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PubMed1996

Diagnostic criteria for selenium toxicosis in aquatic birds: dietary exposure, tissue concentrations, and macroscopic effects.

A feeding study with mallard ducks (Anas platyrhynchos) was conducted during March to July 1988 in Laurel, Maryland (USA), to identify diagnostic criteria for selenium toxicosis in birds. One-year-old male mallards in groups of 21 were fed diets containing 0, 10, 20, 40, or 80 parts per million (ppm) selenium, as seleno-DL-methionine, for 16 weeks. All ducks receiving 80 ppm died. Ducks receiving 40 or 80 ppm selenium consumed less feed than ducks in the other treatment groups. Body weights of ducks receiving 40 or 80 ppm selenium declined during the study. The post-breeding molt was delayed in ducks receiving 40 ppm; most ducks receiving 80 ppm selenium died prior to the onset of molt. At necropsy, numerous abnormalities were observed in ducks that died but only a small number of abnormalities were observed in ducks surviving to the end of the study in the 40 ppm group. Weights of the heart, spleen, and pancreas were mostly lower and weights of the kidney were higher for ducks dying during the study than for euthanized ducks. Liver weights were unaffected. Selenium accumulated in soft tissues approximately in proportion to dietary concentrations. Selenium concentrations in tissues of all ducks that died were different from those of surviving ducks in the 0, 10, and 20 ppm groups, but were not different from those of surviving ducks in the 40 ppm group. Proposed diagnostic criteria for fatal chronic selenosis were derived from body weight, macroscopic abnormalities, organ weights, and concentrations of selenium in the liver. Proposed diagnostic criteria for non-fatal chronic selenosis were derived from body weight, plumage condition, macroscopic abnormalities, concentrations of selenium in the liver, reproductive failure, and alterations of blood and tissue chemistries. Lead or dioxin poisoning have diagnostic criteria most similar to selenium toxicosis.

Administration, Oral↗

PubMedDate not supplied

[Role of selenium in the etiology and prevention of diseases (review)].

The data of reports by Russian and foreign authors on the biological effect of selenium are summarized. Some investigations have revealed its high toxic and carcinogenic properties in the selenium-rich biogeochemical provinces. Low-selenium diet has a human unfavourable impact. Recent studies have provided evidence for that is severe selenium deficiency in the environmental objects and foodstuffs virtually throughout the former USSR. At present selenium is recognized to be an essential trace element for human health. Selenium preparations in therapeutical doses have high antioxidative and anticarcinogenic activities. The types of medicinal plant materials that has a pronounced capacity to selectively accumulate selenium from the soil have been defined. Moreover, there are medicinal plants which are selenium concentrators that have high biological accumulation coefficients. Experimental and clinical findings indicate that selenium-containing drugs and medicinal plants should be recommended as an compulsory food additive in selenium-deficient areas for treatment and prophylaxis.

Antioxidants↗

PubMed2002

Age-related reference values for serum selenium concentrations in infants and children.

BACKGROUND: Children are at particular risk for selenium deficiency, which has potentially serious medical implications. Reliable age-specific reference values for serum selenium concentrations in children are sparse, but are essential for the identification of selenium deficiency and decisions regarding selenium supplementation. METHODS: Using electrothermal atomic absorption spectrometry, we analyzed serum selenium concentrations from 1010 apparently healthy children (age range, 1 day to 18 years) and from 60 patients on a protein-restricted diet because of inborn errors of metabolism. Reference intervals were defined according to recommended guidelines. RESULTS: Medians for serum selenium concentrations showed a statistically significant age dependency: a decrease from the age <1 month (0.64 micromol/L) to 4 months (0.44 micromol/L); an increase to 0.62 micromol/L in the 4-12 months age group; constant values in children between 1 and 5 years of age (0.90 micromol/L); and an additional slight increase to reach a plateau between 5 and 18 years (0.99 micromol/L). Of 43 children older than 1 year and on a protein-restricted diet, 87% showed serum selenium concentrations below the 2.5 percentile. CONCLUSIONS: Because of nutritional changes, serum selenium concentrations are significantly higher in older children than in infants under 1 year of age. The application of age-adjusted reference values may provide more specific criteria for selenium supplementation. Long-term protein restriction in children is reflected by a failure to achieve higher serum selenium concentrations with increasing age.

