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PubMed1990

[Selenium in human environment].

Selenium belongs to the group of elements which may be regarded as useful only in a very narrow range, while in excess doses they exert a harmful action. The content of the element in soil is usually from 0.1 to 2 mg/kg, with the Scandinavian soils have a low level of selenium, not exceeding 0.3 mg/kg. The highest level, exceeding 3000 mg/kg was noted in Northern Ireland. Selenium content in soil over 500 mg/kg produces chronic selenium intoxication in domestic animals. Selenium accumulation by plants is a selective process and depends on the chemical state of the element in soil and pH of soil. It is considered that the daily requirement for selenium is 50-300 mcg for adults, while the toxic dose is regarded as 5 mg daily. The toxic effects of selenium in the environment include inflammatory processes of the extremities in herbivorous animals (the so called Degnal disease in India and the Alkali disease in Great Britain). Selenium deficiency in the environment leads to the so called white muscle disease in these animals in Great Britain. Selenium is considered also to protect the organism in case of poisoning with lead, mercury or cadmium.

Dose-Response Relationship, Drug↗
PubMed1989

Low serum selenium and glutathione peroxidase activity in patients receiving short-term total parenteral nutrition.

Selenium status was determined in 15 consecutive postoperative patients receiving short-term total parenteral nutrition (TPN) using both serum selenium concentration and glutathione peroxidase (GSH-Px) activity as an indicator of body selenium status. The serum selenium concentration was significantly (p less than 0.001) lower in TPN patients (0.52 +/- 0.16 mumol/l, mean +/- SD) than in age- and sex-matched controls (1.08 +/- 0.17 mumol/l). Serum selenium in TPN patients ranged from 0.28 to 0.79 mumol/l and was associated with the duration of TPN. The lowest selenium values was found in patients who had received TPN over 3 weeks (0.35 +/- 0.06 mumol/l) as compared to patients receiving TPN for 1-3 weeks (0.61 +/- 0.13 mumol/l; p less than 0.01). Serum GSH-Px activity in TPN patients was also low (116 +/- 21 U/l) and ranged from 75 to 159 U/l. A significant positive correlation was found between serum selenium and GSH-Px activity (r = 0.520; p less than 0.05) whereas serum selenium and GSH-Px activity did not correlate significantly with liver function tests and body mass index. This study suggests that also short-term TPN patients may be at risk of selenium deficiency.

Adult↗
PubMed1989

Correction of selenium deficiency in hemodialyzed patients.

Selenium is an essential trace element important for glutathione peroxidase activity. Selenium deficiency has been found in association with skeletal and cardiac myopathy and may increase the risk for cardiovascular diseases and for cancer. We studied 39 hemodialysis patients and 15 control subjects. Plasma selenium, plasma glutathione peroxidase activity and erythrocyte glutathione peroxidase activity were lower than in controls (38 +/- 14 vs. 88 +/- 17 micrograms/liter (P less than 0.01); 153 +/- 32 vs. 334 +/- 41 IU/liter (P less than 0.01), 19 +/- 4 vs. 26 +/- 4 IU/g Hb (P less than 0.01), respectively). Plasma selenium and plasma glutathione peroxidase activity were strongly correlated with duration of dialysis. There was no correlation between plasma selenium and protein or calorie intakes. Plasma selenium was lower in patients dialyzed with highly permeable membranes (P less than 0.01). The total muscle mass, assessed by anthropometry, was lower in the patients who had the lowest plasma selenium (P less than 0.01) and plasma glutathione peroxidase activity (P less than 0.05). Interventricular septum hypertrophy, documented by echocardiography, was greater in patients with the lowest plasma selenium and plasma glutathione peroxidase activity (P less than 0.01). Twenty hemodialysis patients had oral supplementation of 500 micrograms/day of sodium selenite for three months, and then, 200 micrograms/day for the next three months. Plasma selenium increased as early as the first week and reached a plateau similar to the control levels after three weeks. Plasma glutathione peroxidase activity increased after two months but remained below controls. Erythrocyte glutathione peroxidase activity reached a higher value than controls after one month.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Interaction of vitamin C and selenium supplementation in the modification of mammary carcinogenesis in rats.

