Selenium and vitamin E deficiency in pigs. II. Influence on plasma selenium, vitamin E, ASAT and ALAT and on tissue selenium.
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Alanine Transaminase↗
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A review of selenium deficiency in grazing ruminants. Part 1: new roles for selenium in ruminant metabolism.
SELENIUM AVAILABILITY: Selenium deficiency has been an important source of loss to the pastoral industries of New Zealand. About 30% of farmed land in New Zealand is considered to be selenium-deficient and continued development of soils and pasture will tend to further decrease the concentration of selenium in pasture. BIOLOGICAL FUNCTIONS: Formerly it was believed that all biological functions of selenium in animals could be attributed to the antioxidant activity of the enzyme glutathione peroxidase. More recently, it has been shown that selenoproteins have roles in immune function and thyroid hormone metabolism. RESPONSES TO SUPPLEMENTATION: Following supplementation of ruminants grazing pastures deficient in selenium, milk production and growth responses are likely to occur in cattle, while in sheep improvements in growth and fertility are most likely. Reproductive dysfunction may not be as important as previously thought in cattle grazing pasture moderately deficient in selenium. The relationship between selenium intake and disease resistance deserves further study. CLINICAL RELEVANCE: Management of selenium deficiency will continue to be important in grazing ruminants. Veterinarians should be aware that many selenoenzymes exist, some with functions quite distinct from the antioxidant role of glutathione peroxidase.
Journal Article↗
Selenium distribution in blood fractions of New Zealand women taking organic or inorganic selenium.
Three groups of 11 New Zealand women each received, for 32 wk, yeast tablets with no added selenium (placebo) or 200 micrograms Se/d in tablets either as selenate or as selenium-enriched yeast (SeMet) in a double-blind selenium trial. Plasma and erythrocyte (RBC) samples were collected bimonthly. Gel filtration of plasma from women taking SeMet revealed two major selenium-containing peaks with most of the selenium in the second peak. In contrast, the first peak contained most of the selenium in plasma from women taking selenate. Chromatography of RBC lysates indicated that the majority of the selenium was with hemoglobin (Hb) in women taking SeMet but was about equally distributed between glutathione peroxidase (GSH-Px) and Hb in women taking selenate. The percentage of selenium associated with GSH-Px was found to be greater in RBCs and plasma of women taking selenate than of those taking SeMet.
Adult↗
Selenium deficiency in cultured adrenocortical cells: restoration of glutathione peroxidase and resistance to hydroperoxides on addition of selenium.
Cultured bovine adrenocortical cells were previously shown to be functionally deficient in selenium and vitamin E when grown in medium supplemented with fetal bovine serum. In the present experiments, the lack of significant bioavailable amounts of selenium in the medium was demonstrated by the finding of only low levels of glutathione peroxidase in the cultured cells (0.008 U/mg protein compared with 0.045 U/mg protein in fresh adrenocortical tissue). When 20 nM selenium as selenite was added to the cultured adrenocortical cells, glutathione peroxidase activity increased continuously over 72 h, with a total increase of about eightfold over this period. Over the same time-course, the highest concentration of cumene hydroperoxide tolerated by the cells without cell death increased progressively from 10 microM to 50 microM. Addition of 1 microM alpha-tocopherol also increased the amount of cumene hydroperoxide tolerated to 50 microM. Cell death was measured by cloning efficiency after removal of cumene hydroperoxide. Addition of either selenium or alpha-tocopherol had little effect on the growth rate of the cells over six passages, even when residual vitamin E was removed from the serum by extraction with ether and residual low molecular weight selenium compounds were removed by dialysis. It is concluded that combined deficiency of selenium and vitamin E, at least in the presence of other components of fetal bovine serum, has little effect on the ability of the cells to survive under normal conditions, as evidenced by continued long-term proliferation. However, the low levels of glutathione peroxidase resulting from selenium deficiency cause an increase susceptibility to peroxide-mediated toxicity. The combined deficiency of selenium and vitamin E impairs the ability of cells to survive under adverse conditions, as well as altering mitochondrial functions, as previously demonstrated.
Adrenal Cortex↗
Low selenium status in alcoholic cirrhosis is correlated with aminopyrine breath test. Preliminary effects of selenium supplementation.