Adolescent↗

PubMed2003

Toenail selenium as biomarker: reproducibility over a one-year period and factors influencing reproducibility.

We assessed the reproducibility of selenium levels in toenails, comparing concentrations in two sets of specimens collected about a year apart, from 80 women (40 pre-menopausal and 40 post-menopausal) in the period October 1990 to February 1992. The women were participants in a prospective study on hormones and diet in relation to prediagnostic breast cancer (the ORDET study) conducted in northern Italy. Toenail selenium was determined by electrothermal atomic absorption spectrometry. The data were log-transformed as they were not normally distributed. To assess reproducibility Pearson correlation coefficients (r) for the two selenium determinations were calculated in pre- and post-menopausal women, according to smoking status and acetone treatment. A weighted kappa statistic (k) assessed inter-quintile agreement between the two sets of measures. Toenail selenium levels were highly reproducible (r = 0.57, p < 0.001), especially in pre-menopausal women (r = 0.66, p <0.001). Smoking lowered selenium levels (mean difference of 0.24 microg/g, p < 0.05 between smokers and non smokers) but did not significantly influence reproducibility. Acetone treatment to remove nail polish did not modify selenium levels but affected inter-quintile agreement, with moderate agreement (k = 0.58, p < 0.001) when acetone was used at both or neither samplings; and fair non significant agreement (k = 0.39, p = 0.06) when acetone was used at one sampling but not the other. As selenium levels in toenails are highly reproducible, notwithstanding variation in selenium levels in food and long-term changes in individuals' food choices, toenail selenium may be a useful biomarker of selenium exposure, particularly since toenail samples provide a measure of long-term exposure. However age, smoking status and acetone treatment are possible causes of misclassification.

Acetone↗

PubMed2004

The facts and controversies about selenium.

Selenium is a trace element, essential in small amounts, but it can be toxic in larger amounts. Levels in the body are mainly dependent on the amount of selenium in the diet, which is a function of the selenium content of the soil. Humans and animals require selenium for normal functioning of more than about 30 known selenoproteins, of which approximately 15 have been purified to allow characterisation of their biological functions. Selenoproteins are comprised of four glutathione peroxidases, three iodothyronine deiodinases, three thioredoxin reductases, selenoprotein P, selenoprotein W and selenophosphate synthetase. Selenium is essential for normal functioning of the immune system and thyroid gland, making selenium an essential element for normal development, growth, metabolism, and defense of the body. Supportive function of selenium in health and disease (male infertility, viral infections, including HIV, cancer, cardiovascular and autoimmune diseases) is documented in great number of clinical examinations. A great number of studies confirm that selenium supplementation plays a preventive and therapeutical role in different diseases. Definitive evidence regarding the preventive and therapeutical role of selenium as well as the exact mechanism of its action should be investigated in further studies. Investigations in Croatia indicate a possibility of inadequate selenium status of people in the area.

Animals↗

PubMed2006

Effect of selenium supplementation on activity and mRNA expression of type 1 deiodinase in mice with excessive iodine intake.

OBJECTIVE: To investigate the effect of selenium supplementation on the selenium status and selenoenzyme, especially the activity and mRNA expression of type 1 deiodinase (D1) in mice with excessive iodine (EI) intake and to explore the mechanism of selenium intervention on iodine-induced abnormities. METHODS: Weanling female BALB/c mice were given tap water or 3 mg/L of iodine or supplemented with 0.5 mg/L or 1.0 mg/L of selenium in the presence of excessive iodine for 5 months. Selenium status, thyroid hormone level, hepatic and renal D1 activity and mRNA expression were examined. RESULTS: Excessive iodine intake significantly decreased the selenium concentration in urine and liver, and the activity of glutathione peroxidase (GSH-Px) in liver. Meanwhile, serum total T4 (TT4) increased while serum total T3 (TT3) decreased. Hepatic D1 enzyme activity and mRNA expression were reduced by 33% and 86%, respectively. Renal D1 enzyme activity and mRNA were reduced by 30% and 55%, respectively. Selenium supplementation obviously increased selenium concentration, activity of GSH-Px and Dl as well as mRNA expression of D1. However, increasing the supplementation of Se from 0.5 to 1.0 mg/L did not further increase selenoenzyme activity and expression. CONCLUSION: Relative selenium deficiency caused by excessive iodine plays an essential role in the mechanism of iodine-induced abnormalities. An appropriate dose of selenium supplementation exercises a beneficial intervention.