The objectives of this study were a) to compare the efficacy of inorganic and organic selenium compounds in protecting against mammary tumorigenesis induced by 7,12-dimethylbenz[a]anthracene [(DMBA); CAS: 57-97-6] in rats and b) to study the interaction of vitamin C with either selenite (inorganic) or seleno-DL-methionine (organic) in chemoprevention. Control Sprague-Dawley rats were fed a purified 5% corn oil diet containing 0.1 ppm selenium. Selenite or seleno-DL-methionine was added to the basal diet in concentrations of 2, 3, or 4 ppm starting 1 week after DMBA administration. The inhibitory response in mammary tumorigenesis with selenium supplementation was dose dependent. Both selenium compounds were found to be equally efficacious in prophylaxis, although at the 4-ppm level a slight reduction in growth was observed. In the second experiment, different concentrations of vitamin C (0.2, 0.5, and 1%) were tested. In general, there was no change with the two lower levels; but a slight, although insignificant, increase in tumor yield was detected in rats supplemented with 1% vitamin C in the diet. The interaction of 0.5% vitamin C with either selenite or seleno-DL-methionine (3 ppm) was studied in the third experiment. Results showed that the protective effect of selenite in tumorigenesis was nullified by vitamin C, whereas the chemopreventive action of seleno-DL-methionine was not affected. It is possible that selenite is reduced by vitamin C to elemental selenium and is therefore not available for uptake by tissues. This hypothesis was indirectly supported by tissue selenium measurements showing that 0.5 or 0.25% of vitamin C in the diet completely negated in blood, liver, and mammary gland the accumulation of selenium induced by 3 ppm of selenite supplementation. Lower levels of vitamin C (less than or equal to 0.1%) were found to have no effect on tissue selenium concentrations. Furthermore, the presence of 0.1% vitamin C in the diet no longer abolished the anticarcinogenic effect of selenite. This study suggests that high levels of vitamin C can interfere with the accumulation of tissue selenium and that an increased titer of this trace element in cells is essential for retarding tumor development.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1986

Interactions of selenium deficiency, vitamin E, polyunsaturated fat, and saturated fat on azoxymethane-induced colon carcinogenesis in male F344 rats.

The effect of the interaction of selenium deficiency, excess vitamin E, and type of fat on colon carcinogenesis induced by azoxymethane (AOM) was studied in male F344 rats. The experimental diets, based on a Torula yeast diet and containing 20% stripped corn oil or 20% stripped lard, were as follows: 1) selenium deficient with adequate (50 mg/kg diet) vitamin E, 2) selenium deficient with excess (750 mg/kg diet) vitamin E, 3) selenium adequate with adequate vitamin E, and 4) selenium adequate with excess vitamin E. Starting at about 3 weeks of age, animals were fed the experimental diets, and at 7 weeks of age all animals except the vehicle-treated controls were given sc injections of AOM (15 mg/kg body wt) once weekly for 2 weeks. Animals were fed the experimental diets until termination of the experiment. Selenium deficiency significantly inhibited the incidence (percentage of animals with tumors) and multiplicity (tumors per animal) of colon adenocarcinomas and adenomas, whereas excess vitamin E had no effect on colon carcinogenesis. There was no interaction between the selenium status and vitamin E; the selenium status and type of fat; vitamin E and type of fat; and among selenium status, vitamin E, and type of fat.

1,2-Dimethylhydrazine↗
PubMed1987

Selenium content of foods purchased or produced in Ohio.

Approximately 450 samples of about 100 types of foods consumed by rural and urban Ohioans were analyzed for selenium. Meat, dairy products, eggs, and grain products produced in Ohio have considerably lower selenium content than corresponding products produced in high selenium areas, such as South Dakota. Retail Ohio foods with interregional distribution tended to be higher in selenium content than corresponding foods produced in Ohio. Best sources of selenium in Ohio foods commonly consumed were meat and pasta products. Poor sources of selenium were fruits, most vegetables, candies, sweeteners, and alcoholic and nonalcoholic beverages. Establishment of an accurate data base for selenium depends on knowledge of the interregional distribution of foods, the selenium content of foods at their production site, and the selenium content of foods with wide local distribution.