The relationship among impaired selenium status, lipid peroxidation, and liver function was examined in 19 hospitalized patients with severe alcoholic cirrhosis. Plasma selenium was found to be significantly lower (mean +/- SD: 54 +/- 13 micrograms/L) than in healthy controls (83 +/- 11 micrograms/L) and plasma malondialdehyde, assessed as thiobarbituric acid reactants, which reflects lipid peroxidation, was increased (2.0 +/- 1.2 mumol/L vs < 1.2 mumol/L in controls). The mean 14C aminopyrine breath test, an indicator of liver function, was lower than normal (2.7 +/- 1.9 vs 6.3 +/- 0.9% in controls) and found to be significantly correlated with plasma selenium (r = 0.59, p < 0.05). A prospective, randomized selenium supplementation trial was conducted in a group of 16 patients who received either daily 100 micrograms selenium as enriched yeast during 4 mo or a placebo. Among the 10 patients who completed the study, plasma selenium significantly increased in the supplemented group (n = 4; before: 58 +/- 10 micrograms/L, and after 101 +/- 12 micrograms/L, p < 0.01) contrary to the placebo group (n = 6, before: 47 +/- 10 micrograms/L, after: 57 +/- 9 micrograms/L, n.s.). 14C aminopyrine breath test improved in three out of four selenium-supplemented patients and in three out of six placebo patients, but the small number of patients did not allow statistical evaluation. These results demonstrate that low selenium status in alcoholic cirrhosis is correlated to liver function and could be improved by supplementation.
Adult↗
Selenium supplementation: plasma glutathione peroxidase an indicator of selenium intake.
Plasma glutathione peroxidase activity is markedly reduced in dietetically treated patients with PKU or MSUD in comparison to health children of the same age. This is due to the low selenium content of their diet. During supplementation with yeast rich in selenium (200 micrograms selenium per day) for 3 months 2 healthy adults did not show any significant change of their plasma GSHPx activity. 5 dietetically treated patients with PKU or MSUD and a reduced selenium state showed a rapid increase of the plasma GSHPx activity after selenium supplementation were started with 120 micrograms Se/m2 x d. The values doubled within the first two days and reached a plateau after 1--3 weeks. The patients showed no clinical anomalities before or during the selenium supplementation besides the inherited defect of amino acid metabolism. Plasma GSHPx activity seems to be a good indicator of short-term changes of selenium intake in patients with reduced selenium state.
Child↗
Nicotinic acid hydroxylase from Clostridium barkeri: electron paramagnetic resonance studies show that selenium is coordinated with molybdenum in the catalytically active selenium-dependent enzyme.
Nicotinic acid hydroxylase from Clostridium barkeri contains selenium in an unidentified form that is dissociated as a low molecular weight compound upon denaturation of the enzyme. Other cofactors of this enzyme are molybdopterin, FAD, and iron-sulfur clusters. In the current study, we show that the enzyme, as isolated, exhibits a stable Mo(V) electron paramagnetic resonance (EPR) signal ("resting" signal) and that this signal is correlated with the selenium content and nicotinate hydroxylase activity of the enzyme. Substitution of 77Se for normal selenium isotope abundance results in splitting of the Mo(V) EPR signal of the native protein without affecting the iron signals of the FeS clusters. The Mo(V) EPR signal and nicotinic acid hydroxylase activity of enzyme isolated from cells grown in selenium-deficient medium are barely detectable. In contrast, the EPR signals of the FeS clusters, the electronic absorption spectrum, the NADPH oxidase activity, and the chromatographic behavior are changed little and are typical of active selenium-containing enzyme. An EPR signal indicative of the presence of molybdenum in the selenium-deficient enzyme also is exhibited. From these results, we conclude that a dissociable selenium moiety is coordinated directly with molybdenum in the molybdopterin cofactor and, moreover, this selenium is essential for nicotinic acid hydroxylase activity.
Bacterial Proteins↗
Hepatic cytosolic non selenium-dependent glutathione peroxidase activity: its nature and the effect of selenium deficiency.
Recent work had indicated the presence of a non selenium-dependent glutathione peroxidase activity in rat liver in addition to the selenium-dependent activity. The present study was undertaken to learn whether the glutathione S-transferases are reponsible for the non selenium-dependent glutathione peroxidase activity and to study the effect of selenium deficiency on those enzymes. Glutathione S-transferase B was purified by an established method using carboxymethyl cellulose ion exchange chromatography and studied. It exhibited glutathione peroxidase activity toward cumene hydroperoxide and t-butyl hydroperoxide. A limiting Km of 0.55 mM was determined for cumene hydroperoxide. Sulfobromophthalein was found to be a competitive inhibitor with respect to cumene hydroperoxide of the glutathione peroxidase activity of glutathione S-transferase B. Selenium deficiency caused an increase in glutathione S-transferase activity. These results establish that glutathione S-transferase B contributes to the non selenium-dependent glutathione peroxidase activity in rat liver and show that it increases in selenium deficiency when the selenium-dependent glutathione peroxidase is decreased.
