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PubMed2002

Blood selenium concentrations and enzyme activities related to glutathione metabolism in wild emperor geese.

In 1998, we collected blood samples from 63 emperor geese (Chen canagica) on their breeding grounds on the Yukon-Kuskokwim Delta (YKD) in western Alaska, USA. We studied the relationship between selenium concentrations in whole blood and the activities of glutathione peroxidase and glutathione reductase in plasma. Experimental studies have shown that plasma activities of these enzymes are useful biomarkers of selenium-induced oxidative stress, but little information is available on their relationship to selenium in the blood of wild birds. Adult female emperor geese incubating their eggs in mid-June had a higher mean concentration of selenium in their blood and a greater activity of glutathione peroxidase in their plasma than adult geese or goslings that were sampled during the adult flight feather-molting period in late July and early August. Glutathione peroxidase activity was positively correlated with the concentration of selenium in the blood of emperor geese, and the rate of increase relative to selenium was greater in goslings than in adults. The activity of glutathione reductase was greatest in the plasma of goslings and was greater in molting adults than incubating females but was not significantly correlated with selenium in the blood of adults or goslings. Incubating female emperor geese had high selenium concentrations in their blood, accompanied by increased glutathione peroxidase activity consistent with early oxidative stress. These findings indicate that further study of the effects of selenium exposure, particularly on reproductive success, is warranted in this species.

Alaska↗
PubMed2002

Selenium supplementation and lung cancer incidence: an update of the nutritional prevention of cancer trial.

Interest in the chemopreventive effects of the trace element selenium has spanned the past three decades. Of >100 studies that have investigated the effects of selenium in carcinogen-exposed animals, two-thirds have observed a reduction in tumor incidence and/or preneoplastic endpoints (G. F. Combs and S. B. Combs, The Role of Selenium in Nutrition Chapter 10, pp. 413-462. San Diego, CA: Academic Press, 1986, and B. H. Patterson and O. A. Levander, Cancer Epidemiol. Biomark. Prev., 6: 63-69, 1997). The Nutritional Prevention of Cancer Trial, a randomized clinical trial reported by Clark et al. (L. C. Clark et al., JAMA, 276: 1957-1963, 1996), showed as a secondary end point, a statistically significant decrease in lung cancer incidence with selenium supplementation. The adjusted hazard ratio (HR) was 0.56 [95% confidence interval (CI), 0.31-1.01; P = 0.05]. These results were based on active follow-up of 1312 participants. This reanalysis used an extended Nutritional Prevention of Cancer Trial participant follow-up through the end of the blinded clinical trial on February 1, 1996. The additional 3 years added 8 cases to the selenium-treated group and 4 cases to the placebo group, and increased follow-up to 7.9 years. The relative risk of 0.70 (95% CI, 0.40-1.21; P = 0.18) is not statistically significant. Whereas the overall adjusted HR is not significant (HR = 0.74; 95% CI, 0.44-1.24; P = 0.26), and the HR for current and former smokers was not significant, the trend is toward a reduction in risk of incident lung cancer with selenium supplementation. In a subgroup analysis there was a nominally significant HR among subjects with baseline plasma selenium in the lowest tertile (HR = 0.42; 95% CI, 0.18-0.96; P = 0.04). The analysis for the middle and highest tertiles of baseline showed HRs of 0.91 and 1.25. The current reanalysis indicates that selenium supplementation did not significantly decrease lung cancer incidence in the full population, but a significant decrease among individuals with low baseline selenium concentrations was observed.

Aged↗
PubMed2003

The controversy surrounding selenium and cardiovascular disease: a review of the evidence.