Food Analysis↗
PubMed1987

Selenium content of a core group of foods based on a critical evaluation of published analytical data.

References published since 1960 that report analyses of selenium in foods were collected and evaluated according to criteria in five categories: number of samples, analytical method, sample handling, sampling plan, and analytical quality control. Data were grouped by food item and rated according to the criteria that had been developed specifically for evaluating the quality of selenium data. Ratings assigned to the data from each study yielded a Quality Index, indicating which data would be included in the calculation of the mean selenium value for each food item. The Quality Indexes for acceptable studies were summed to determine a Confidence Code, intended to indicate the relative degree of confidence the user can have in each mean selenium value. The selection of selenium core foods was based on their selenium concentration and frequency of consumption. Foods were ranked by multiplying selenium concentration by the amount consumed by the 36,255 individuals who provided 3-day dietary intake data in the U.S. Department of Agriculture's 1977-78 Nationwide Food Consumption Survey. Mean, minimum, and maximum selenium values, Confidence Codes, ranks, and references have been compiled for 114 food items. The five most highly ranked food aggregates (beef, white bread, pork, chicken, and eggs) provided half of the selenium accounted for in the diets of the survey respondents.

Diet↗
PubMed1982

Selenium and the acute effects of the carcinogens, 2-acetylaminofluorene and methylazoxymethanol acetate.

Selenium inhibits the development of 2-acetylaminofluorene-induced hepatic tumors and methylazoxymethanol-induced colon tumors. It has been suggested that selenium exerts these protective effects by inhibiting metabolic activation of the carcinogen. We have studied the effects of selenium upon the acute inhibition of RNA and DNA synthesis induced by 2-acetylaminofluorene or methylazoxymethanol in intact liver, regenerating liver, and colon of weanling male Sprague-Dawley rats. Some animals received selenium in the drinking water (4 ppm) for 1 week, while others received a single injection of selenium (1 mg/kg i.p.) prior to being treated with the carcinogens. No protection against the effects of the carcinogens on RNA or DNA synthesis was noted with either treatment of selenium. Disulfiram did protect against the 2-acetylaminofluorene-induced inhibition of hepatic RNA synthesis, and pyrazole prevented the inhibition of RNA synthesis induced by methylazoxymethanol in both liver and colon. Serum selenium levels are reported. The data indicate that selenium does not influence the acute alterations induced by the carcinogens 2-acetylaminofluorene or methylazoxymethanol and suggest that the tumor-preventive effects of selenium are probably due to a mechanism other than interference with carcinogen activation and interaction with cellular macromolecules.

2-Acetylaminofluorene↗
PubMed1983

Modification of the effects of aflatoxin B1 and warfarin in young pigs given selenium.

Selenium may be related to the hepatic metabolism of the coumarin compounds aflatoxin B1 and warfarin. Selenium evidently increased the pharmacologic activity of warfarin, probably due to a displacement of warfarin from albumin by selenium, the close relationship among selenium, vitamin E, and sulphur-containing groups (eg, glutathione), or the antioxidant effect of selenium. A diet containing selenium in a concentration of 2.5 mg/kg of feed was protective against the toxic effects of both coumarins in pigs given 4 daily oral doses of 0.2 mg/kg of body weight. Selenium, as glutathione peroxidase, at least in part, protects the hepatic cells against the toxic effects of aflatoxin B1 and warfarin. The protection was demonstrated by alteration of clinical responses and hematologic (prothrombin times), electrophoretic, and clinical chemistry values. It also was demonstrated that selenium at 2.5 mg/kg of feed does not produce toxic effects; however, dietary selenium at a concentration of 5 mg/kg (and in the presence of both toxic agents) was toxic for young pigs within the 3-week experimental period. Warfarin was more active as an anticoagulant than aflatoxin B1.