Animals↗
Effect of selenium on appetite in the selenium-deficient chick.
Experiments were conducted to determine the initial effects of oral selenium administration on selenium-deficient chicks. Administration of 5 microgram selenium as seleno-DL-methionine increased voluntary feed consumption within 2-3 hours, whereas selenite did not have a significant effect until 3-4 hours. Spontaneous activity, body weight gain and plasma glucose concentration increased 6-8 hours after selenium administration. The earliest response in the specific activity of selenium-dependent glutathione peroxidase occurred in plasma at 8 hours and in liver at 24 hours after selenium administration. The onset of pancreatic atrophy, however, was not affected by the level of feed intake suggesting that the effect of selenium upon appetite may be distinct from the involvement of selenium in nutritional pancreatic atrophy and fibrosis.
Animals↗
Effect of selenium supplementation on thyroid hormone metabolism in an iodine and selenium deficient population.
OBJECTIVE: Severe selenium deficiency has been documented in northern Zaïre, already known as one of the most iodine deficient regions in the world and characterized by a predominance of the myxoedematous form of cretinism. This has been attributed to the double deficiency of essential trace elements. A short selenium supplementation programme was conducted in this area to evaluate the effects of a selenium supplementation on thyroid diseases. DESIGN: Placebo or selenium 50 micrograms as selenomethionine was administered once daily for 2 months. Blood and urine samples were collected before and after supplementation. PATIENTS: Fifty-two healthy schoolchildren from northern Zaire. MEASUREMENT: Selenium status, thyroid function and urinary iodide were determined. RESULTS: After 2 months of selenium supplementation, mean +/- SD serum T4 decreased from 73.1 +/- 45.4 to 48.3 +/- 23.7 nmol/l (P less than 0.001), serum FT4 from 11.8 +/- 6.7 to 8.4 +/- 4.1 pmol/l (P less than 0.01), and serum rT3 from 124 +/- 115 to 90 +/- 72 pmol/l (P less than 0.05), without significant change in serum T3 and serum TSH. CONCLUSION: Deiodinase type I which has been shown to be a seleno-enzyme could account for the changes in thyroid hormones in our subjects. Our data show that selenium plays a definite role in thyroid hormone metabolism in humans. Selenium could be an important cofactor in the clinical picture of iodine deficiency in Central Africa and could be involved in the aetiology of both forms of cretinism.
Administration, Oral↗
Response of rat selenoprotein P to selenium administration and fate of its selenium.
Selenoprotein P is a glycoprotein that contains greater than 60% of the selenium in rat plasma. Physiological experiments were undertaken to gain insight into selenoprotein P function. Selenium-deficient rats were injected with doses of selenium ranging from 25 to 200 micrograms/kg, and the appearance of selenoprotein P was compared with the appearance of glutathione peroxidase activity in plasma and in liver. Selenoprotein P concentration increased to 35% of control by 6 h, whereas glutathione peroxidase activity increased minimally or not at all. Moreover, in rats given 100 and 200 micrograms selenium/kg, selenoprotein P reached 75% of its concentration in control rats at 24 h, whereas glutathione peroxidase activity reached only 6% of control. Cycloheximide pretreatment blocked the appearance of selenoprotein P in response to selenium injection. Male and female rats had similar concentrations of selenoprotein P. Partially purified selenoprotein P and plasma glutathione peroxidase labeled with 75Se were administered intravenously to selenium-deficient and control rats. 75Se given as selenoprotein P disappeared more rapidly from plasma than did 75Se given as glutathione peroxidase. Selenium deficiency did not significantly affect 75Se disappearance from plasma. At 2 h, brain, but not other tissues, took up more 75Se in selenium-deficient rats than in control rats when 75Se was given as selenoprotein P. This suggests that brain has a specific uptake mechanism for selenium given in the form of selenoprotein P. These results demonstrate that several physiological properties distinguish selenoprotein P from glutathione peroxidase. However, they do not clearly indicate its function.