Selenium is an essential trace element that is an integral part of many proteins, with catalytic and structural functions. The antioxidant properties of some selenoproteins, such as glutathione peroxidase, may be particularly important in carcinogenesis and heart disease. The content of selenium in food depends on the selenium content of the soil where the plants are grown or the animals are raised. Moreover, the metabolism of selenium is determined by its dietary form: some forms are better utilized than others. Therefore, wide variations have been found in selenium status in different parts of the world. In animal studies, selenium deficiency is associated with cardiomyopathy and sudden death, as well as reduced T-cell counts and impaired lymphocyte proliferation and responsiveness. Abnormalities in liver function, brain, heart, striated muscle, pancreas and genital tract have also been reported. In humans, selenium deficiency has been implicated in the etiology of cardiovascular disease and other conditions in which oxidative stress and inflammation are prominent features, but there is still only limited evidence from epidemiological and ecological studies for this, and the therapeutic benefit of selenium administration in the prevention and treatment of cardiovascular diseases remains insufficiently documented. Interventions studies are currently in progress to assess the benefits of selenium supplements in primary and secondary prevention of atherosclerosis. The results to date are inconclusive and further controlled trials are needed.

Animals↗
PubMed2002

[Cereal products as a source of selenium in Polish food rations].

The aim of the study was to update the data concerning the level of selenium in cereal products and to determine its uptake with daily food rations and percentage of cereal products in the 24-hour pool of selenium ingested. Selenium was determined fluorometrically after the reaction of Se (IV) with 2.3-diaminonaphthalene and extraction of naphtho-[2.3-d]-2-seleno-1.3-diazole to cyclohexane. Compared to the results found several years ago, the selenium levels observed in cereals, flour and bakery products were significantly lower. The mean levels of selenium in the above-mentioned products ranged from 22.9 micrograms/kg to 53.0 micrograms/kg and were markedly lower compared with pasta which reach to level 528 micrograms/kg, especially when pasta was made from semoline or contained eggs. The average daily intake of selenium with reconstructed rations was 37.9 micrograms while with home made rations 60.4 micrograms. The values calculated on the basis of the data collected in the 80-ties were significantly stray to analytical results, and those based on our findings was comparable. The percentage of the most important products in the daily selenium pool changed significantly after taking into account these new results because according to the data from 80-ties, the major sources of selenium in home and reconstructed rations were cereal products which share to 48%. According to the new results the main source of selenium in daily rations were meat one its products about 26% and cereal products somewhat less than 20%.

Edible Grain↗
PubMed2003

Prediagnostic serum selenium concentration and the risk of recurrent colorectal adenoma: a nested case-control study.

Several studies have suggested that selenium may help to prevent colorectal neoplasia. To investigate the relation between prediagnostic serum selenium concentrations and colorectal adenomas, we conducted a nested case-control study using data from a large, multicenter, adenoma prevention trial. Cases comprised a total of 276 patients who developed a colorectal adenoma between the year 1 and year 4 follow-up exam. Controls were 276 patients who did not develop an adenoma during this time interval, matched to case subjects on age, sex, and clinical center. Total and bound selenium concentrations were measured from baseline or year 1 serum samples using instrumental neutron activation analysis. We estimated the odds ratios of colorectal adenoma in relation to serum selenium concentrations adjusting for age, clinical center, and sex. Compared with the lowest quintile, the odds ratio for the highest quintile was 0.76 (95% confidence interval, 0.44-1.30) for total selenium and 0.60 (95% confidence interval, 0.34-1.05) for bound selenium, and there was no apparent trend in risk (P for trend = 0.50 for total selenium and P for trend = 0.20 for bound selenium). Thus, our findings do not indicate a clear association between serum selenium concentrations and adenoma recurrence.

Adenoma↗
PubMed1992

Effects of selenium on ribonucleic acid synthesis and degradation in rat liver.