Animals↗

PubMed1990

[Selenium and pregnancy].

Selenium is an essential trace element with protective properties against endogenous or exogenous aggression, mainly due to the hyperproduction of oxygen derivatives. During pregnancy, a depletion in plasma selenium occurs regulated by hormones from the placenta. Selenium requirement is simultaneously increased which is partly satisfied by the increased retention of the element resulting from a decrease in selenium urinary excretion. The foetus accumulates selenium at the end of pregnancy by storing it in the liver. However, after birth, selenium stores rapidly deplete. Selenium deficiency is apparently not responsible for pregnancy or delivery problems in man. However, the infant is exposed to pronounced deficiency symptoms or to the worsening of some diseases liable to affect the young baby, particularly if premature because the usual selenium dietary intake is marginal in this country, selenium supplementation with 25 to 50 micrograms selenium per day is advisable and should be considered among other trace elements as a food supplement for pregnant and lactating woman.

Female↗

PubMed1986

Differential effects of selenium on normal and neoplastic canine mammary cells.

Four different canine mammary tumor (CMT) cell lines and a nonneoplastic primary culture of mammary cells were examined for their in vitro responsiveness to selenium supplementation. These cell lines were found to vary in their metabolic response to increasing concentrations of selenium. Sensitivity to selenium, as sodium selenite, increased with increasing concentrations of this trace element in all of the neoplastic lines. These data also suggest that increasing the plating density of tumor cells further increases the sensitivity to selenium. A relatively selenium-sensitive cell line (CMT-13) and relatively insensitive cell line (CMT-11) were characterized on the basis of reduced growth resulting from selenium supplementation. Increasing the concentration of selenium to 0.75 microgram/ml depressed the growth of CMT-13 and CMT-11 cells by 75% and 11%, respectively, while no inhibition was observed in nonneoplastic cells. These cell lines also varied in their sensitivity to different forms of selenium. Selenodiglutathione was the most effective form of selenium examined that inhibited tumor cell growth. The sensitivity of the neoplastic lines was selenodiglutathione much greater than sodium selenite much greater than selenocystine greater than selenomethionine. None of the forms of selenium examined inhibited the growth of the nonneoplastic mammary cells in culture. Supplementation with sodium selenite (1 microgram Se per ml) for 60 min resulted in a dramatic depression in RNA biosynthesis in CMT-13, but not CMT-11 or nonneoplastic cells.

Animals↗

PubMed1989

[The optimal selenium supplementation in reproducing sows].

In two trials with sows of German Landrace at different dietary selenium levels glutathione peroxidase activity (GSH-Px activity) in plasma was determined at day 60, 90 and 110 of gestation, day 5, 15 and 25 of lactation and day 7 post weaning. In three groups of five first-litter gilts receiving 0.1, 0.3 and 0.5 mg selenium per kg diet, GSH-Px activities dropped within the treatments, independent of dietary selenium, from day 60 of gestation to a minimum at day 5 and 15, respectively, of lactation and increased again after weaning. Highest enzyme activities were observed at the 0.5 level. In another trial, 127 reproductive cycles of sows in first, second and third parity, respectively, with 0.1, 0.5 and 0.9 mg dietary selenium were investigated. GSH-Px activity showed results comparable to those of the former trial. Selenium content of plasma increased linearly as dietary selenium increased. In all cases, results of GSH-Px activity and of plasma selenium were confirmed by regression analysis. Reproductive performance ameliorated with increasing dietary selenium. Especially piglet's gain from birth to weaning and litter weight at weaning increased significantly. Furthermore, percentage of still born piglets showed a minimum at the selenium supplementation of 0.5 mg/kg diet. The pattern of GSH-Px activity in plasma and the improved reproductive performance of animals imply that the requirement of the sow during the reproductive cycle is met a level of 0.5 mg selenium per kilogram diet.