Animals↗
Subcellular distribution of selenium in the liver from rats fed selenium from fish: selenocystine and inorganic selenite.
Four groups of rats of a normal selenium status were given different selenium compounds during a long-term feeding experiment (28 days). The selenium supplementations (per kg diet) were sodium selenite (1 mg), selenocystine (2 mg), and two different concentration levels of selenium from fish (0.1 and 1 mg). Differential pelleting of liver homogenates demonstrated that selenium was present in all the subcellular fractions, with a recovery of 55-60% in the cytosols. Gel permeation high-performance liquid chromatography of the cytosol fractions demonstrated the presence of protein-bound selenium at a molecular weight of 70,000 daltons. The subcellular distributions as well as the protein binding of selenium in the cytosols were identical in all dietary groups. This indicates a similar long-term liver metabolism of the four selenium compounds tested in the rat.
Animals↗
Selenium content of feeds and effect of dietary selenium on hair and blood serum.
A selenium depletion diet (.025 ppm selenium) was fed to two male Holstein calves for its effect on concentrations of selenium in serum. By 90 days, selenium in serum was depressed from .022 ppm to .013 ppm, and one of two calves had died of "possible white muscle disease." Repletion was rapid in that a diet containing .200 ppm selenium increased selenium in serum to .028 ppm within 2 wk. Dietary .280 ppm selenium increased it to .051 ppm in 1 wk. Eleven cows and eleven calves showed averages of .030 ppm in serum (range of .013 to .051 ppm) fed a diet of corn silage (.039 ppm) and supplement (.090 ppm). A sampling of feedstuffs showed a wide range of selenium among feedstuffs (.023 for corn cobs to 2.663 ppm for dried egg albumin) and a wide range within one type feedstuff (shelled corn, .017 to .219 ppm).
Animal Feed↗
Retention of selenium in tissues of calves, lambs, and pigs after parenteral injection of a selenium-vitamin E preparation.
Four each healthy weaned calves, lambs, and pigs raised in Indiana without selenium supplementation were killed, and their tissues were fluorometrically analyzed to establish base line selenium concentrations. The following mean selenium content (in ppm, wet weight) was found in calves, lambs, and pigs, respectively: liver, 0.12, 0.16, and 0.19; renal cortex, 0.63, 0.89, and 0.70; muscle, 0.05, 0.05, and 0.06. Eight each additional healthy weaned calves, lambs, and pigs were injected with a commercial selenium-vitamin E preparation at dose levels of 0.0825, 0.055, or 0.06 mg of Se (as selenite) per kilogram of body weight, respectively. Selenium content of tissues was measured in animals killed at 1, 7, 14, and 23 days after injection. In calves, concentrations in liver and kidney rapidly increased to moderate values and then slowly decreased, with mean concentrations after 23 days still somewhat greater than base line values. Concentrations for injection site tissue also rapidly increased to moderate values, but had decreased to base line values by 23 days after injection. In lambs, selenium content of liver was moderately increased after injection, but had decreased to base line values after 14 days; kidney and injection site did not have increased selenium content after injection. In pigs, liver and kidney had moderate initial increases in concentration of selenium, but these were at base line values after 14 days, and increase did not occur at injection sites.
Adipose Tissue↗
Comparison of selenium distribution in mice organs after the supplementation with inorganic and organic selenium compound selenosemicarbazide.
Studies on selenium organ content and its function in living organisms just like studies on other elements provide interesting results although their interpretation is not always clear. The aim of our study was to determine the concentration and distribution of selenium in several organs and tissues in mice after supplementation with our newly synthesized organic compound of selenium selenosemicarbazide (4-o-tolyl-selenosemicarbazide of o-chlorobenzoic acid) as compared to the effects of the supplementation with inorganic compounds. SWISS mice were fed with both types of compounds at the dose of 10(-3) g Se per kg for the period of 10 days. The concentrations of selenium in brains of mice treated with selenocarbazide and sodium selenite were higher than in controls (38.04 micrograms g-1 and 32.00 micrograms g-1 vs. 26.18 micrograms g-1). There was a statistically significant increase in the selenium contents in lungs after supplementation with selenosemicarbazide and sodium selenite (11.81 micrograms g-1 and 6.79 micrograms g-1 vs. 1.75 micrograms g-1 in controls). We found a statistically insignificant increase in selenium contents in intercostal muscles after supplementation with inorganic selenium compounds and a statistically significant increase after the supplementation with selenosemicarbazide (10.13 micrograms g-1; 14.21 micrograms g-1 and 28.84 micrograms g-1, respectively). Our investigations lead to a conclusion that 4-o-tolyl-seleno-semicarbazide of o-chlorobenzoic acid, an organic selenium compound may be more easily absorbed than inorganic sodium IV selenite.