Six groups of weanling rats were fed a low-selenium based diet containing less than 0.01 mg/kg of Se in the diet or the basal diet supplemented with five levels of selenium as selenite (0.1, 0.2, 0.3, 0.4 and 0.5 mg/kg) for at least 16 to 18 weeks. For determination of the effect of selenium on ribonucleic acid (RNA) synthesis in rat liver, rats of each dietary group were injected with a single dose of (5-3H)-uridine, and 3 hours later their livers were removed and subjected to cell fractionation. The radioactivities in the nuclear and cytoplasmic RNA were taken as a measure of the RNA synthesis rate. With selenium supplementation between 0.2 and 0.5 mg/kg diet, the radioactivities, amounts of RNA, as well as RNA/DNA ratios in both nuclear and cytoplasmic fractions of rat liver all increased significantly. In addition, at similar levels of selenium supplementation, statistically significant increments of glutathione peroxidase (GSH-Px) activity and reductions in lipid peroxide in liver were also observed. For assessment of RNA degradation, activities of ribonucleases (RNase) and RNase inhibitor in rats fed the low-selenium diet or a selenium-supplemented diet were determined. The activities of acid RNase and both free and latent alkaline RNase in liver homogenate were not affected by selenium deficiency; however, the level of RNase inhibitor present in the supernatant fraction increased significantly with selenium supplementation at 0.2 mg/kg diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Has the increase in selenium intake led to a decrease in caries among children and the young in Finland.

Finland is poor in selenium. Selenium deficit leads to muscular dystrophy in animals. Since 1962, selenium has been added in Finland to some animal foodstuffs, since 1968 to all animal foodstuffs. Addition of selenium to fertilizers started in 1984. Intake of selenium by man and cattle today is roughly 1.0 times higher than it was before selenium supplementation. Collagen is the most important component of the organic matrix of the tooth. Selenium can replace sulphur in bonds of collagen. The resulting bond is stronger than a sulphur bond. Since selenium supplementation, the conditions of the teeth of children and young people has improved considerably. The author believes that selenium supplementation has reduced the incidence of caries in young Finns.

Adolescent↗
PubMed2003

Effects of oral selenium supplementation on mastitis markers and pathogens in Estonian cows.

The effects of selenium supplementation on mastitis parameters in milk and on glutathione peroxidase (GPx) levels in blood were evaluated. Fifty-five Estonian dairy cows were allocated to selenium-supplemented (n=39) and nonsupplemented (n=16) groups. The supplemented group received 0.2 ppm organic selenium in the form of selenium yeast in their diet daily for 8 weeks. The nonsupplemented cows received their standard diet with no selenium supplementation. Mastitis parameters (i.e., bacteriologic findings and somatic cell count, N-acetyl-beta-D-glucosaminidase, and bovine serum albumin concentration) and GPx levels were monitored. The increase in the activity of GPx was significantly (P<.001) greater in selenium-supplemented cows than in nonsupplemented ones. Milk samples from each quarter were examined before and 8 weeks after initiation of the study. The proportion of quarters still pathogen-free after 8 weeks was significantly (P<.01; odds ratio [OR]=9.7) higher in selenium-supplemented cows than in nonsupplemented cows. However, when quarters milk-tested as pathogen-infected at the start of the study were reexamined after 8 weeks, there was no significant (P=.14; OR 3.6) difference in the proportion of pathogen-free quarters between selenium-supplemented cows and nonsupplemented cows. Differential positive rate (Youden's index) revealed that individual quarters were more prone to be infected by pathogens when the blood GPx activities in cows were below the cutoff value of 3.3 microkat/g hemoglobin than when GPx activity was above this value. It was concluded that selenium supplementation in cows with low GPx activity seems to support udder defense mechanisms that favor reduction of the incidence of new mastitis cases.

Acetylglucosaminidase↗
PubMed2003

Selenium and nitrate removal from agricultural drainage using the ALWPS technology.