Animal Feed↗

PubMed1989

Selenium status in Sudanese children with protein-calorie malnutrition.

In 68 Sudanese children with severe protein-energy malnutrition, age 1-4 years, the selenium status was investigated and the results were compared with those of healthy Sudanese and German children. The median selenium content in plasma of healthy Sudanese children (x = 59 micrograms/L) and with those of marasmus (x = 57 micrograms/L) were found to be in the same range. It was lower than in healthy German children (x = 82 micrograms/L). Patients with marasmic kwashiorkor exhibited still lower values (x = 42 micrograms/L. Within each group of malnourished children (marasmus, marasmic kwashiorkor, kwashiorkor) there were patients with low and with "normal" selenium values (taking the values of healthy German children as normal). Hair selenium values were not different between marasmic Sudanese children and healthy German children, probably due to reduced hair growth in malnourished children. Plasma glutathione peroxidase activity was reduced concomitantly with plasma selenium in the patients with protein-calorie malnutrition. There was a good correlation between plasma selenium and plasma glutathione peroxidase activity. A follow-up study showed that plasma selenium decreased during rehabilitation in those patients who had a "normal" value before treatment. This is probably due to the low selenium content of the two dietary formulae used, which contained 18 and 25 micrograms/L Se of formula,. It remains questionable whether the low selenium states and low selenium intake exhibit a healthy risk inhibiting further rehabilitation of the patients with severe protein-calorie malnutrition.

Child, Preschool↗

PubMed1989

The effect on atopic dermatitis of supplementation with selenium and vitamin E.

Reduced concentrations of selenium in whole blood, plasma and white cells and reduced activity of selenium-dependent glutathione peroxidase in red cells have been found in atopic dermatitis. To determine the effect of selenium supplementation on this disease, the normal daily diet of 60 adults with atopic dermatitis was supplemented with selenium-enriched yeast for 12 weeks in a randomised double-blind study. Group 1 took 600 micrograms of selenium alone, Group 2 600 micrograms of selenium plus 600 IU of vitamin E and Group 3 a placebo. After 12 weeks, there was a significant increase in the concentration of selenium in whole blood and the activity of selenium dependent glutathione peroxidase in platelets in Groups 1 and 2 and the concentration of vitamin E in plasma in Group 2. There was no significant difference between the three Groups in the severity of the eczema or the concentration of selenium either before or after the 12 weeks of supplementation. The results suggest that although selenium-enriched yeast supplement was absorbed and bioavailable it does not enter the skin or produces a worthwhile improvement in atopic dermatitis.

Adult↗

PubMed1989

Porcine focal symmetrical poliomyelomalacia: test for an interaction between dietary selenium and niacin.

Experiments were conducted to test the hypothesis that dietary supplementation with nicotinamide would retard or eliminate the signs of selenium induced porcine focal symmetrical poliomyelomalacia (PFSP). Mixed-sex feeder pigs, approximately five weeks old, were divided into four groups and daily received, by oral capsule, the following treatments: no supplementation (control); 2.86 mg sodium selenite per kg body wt (selenium only); 44 mg nicotinamide per kg body wt (niacin only); or both the niacin and selenium (niacin + selenium). Over the ten day treatment body weights and behavior scores were recorded, as well as collection of fluid (blood, serum, urine) samples. Upon death, tissue samples (kidney, liver, brain, spinal cord and muscle) were obtained. All of these samples were analyzed for total selenium and bioactive niacin compounds. After gross pathological analysis, 11 samples from specific brain and spinal cord regions were taken for fixation and processing for histological analysis by light microscopy. The selenium only group showed behavior signs related to PFSP after two days of treatment with the average time of death at 6.5 days. Tissue levels of selenium were elevated and histological analyses established the expected lesions of PFSP. No disorders were noted in the control and niacin only groups. The niacin + selenium groups had slightly retarded changes in behavior scores (first differences from controls on day 4) but their mean day of death (7.5 days of treatment) did not differ from that of the selenium only groups. Histological analyses of these tissues revealed similar lesions to the selenium only group, but they may have been of lesser magnitude. The data were consistent with, but only partially supportive of, the above hypothesis.