Administration, Oral↗
Selenium status and absorption of zinc (65Zn), selenium (75Se) and manganese (54Mn) in patients with short bowel syndrome.
Selenium level and activity of glutathione peroxidase in plasma were studied in seven patients with extensive short bowel resection due to Crohn's disease, before and during 27-54 weeks of intake of a vitamin and trace element supplement containing 50 micrograms of selenium as sodium selenite. Initial levels of selenium were normal in all except one of the patients. The supplementation had no or minor effects on plasma selenium levels and glutathione peroxidase activity. The absorption of zinc, manganese and selenium was measured with a radionuclide technique before and/or after the supplementation period in five of the patients. The absorption of zinc and manganese was similar to that observed earlier in healthy subjects, while the absorption of selenium was significantly lower. The results indicate that a higher selenium intake or a different form of selenium is needed in these patients to compensate for the impaired bowel function.
Adult↗
[Dynamics of selenium in the blood serum of sows after a supplementary feeding dose of vitamin E and selenium during pregnancy].
The influence of peroral and parenteral supplementation with selenium compounds and vitamin E was studied in sows during gravidity, as exerted on the concentration of selenium in the blood serum of the tested sows. The experiment was conducted with 18 sows at the age of two to three years. The averge selenium level in the blood serum of the sows given an oral supplement of selenium and vitamin E was blood serum of the sows given an oral supplemnent of selenium and vitamin E was 2.278 mumol .1-1 on the 110th day of gravidity and 2.405 mumol .1-1 on the 20th day of lactation; adter s. c. injection of the preparation Selevit inj. Spofa the average concentration of selenium was kept at the same level from the 110th day to the 20th day of lactation (2.152 mumol .1-1). In the control sows the average value of blood serum selenium level was significantly lower at the same time intervals (1.772 and 1.645 mumol .1-1). Both ways of supplementation favourably influenced the selenium level in the blood serum of sows, particularly in the last stage of gravidity and in the first stage of lactation.
Animal Feed↗
Effect of acute selenium restriction on whole body endogenous selenium and the selenite-exchangeable metabolic pool in the adult rat.
The time course of changes in whole body endogenous selenium (Se(end)) was investigated during a short-term (7-day) selenium restriction study in the adult rat. The method of continuous feeding with a stable isotope of selenium was used to permit normal intake of selenium while distinguishing between the dietary and endogenous components of body selenium. Additionally, the effect of short-term selenium restriction on the time course of the selenite-exchangeable metabolic pool (Se-EMP) was investigated. Two groups of adult male rats were intubated with the in vivo stable isotope (74)SeO(3)(2-), then fed a Torula yeast diet (selenium <0.02 microg/g) and either deionized water (-Se group) or deionized water containing selenium as (76)SeO(3)(2-) (0.1 microg selenium/ml) (+Se group). Three animals from each group were killed at 24-hour intervals. Whole body Se(end) and the estimated size of Se-EMP (W(Se-EMP)) were determined using hydride generation-inductively coupled plasma mass spectrometry for isotopic measurements. Whole body Se(end) decreased linearly in the +Se group (Se degrees (end): 54.4 microg; Se(end) at 3 days: 49.3 +/- 2.1; Se(end) at 7 days: 45.2 +/- 2.2). The decrease was exponential for the -Se group (Se degrees (end): 54.4 microg; Se(end) at 3 days: 42.9 +/- 0.3; Se(end) at 7 days: 42.2 +/- 0.7). The value of W(Se-EMP,pl) (microg) was 19.8 +/- 0.6 at 1 day and 19.7 +/- 1.0 at 7 days for the +Se group. The corresponding values for the -Se group were 15.7 +/- 1.5 and 18.8 +/- 0.4. All respective values of W(Se-EMP,pl) for the -Se group were significantly smaller than for the +Se group (P < 0.05), with the exception of values at days 6 and 7. The value of W(Se-EMP,urine) (microg) was 2.1 +/- 0.2 at 1 day, increasing rapidly to 23.5 +/- 1.5 at 7 days for the +Se group. The corresponding values for the -Se group were 3.0 and 23.1.
Journal Article↗