Monthly Maximum Discharge Limits (MMDL) have been established for selenium in irrigation drainage by the State of California and the U.S. Environmental Protection Agency following observations of avian teratogenesis at the Kesterson Reservoir in the San Joaquin Valley of California. As a result of these and other adverse effects, farmers and drainage districts on the western side of the San Joaquin Valley must reduce selenium concentrations in irrigation drainage discharged to the San Joaquin River. Drainage treatment will be required in the near future to meet existing MMDL and future Total Maximum Discharge Limits (TMDL) for the San Joaquin River. A 0.4-hectare Algal Bacterial Selenium Removal (ABSR) Facility was designed and constructed at the Panoche Drainage District in 1995 and 1996 using the Advanced Integrated Wastewater Pond Systems or AIWPS Technology. Each of two physically identical systems combined a Reduction Pond (RP) with a shallow, peripheral algal High Rate Pond (HRP). A Dissolved Air Flotation (DAF) unit and a slow sand filter were used to remove particulate selenium from the effluent of each system. The two systems were operated under different modes of operation and the bacterial substrate varied in each system. The rates of nitrate and selenium removal were compared. Microalgae were harvested using DAF and used as a carbon-rich substrate for nitrate- and selenate-reducing bacteria. Mass removals of total soluble selenium of 77% or greater were achieved over a three-year period. Nitrate and selenate were removed by assimiliatory and dissimiliatory bacterial reduction, and nitrate was also removed by algal assimilation. The final removal of particulate selenium is the focus of ongoing investigations. The removal of particulate selenium is expected to increase the overall removal of selenium to greater than 90% and would allow farmers and drainage districts to discharge irrigation drainage in compliance with regulatory discharge limits.

Agriculture↗
PubMed2004

DNA stability and serum selenium levels in a high-risk group for prostate cancer.

The essential micronutrient, selenium, is at low levels in the New Zealand diet. Selenium is a component of a number of proteins involved in the maintenance of genomic stability, and recommended daily allowances (RDA) are set on saturation levels for glutathione peroxidase (GPx), a key enzyme in surveillance against oxidative stress. It has been assumed but not proven that this level will be adequate for other key selenoenzymes. The "Negative Biopsy Trial" identifies a group of New Zealand individuals at high risk of prostate cancer, whose serum selenium levels will be monitored and who will be supplemented with a yeast-based tablet, with or without selenium, over an extended time. Access to patients on this trial provides the opportunity to ask the more generic question as to whether selenium levels in this population are adequate to maintain genomic stability. The single cell gel electrophoresis (comet) assay was used to study DNA damage in blood leukocytes harvested from these volunteers. Average serum selenium levels before randomization was 97.8 +/- 16.6 ng/ml, low by international standards. For the half of the population below this mean value, lower serum selenium levels showed a statistically significant inverse relationship (P = 0.02) with overall accumulated DNA damage. Although other interpretations cannot be excluded, the data suggest that the selenium intake in half of this population is marginal for adequate repair of DNA damage, increasing susceptibility to cancer and other degenerative diseases. It also raises the question as to whether glutathione peroxidase saturation levels are appropriate indicators of the optimal selenium levels for a given population.

Aged↗
PubMed2006

[Influences of excess iodine on thyroid hormone concentrations in cerebrum of filial mice and intervention of selenium].

OBJECTIVE: To study the influence of excessive iodine intake on thyroid hormones in cerebrum of filial mice and intervention of selenium. METHODS: 60 Balb/c mice were divided randomly into 4 groups: control group, iodine group, selenium group and iodine plus selenium group and given tap water, tap water containing iodine 3000 microg/L, tap water containing selenium 200 microg/L and tap water containing iodine plus selenium 200 microg/L respectively as drinking water. At the end of the fourth month, the mice mated. Thyroid hormones and TSH in serum and in cerebrum of filial mice were determined at the postnatal 0, 14th and 28th day. RESULTS: At the postnatal 14th day, serum TT4 level was lower significantly, and serum TSH was higher in iodine group than those in control group and in the iodine plus selenium group. At the postnatal 0 day and 14th day, thyroid hormone concentrations in the cerebrum of progeny of mice were lower significantly in iodine group than those in control group, selenium group and iodine plus selenium (P < 0.05). No significant difference was observed among the four groups in TT4, TT3 and rT3 concentrations in serum and cerebrum at the postnatal 28th day. CONCLUSION: Excessive iodine intake can change thyroid hormone concentrations in the cerebrum of progeny of mice and selenium supplementation exerted favorable effects on it.

Animals↗
PubMed2006

Evaluating selenium poisoning.