Animals↗

PubMed1989

Selenium toxicosis in three California sea lions (Zalophus californianus).

Selenium poisoning occurs worldwide in nearly all domestic animals. Acute selenium poisoning is associated with feeding high levels or injecting excessive amounts of selenium and is usually fatal. The acute poisoning may cause gastrointestinal disturbance, muscle weakness, depression of the central nervous system, prostration and death (1-2). Chronic selenium poisoning in cattle, sheep and horses may result from the consumption of seleniferous plants over an extended period of time. Chronic selenium results in ataxia, incoordination, partial blindness, paralysis, loss of hair or wool, abnormal hoof growth and possibly abnormal changes in behavior (1). There is little information regarding the clinical signs and pathology of selenium toxicosis in marine mammals. Likewise, there is little information regarding normal tissue levels or toxicologically significant levels of selenium in these species. The results of these investigations in sea lions, based on clinical signs, pathologic findings and tissue levels of selenium, suggest subacute or chronic selenium poisoning was most likely from dietary fish high in selenium.

Animals↗

PubMed1986

Selenium in food and nutrition in Finland. An overview on research and action.

For geochemical reasons Finland is a low-selenium area. In the 1960's several diseases associated with serious Se deficiency were observed in domestic animals. Selenium medication of animals and selenium supplementation of animal feeds from 1969 effectively eliminated these diseases. An extensive study of the trace element content of foods consumed in Finland in the 1970's demonstrated that the dietary intake of selenium was exceptionally low (25 micrograms/day/10 MJ) during the years when domestic grains were used. A study carried out in 1981 showed that supplementation of healthy middle-aged men with high selenium wheat or yeast or selenate double the glutathione peroxidase activity in platelets. Prospective epidemiological studies based on cohorts that were followed in the 1970's suggested that low selenium (less than 45 ng/ml serum) might be a risk factor for cardiovascular diseases and cancer. Technologies to increase the selenium content of foods and feeds were developed and an official decision was reached to add, starting in 1984, sodium selenate to the main fertilizers to increase the selenium content of domestic grain to about 100 micrograms/kg. This measure will increase the average selenium intake above 50 micrograms/d even in the years when grain with a high selenium content is not imported.

Animal Husbandry↗

PubMed1986

Perspectives in metal carcinogenesis. I. Selenium.

This review has focused primarily on the sources of exposure to selenium and its role as an antioxidant as well as its anticarcinogenic and antimutagenic properties. Selenium is an essential trace element and a constituent of glutathione peroxidase in human erythrocytes. Numerous studies with animals have demonstrated that it is a potent inhibitor of virally- and chemically-induced tumorigenesis when administered continuously in a variety of tumor systems (predominantly in the skin, liver, colon, and mammary gland). The mechanisms by which selenium inhibits tumorigenesis is not definitely known. Several epidemiological studies have demonstrated statistically significant inverse associations between human cancer mortalities in different populations. In these studies, the regional availabilities of selenium were measured via a variety of means, including blood selenium levels, the concentration of selenium in grains and forage crops or from calculated apparent selenium intake estimated from food consumption and consumption data. These animal and human studies demonstrating inverse associations between tumorigenesis and selenium levels have led to suggestions that selenium be considered a prophylactic agent in the chemoprevention of tumorigenesis. It would appear prudent to avoid the unnecessary supplementation of normal diets with selenium.

Air Pollutants↗

PubMed1986

The serum selenium concentration of patients with acute myocardial infarction.

Serum selenium concentration was determined in 49 patients with acute myocardial infarction within 4 hours after the beginning of the symptoms. The mean serum selenium concentration of the patients was significantly lower than that of healthy controls (55 +/- 15 micrograms/l vs. 78 +/- 11 micrograms/l). Among the 49 patients with acute myocardial infarction 20 (41%) had serum selenium concentration below the 95% percentile of the healthy control group. It is concluded that the low serum selenium concentration was present in these patients before the acute event and was not a consequence of the myocardial infarction. No relationship was found in this study between the serum selenium concentration and the severity of myocardial infarction if the number of coronary vessels occluded is taken as the criterion of severity. Serum selenium concentration was similar in patients with 1 or more coronary vessels occluded. Patients with anterior or posterior myocardial infarction had similar serum selenium concentrations. A positive correlation was observed between serum selenium concentration and total serum creatine kinase (CK) activity and serum myoglobin (MB). The serum selenium concentration correlated negatively with the ratio CK-MB/total CK activity, which can be interpreted as minor injury of mitochondria during infarction in patients with normal serum selenium concentration.