Aflatoxin B1↗
PubMed1984

Dietary intake and sources of selenium in young Finnish women.

Dietary intake of selenium by 29 young Finnish women was estimated using the 7-day record method. The mean daily selenium intake was 31 micrograms by calculation. The main dietary sources of selenium were fish and eggs (29.5 per cent of the total intake), cereals (28.1 per cent) and milk (18.7 per cent). Using multiple regression analysis, it was shown that selenium intake cannot be explained by the consumption of nine main food groups because of the large variation in selenium content of different foods in each of the food groups. The 95 per cent confidence limits for an individual's selenium intake showed that the 7-day record method gave an estimate within 35 per cent of the long-term selenium intake. The high intra-individual variation in the selenium intake found in the present study warrants particular attention when dietary data on selenium intake are considered in relation to health parameters.

Adult↗
PubMed1984

Effect of an inorganic and organic form of dietary selenium on the promotional stage of mammary carcinogenesis in the rat.

The relative effectiveness of either sodium selenite or selenomethionine in the inhibition of mammary carcinogenesis was studied in virgin female Sprague-Dawley rats. In one experiment, rats were given 50 mg of 1-methyl-1-nitrosourea per kg of body weight s.c. at 50 days of age. Beginning 7 days post-1-methyl-1-nitrosourea, they were assigned to a basal diet containing 0.1 ppm of selenium or basal diet supplemented to contain either 4, 5, or 6 ppm of selenium as sodium selenite or 5 or 6 ppm of selenium as selenomethionine. Selenium treatment was continued until termination of the study 135 days after 1-methyl-1-nitrosourea treatment. Sodium selenite, at the 5-ppm level, was the most effective chemopreventive agent. The highest level of selenomethionine (6 ppm) caused grossly apparent liver damage. No liver damage was noted in sodium selenite-treated rats. In a second experiment, rats were given 5 mg of 7,12-dimethylbenz(a)anthracene at 50 days of age. Beginning 7 days after 7,12-dimethylbenz(a)anthracene treatment, rats were assigned randomly to the control group or to one of two selenium treatment groups receiving either 3.4 ppm of selenium as sodium selenite or 3.4 ppm as selenomethionine in their drinking water. Selenium supplementation was continued throughout the study until its termination at 111 days postcarcinogen . Sodium selenite significantly reduced cancer incidence and the average number of cancers per rat. Treatment with selenomethionine was less effective and caused severe liver damage. Although both sodium selenite and selenomethionine can inhibit some aspect of the postinitiation stage(s) of mammary carcinogenesis, selenium provided as sodium selenite was the more effective and less toxic of the two chemicals. Increasing the dose of sodium selenite above 5 ppm did not enhance the inhibitory activity of selenium.

Animals↗
PubMed1981

Effects of selenium on mouse mammary tumorigenesis and glutathione peroxidase activity.

The effects of supplemental selenium on 7,12-dimethylbenz(a)anthracene (DMBA)-induced and murine mammary tumor virus (MuMTV)-induced mammary tumorigenesis were investigated in BALB/c mice. Selenium (4-10 ppm), administered in the drinking water, inhibited mammary tumor formation in DMBA-treated mice. The higher doses of selenium (7-10 ppm) were tolerated well by the DMBA-treated mice and blocked mammary tumor formation by 80-90%. In addition, selenium at the lowest dose (4 ppm) inhibited the tumor-producing capabilities of a MuMTV-positive preneoplastic nodule outgrowth line by greater than 75%. The inhibition of tumor formation could not be attributed to an alteration in virus expression because there was no qualitative difference in the expression of of MuMTV proteins between selenium-treated and -untreated mice. Additionally, selenium-dependent glutathione peroxidase activity was detectable in normal virgin and preneoplastic mammary tissues of mice raised on a commercial diet and was increased 2-fold by 4 ppm supplemental selenium in the drinking water. These results demonstrate that supplemental selenium is an effective inhibitor of both chemical- and viral-induced mouse mammary tumorigenesis, and secondly, that the neoplastic transformation in, as well as the development of, preneoplastic lesions is sensitive to selenium-mediated inhibition.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1983

Selenium inhibition of 1,2-dimethylhydrazine-induced colon carcinogenesis.