Selenium poisoning in humans is reviewed from the perspective of the clinical laboratory. While evaluation of selenium poisoning is straightforward when the analytic results are markedly elevated and the patient is acutely symptomatic, distinguishing toxic from non-toxic elevations is a more frequent issue and more challenging. A significant problem is that selenium is determined as its total concentration in spite of the fact that different chemical forms of selenium have different toxic potentials. In the published reports reviewed herein, serum selenium concentrations span the following ranges: 400-30,000 micro g/L associated with acute toxicity, 500-1400 micro g/L associated with chronic toxicity, and <1400 micro g/L free of toxicity; the category is determined by signs and symptoms in the patient. Most reports that describe acute selenium poisoning involve ingestion of inorganic compounds such as selenious acid, found in gun-bluing agents, and fatalities that occur within the first day are associated with postmortem blood selenium levels >1400 micro g/L. Tissue selenium levels show a complex pattern and significant elevations in organs such as kidney are not always indicative of toxicity. As with many trace elements, measuring selenium concentrations in body fluids and tissues tends to be easier than understanding what the results mean.

Acute Disease↗
PubMed1991

Evaluation of multiple reticulorumen selenium pellets as a health risk in growing Hereford steers.

Five groups of Hereford steers were monitored for 293 days. One group of 3 was not given selenium supplementation; the other 4 groups of 3 steers each were given 2, 4, 6, or 8 reticulorumen selenium pellets. Health, body weight, and blood selenium concentration were monitored during the study. At the finish, steers were slaughtered, and various tissues from the carcasses were analyzed for selenium content. Initial blood selenium concentration did not differ significantly among groups. However, significant (alpha = 0.01) difference among means was detected during the early period of rapid increase in blood selenium concentration in steers of supplemented groups. Means of maximal blood selenium concentration also differed among groups; however, even the highest value, 0.253 micrograms/g, was lower than the 3 micrograms/ml reported in chronic clinical cases of toxicosis in the literature. Carcass analysis indicated significant (alpha = 0.05) differences in selenium concentrations among treatment groups for almost all tissues tested. Only kidney samples (7.9 micrograms/g) from steers of the 8-pellet treatment group exceeded published normal values (7.6 micrograms/g). Health variables for most dates were not significantly different among groups, and selenium toxicosis was not evident in any steer. Analysis did not indicate risk to human beings consuming tissues from these steers.

Analysis of Variance↗
PubMed1991

Scientific rationale for the 1989 recommended dietary allowance for selenium.

During the past 15 years, our knowledge of human selenium requirements has improved greatly, primarily because of research conducted in the People's Republic of China. Dietary surveys demonstrated that Keshan disease, a juvenile cardiomyopathy, was absent in parts of China where the food supply provided at least 19 and 13 micrograms selenium per day for men and women, respectively. Such intakes can be regarded as minimum daily requirements for selenium. Chinese scientists also carried out a study in an area where Keshan disease was prevalent to determine the amount of dietary selenium needed to maximize the activity of the selenium-containing enzyme, glutathione peroxidase, in plasma. For a man weighing 60 kg, enzymatic activity reached a plateau at selenium intakes of about 40 micrograms per day. These data were used by the US National Research Council as the basis for its 1989 Recommended Dietary Allowance (RDA) for selenium. The RDA was calculated as 70 and 55 micrograms per day for adult men and women, respectively, after correcting for differences in body size and taking into consideration possible individual variations in requirements. This RDA is readily satisfied by typical diets in countries with relatively selenium-rich soils, such as the United States. In selenium-poor areas of the world (eg, China, New Zealand, Scandinavia), diets would not readily furnish such intakes.

Animals↗
PubMed1990

Activity of methylated forms of selenium in cancer prevention.