Aged↗

PubMed1986

Selenium deficiency and detoxication functions in the rat: short-term effects of cadmium.

Weanling rats were fed a Torula yeast-based selenium-deficient diet with or without supplementation of sodium selenite (0.2 ppm selenium) in the drinking water. After 5-6 weeks on the diet regimens, the liver glutathione peroxidase activity of the selenium-deficient groups had decreased to about 1% of the supplemented groups, and the rats were then used in experiments. Cadmium-induced effects on the drug-metabolizing system of the liver were measured as the microsomal capacity to perform N- and C-oxygenation of N, N-dimethylaniline. Cadmium in vitro caused a decrease of the cytochrome P-450-dependent C-oxygenation. This effect tended to be more prominent in the selenium-deficient groups. On the other hand, N-oxygenation was increased when cadmium was added in vitro, and no significant difference was found between selenium-deficient and -supplemented groups. However, as was found for the capacity to perform C-oxygenation, there was a tendency for lower N-oxygenation in the selenium-deficient rat. Lipid peroxidation, measured as thiobarbituric acid reactive substances in liver homogenates, was higher in selenium-deficient groups after in vivo treatment or in vitro addition of cadmium, and preincubation or phenobarbital induction enhanced this selenium-dependent difference. Although, the selenium-deficient rat seems more susceptible to cadmium-induced disturbances, 5-6 weeks of selenium deficiency was not enough to cause prominent impairment on the drug-metabolizing system as measured here and with the doses used in the present study.

Aniline Compounds↗

PubMed1983

Synergistic effect of vitamin E and selenium in the chemoprevention of mammary carcinogenesis in rats.

The present study showed that vitamin E, although ineffective by itself, was able to potentiate the ability of selenium to inhibit the development of mammary tumors induced by dimethylbenz(a)anthracene (DMBA) in rats. Animals were maintained on a high-polyunsaturated fat (20% corn oil) diet in order to increase the degree of oxidant stress; additional selenium and/or vitamin E were present at a concentration of 2.5 and 1000 mg/kg of diet, respectively. It should be noted that rats tolerated these levels of supplementation very well with no obvious undesirable effect. Furthermore, our results indicated that vitamin E facilitated the anticarcinogenic action of selenium only when it was present during the proliferative phase. We then proceeded to examine whether DMBA administration would lead to any persistent damage in tissue peroxidation or changes in activities of enzymes associated with peroxide metabolism. It was found that DMBA resulted in an acute but modest increase in lipid peroxidation at 24 hr after carcinogen treatment. This perturbation was only of a transient nature. By comparing the response in a target tissue (mammary fat pad) and a non-target tissue (liver), it can be inferred that DMBA may have a differential effect on the degree of oxidant stress. The antagonistic effect of selenium and vitamin E in suppressing lipid peroxidation was then evaluated. Several conclusions can be drawn regarding the antioxidant potency of these agents in conjunction with their efficacies in cancer prevention. First, although vitamin E is a more effective antioxidant than selenium, it is apparent that systemic suppression of lipid peroxidation by vitamin E subsequent to a carcinogenic insult is not sufficient to inhibit tumor formation. Vitamin E supplementation increases significantly the microsomal hydroperoxidase activity. At the present time, it is unclear what role, if any, this enzyme plays in the synergistic effect of vitamin E and selenium in the inhibition of tumorigenesis. Secondly, the anticarcinogenic action of high levels of selenium is not related to its biochemical function in the regulation of the selenium-dependent glutathione peroxidase. The explanation for this is that the enzyme is already operating at near maximal capacity under normal physiological conditions. Additional selenium will not further increase its activity, since the enzyme protein becomes the limiting factor. Finally, vitamin E may be able to provide a more favorable climate against oxidant stress, thereby potentiating the action of selenium via some other mechanism.

9,10-Dimethyl-1,2-benzanthracene↗