The inhibitory effect of selenium (Na2SeO3) on 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in male Sprague-Dawley rats is presented. A 4-ppm selenium supplement to the drinking water was provided concurrently with DMH treatment and continued until death or sacrifice. Rats were administered 10 weekly injections of 10 mg DMH per kg body weight. Thirtyone weeks following the tenth DMH injection, all surviving animals were sacrificed. At sacrifice, the colon tumor incidence in DMH-only controls was 8 of 28 (29%). Selenium supplementation significantly (p less than 0.01) reduced the colon tumor incidence to 1 of 37 (3%). The cumulative colon tumor incidence for all animals found dead or sacrificed was also significantly (p less than 0.05) reduced from 11 of 40 in DMH controls to 3 of 40 in DMH-selenium-supplemented rats. The total number of colon tumors was reduced from 13 to 3, and the average number of tumors per rat from 1.2 to 1.0 by supplemental selenium. The majority (greater than 65%) of all tumors were located in the distal colon. The serum glutamic oxaloacetic transaminase, alkaline phosphatase, and complete blood count were normal and equivalent for the DMH only, DMH-selenium, and untreated control groups in this study. The glutathione S-transferase activity in liver cytosol preparations was increased from 39.6 +/- 7.3 (S.D.) microM product/min/mg (DMH only) to 67.6 +/- 5.8 microM product/min/mg by selenium only and to 54.3 +/- 10.6 microM product/min/mg in selenium-DMH-treated rats. Protection by selenium may in part be attributed to enhanced detoxification of carcinogenic electrophiles.

1,2-Dimethylhydrazine↗
PubMed1995

Pathogenesis of diquat-induced liver necrosis in selenium-deficient rats: assessment of the roles of lipid peroxidation and selenoprotein P.

A dose of diquat below the amount injurious to selenium-replete animals causes lipid peroxidation and massive liver necrosis in selenium-deficient rats. The current study was undertaken to characterize the lipid peroxidation with respect to the liver injury and to correlate the presence of several selenoproteins with the protective effect of selenium. Lipid peroxidation was assessed by measurement of F2 isoprostanes. Diquat caused an increase in liver and plasma F2 isoprotanes. A gradient of these compounds was detected across the liver in some animals, indicating that this organ was a source of some of the plasma F2 isoprostanes. A time-course experiment showed that liver F2 isoprostane concentration increased before plasma alanine transaminase (ALT) levels rose. Selenium-deficient rats were injected with selenium doses from 2 to 50 micrograms/kg and studied 12 hours later. A dose of 10 micrograms/kg or more prevented diquat-induced lipid peroxidation and liver injury. This dose increased plasma selenoprotein P substantially, and a dose-response was present. Liver cellular and plasma glutathione peroxidase activities remained below 2% of their values in control rats for all selenium doses. In selenium-deficient rats given diquat, hepatic lipid peroxidation precedes hepatic necrosis and could therefore be an important mechanism of the necrosis. Selenoprotein P levels were increased by selenium injections, which protected against diquat injury, but glutathione peroxidase activity was not increased. This is consistent with selenoprotein P being the mediator of the selenium effect.

Animals↗
PubMed1993

Selenium status and lipoproteins in healthy and diabetic children.