The anticarcinogenic activity of selenium in animal models is well established. The active forms of selenium involved have not been identified to date, but conversion of selenium via hydrogen selenide (H2Se) to methylated forms such as dimethylselenide and trimethylselenonium ion is an important metabolic fate. By controlling the entry of selenium into various points within this pathway through selection of appropriate starting compounds, it is possible to pinpoint more closely the form(s) of selenium responsible for its anticarcinogenic activity. Selenobetaine in the chloride form [(CH3)2Se+CH2COOH] and its methyl ester are extensively metabolized in the rat to mono-, di-, and trimethylated selenides, largely bypassing the inorganic H2Se intermediary pool. The chemopreventive efficacy of these selenobetaines was determined at 1 and 2 ppm selenium supplemented in the diet throughout the duration of the experiment using the dimethylbenz(a)anthracene induced mammary tumor model in rats. There was a dose-dependent inhibitory response to both compounds, and they appeared to be slightly more active than selenite. These doses were without any adverse effects on the animals. Coadministration of selenobetaine with arsenite (5 ppm arsenic) enhanced the tumor-suppressive effect of selenobetaine, although arsenic by itself was totally inactive. Arsenite is known to inhibit certain steps in selenium methylation. The substantial prophylactic efficacy of methylated selenides and the enhancement by arsenite suggest that partially methylated forms of selenium may be directly involved in the anticarcinogenic action of selenium.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1990

[The effect of selenium on hepatocarcinogenesis of rats induced by aflatoxin B1].

This experiment was designed to observe the effects of 3 ppm and 6 ppm selenium in water on preneoplastic lesions in liver and hepatocarcinogenesis induced by AFB1. In the group administered selenium, the number of hyperplastic foci and enzyme altered foci was much less than that in the AFB1 group. From the 52nd to 79th week, cancers were observed in 11 of 18 rats in the AFB1 group, while none was found in the selenium treated groups. These results reveal that selenium can inhibit the formation of hyperplastic foci and enzyme--altered foci as well as hepatocarcinogenesis induced by AFB1, but selenium can neither prevent the enlargement nor accelerate the regression of the foci already developed after administration of carcinogens. Additionally, toxic effect of selenium was found in 6 ppm selenium group; the number and size of foci were greater in 6 ppm selenium group than those in 3 ppm group. Therefore, adequate amount of selenium is probably the link to achieve better inhibitory effect.

Aflatoxin B1↗
PubMed1990

Serum selenium in children during anti-cancer chemotherapy.

Serum selenium concentration as an indicator of selenium status was studied during a 6-month period in 24 children with acute leukaemia or solid tumours. At diagnosis low serum selenium values were found in children with acute leukaemia compared to children with solid tumours (P = 0.001), while there were no differences in the protein nutritional status of these children as assessed by serum albumin and prealbumin. During the corticosteroid treatment serum selenium levels increased (mean of 111 per cent) in children with acute leukaemia. The concentrations of serum selenium remained within the reference range of healthy Finnish children from week 16 onwards in children with acute leukaemia and throughout the study period of 24 weeks in children with solid tumours. The results suggest redistribution of the endogenous selenium stores since no selenium supplementation was used, and demonstrate that serum selenium is not a valid indicator of selenium status in these cases.

Acute Disease↗
PubMed1990

Selenium and amino acid composition of selenoprotein P, the major selenoprotein in rat serum.

Selenoprotein P is the second plasma selenoprotein to be purified. It is a glycoprotein and has been shown to be distinct from plasma glutathione peroxidase. This study characterizes selenoprotein P further. Deglycosylation of the protein shifts its migration on sodium dodecyl sulfate-polyacrylamide gel electrophoresis from Mr 57,000 to Mr 43,000, indicating it has a substantial carbohydrate component. Measurement of selenium indicates a selenium content of 7.5 +/- 1.0 atoms/molecule based on a polypeptide weight of 43,000. Amino acid analysis accounts for all the selenium as selenocysteine. The protein is also rich in cysteine (17 residues) and histidine (23 residues). Fragmentation of selenoprotein P by trypsin and by cyanogen bromide produces peptides with varying selenium content. This indicates that selenium-rich regions of the protein exist. The concentration of selenoprotein P determined by radioimmunoassay in serum from control rats is 26.3 +/- 4.5 micrograms/ml and in serum from selenium-deficient rats it is 2.7 +/- 0.8 micrograms/ml. Depletion of selenoprotein P from control serum using an immunoaffinity column indicates that over 60% of serum selenium in the rat is contained in this protein. These results demonstrate that selenoprotein P is the major form of selenium in rat serum. It is the first selenoprotein described which has more than one selenium atom/polypeptide chain.

Amino Acids↗