received an infusion (106 microg Se) on the day before consuming foods low in Se and a second infusion (113 microg Se) 63 days later. Blood and 24-hour urine samples were collected each day for 7 days after the first infusion and on days 22, 43, and 62 following the first infusion. Urine and blood were also collected daily for the next 7 days after the second infusion. Plasma total Se concentration increased for 7 days after each of the two infusions and urine Se decreased exponentially following both the first and second infusions. The excretion of trimethylselenonium followed the same pattern as the total urinary Se. Surprisingly, there was not a significant difference in selenite retention between the two infusion periods, and the data indicated that, regardless of the chemical form of Se present in various organs, its catabolism leading to excretion in urine followed the same pathway as that of selenite. Labeled Se was incorporated predominantly in the plasma selenoprotein P fraction and the half-life of Se in this fraction was determined to be 1.9 to 2.9 days. Thus, a longer depletion period is required in these subjects to obtain more significant changes.
Novel selenium analogues of diiodo(ethylenedithio)diselenadithiafulvalene (DIETS) have been successfully derived from 1,3-diselenole-2-thione, which could be synthesized without the use of the highly toxic reagent CSe(2).
The efficacy of selenium dioxide (SeO2) was similar to sodium selenate (Na2SeO4 x 10H2O), in terms of increasing and maintaining blood Se concentrations, when administered orally twice daily to give 0.64 mg of Se/day to grazing dairy cows for 55 days.
AIM: To determine the relationships between blood selenium (Se) concentrations or glutathione peroxidase activity (GSH-Px), and milk Se concentrations in dairy cows. METHODS: Seventy-two Friesian dairy cows were either untreated or injected with 0.5, 1.0 or 2.0 mg Se/kg liveweight as barium selenate (BaSeO4) formulations, resulting in 6 groups of animals with mean blood Se concentrations that varied from 212 to 2272 nmol/l. Milk samples were collected on Days 104 and 188, and blood samples were collected prior to treatment and on Days 41, 76, 104, 188, 244, and 292 after Se injection. RESULTS: Significant quadratic relationships between blood Se and milk Se concentrations, as well as blood GSH-Px activity and milk Se concentrations, were evident at Days 104 and 188. Using combined data, these were represented by the equations: milk Se = 27.3 + 0.073 blood Se -0.00001 (blood Se)2; R2=0.79, p<0.005, and; milk Se = 34.8 + 4.99 GSH-Px -0.068 (GSHPx)2; R2=0.79, p<0.005. CONCLUSIONS: The Se status of dairy cows can be assessed from milk Se concentrations. CLINICAL SIGNIFICANCE: Bulk-tank milk Se concentrations could be evaluated as a method to assess the Se status of dairy herds.
AIMS: To quantify the relationship between blood selenium (Se) concentration and growth response to Se supplementation in lambs, in order to assess the reliability of current reference ranges and to predict the magnitude of likely responses to supplementation. METHODS: Data from 24 Se-supplementation growth-response trials which used the following general protocol were collated and analysed: in each trial, weaned lambs (n=20-30) were allocated randomly to untreated or to Se-supplemented groups. Supplemented groups received 5 mg Se/month as Na2SeO3 in 20 trials, and 1 mg Se/kg liveweight as BaSeO4 in 4 trials. The duration of the trials was 150-196 days, during which time all lambs were weighed every 4-6 weeks and blood samples were taken at various intervals from 10 lambs/group. RESULTS: Among the 24 trials, flock mean blood Se concentrations of the untreated lambs ranged from 32-569 nmol/l, and growth rate of supplemented lambs was -3 to 63 g/day higher than that of untreated lambs. The relationship between blood Se concentration (X) and growth response (Y) was described by the following hyperbolic-decay equation: Y = -2.6 (SE 3.6) + 1850 (SE 230) / X; (R2=0.74). CONCLUSIONS: For Se-deficient lambs, the potential for a growth response to Se supplementation was strongly related to blood Se concentration. Economically significant liveweight gains of 10 g/day were observed when initial blood Se concentrations were 130 nmol/l. CLINICAL RELEVANCE: Blood Se concentrations can be used to diagnose Se deficiency in lambs and to predict the magnitude of likely growth responses to Se supplementation.
Selenodiglutathione (SDG), the initial metabolite of selenite, is shown to be a more powerful inhibitor of cell growth in vitro than selenite itself. This has been established both with mouse erythroleukaemia (MEL) cells and an ovarian cell line (A2780) which is known to contain wild-type p53. Other seleno-compounds, such as selenomethyl selenocysteine (SMS) and dimethyl selenoxide (DMS), which are potent chemopreventive agents and are known to be metabolized to methylated selenium derivatives directly rather than via SDG, are also growth inhibitory to both MEL and A2780 cells, although less so than SDG or selenite. However, cells growth-inhibited by DMS are more viable than cells growth-inhibited to the same extent by SDG or selenite, suggesting that the methylated seleno-compounds may inhibit cell growth in a different manner from that of SDG or selenite. Our studies of the mechanism of growth inhibition by SDG, have established two facts. First, SDG induces p53 protein levels in cells that contain wild-type p53 (A2780 cells), suggesting that SDG induces the DNA damage-recognition pathway. Secondly, SDG induces apoptosis in MEL cells, as judged by flow cytometry and formation of nucleosomal DNA ladders. However, since p53 mutations have been found to be targetted events in all MEL cells examined, our evidence suggests that induction of apoptosis by SDG is not absolutely dependent on the p53 response pathway.