Selenium and the selenium-dependent glutathione peroxidase (GSH-Px) were measured in healthy and diabetic children from Germany and Hungary. Hyperglycemia and hyperlipidemia are present in diabetes mellitus and they are associated with increased lipid peroxidation. The selenium content of erythrocytes, whole blood and plasma, as well as of plasma glutathione peroxidase activity, were found to be low in the healthy Hungarian children compared to the healthy Germans. Both groups of diabetics had significantly higher blood selenium (1.05 +/- 0.14 versus 0.86 +/- 0.1 mumol/L in Hungarians, 1.34 +/- 0.21 versus 1.12 +/- 0.22 mumol/L in Germans) and higher plasma selenium (0.89 +/- 0.15 versus 0.68 +/- 0.01 mumol/L in Hungarians and 1.01 +/- 0.2 versus 0.88 +/- 0.19 mumol/L in Germans) than the healthy children of the same countries. In all diabetic children the plasma glutathione peroxidase activity and triglycerides were higher and the plasma HDL-cholesterols (HDLC = high density lipoprotein-cholesterol) lower than those in healthy controls. The patients showed linear correlations between blood glucose and plasma glutathione peroxidase activity, as well as in erythrocyte glutathione peroxidase activity with triglycerides (TG) and an inverse correlation with HDL-cholesterol. Plasma selenium correlated only in healthy children with triglycerides, cholesterol and HDL-cholesterol. Irrespective of the geographical region diabetics had a higher selenium status than healthy children. In addition, we found correlations between selenium and lipoproteins in the reference group. The mode of glycation, oxidative procedures and the selenium binding to lipoproteins could explain the different associations in the healthy and diabetic children.

Adolescent↗
PubMed1993

[Complex study of selenium levels in healthy subjects in Hungary].

Selenium supply of different populations might vary substantially according to the geographical location and eating habits. The authors pioneered in surveying the selenium supply of the Hungarian population in diverse parts of the country. The former was achieved by the study of multiple parameters characteristic of the human body's selenium status. Selenium levels were determined in sera of blood donors and in toe and fingernails of healthy village and city populations. Measurements in sera and in nails were performed by electrothermic atomic absorption spectroscopy and by flourimetric method, respectively. The average selenium concentration in sera was 0.70 micromol/liter, in fingernails was 0.61 mg/kg, in toenails it was 0.56 mg/kg. The average selenium concentration was significantly higher in the south-eastern and significantly lower in the south-western regions of the country compared to the northern countries. Similar regional differences could be observed in the average selenium content of both toe and fingernails. According to the findings, selenium deficiency could be verified even in the majority of persons with the highest selenium levels.

Adolescent↗
PubMed1993

A prospective cohort study on selenium status and the risk of lung cancer.

Selenium has been suggested to be anticarcinogenic and to play a role in the cellular defense against oxidative stress. The association between toenail selenium (a marker of long-term selenium status) and lung cancer was investigated in a cohort study of diet and cancer that started in 1986 among 120,852 Dutch men and women aged 55-69 years. After 3.3 years of follow-up, 550 incident cases of lung carcinoma were detected. Toenail selenium data were available for 370 lung cancer cases and 2459 members of a randomly selected subcohort. The rate ratio of lung cancer for subjects in the highest compared to the lowest quintile of toenail selenium, after controlling for age, gender, smoking, and education, was 0.50 (95% confidence interval, 0.30-0.81), with a significant inverse trend across quintiles (P = 0.006). The protective effect of selenium was concentrated in subjects with a relatively low dietary intake of beta-carotene or vitamin C. The rate ratio in the highest compared to the lowest quintile of selenium was 0.45 in the low beta-carotene group (95% confidence interval, 0.22-0.92; trend P = 0.028) and 0.36 in the low vitamin C group (95% confidence interval, 0.17-0.75; trend P < 0.001). The results of this study support an inverse association between selenium status and lung cancer and suggest a modification of the effect of selenium by the antioxidants beta-carotene and vitamin C.

Adenocarcinoma↗
PubMed1994

Plasma selenium level in cancer patients.

Selenium has been shown to be a cancer preventive agent. A few studies have shown that increased selenium level is associated with decreased cancer incidence and decreased cancer mortality. The present study was carried out to find out the relationship of selenium level with site, extent of disease, recurrence of disease, histopathological diagnosis, anaemia and serum protein level of cancer patients. Plasma selenium level were studied in 100 patients and mean selenium level of 75.35 ng/ml in cancer patients was significantly less than control values (116.99 ng/ml) in normal healthy individuals (P < 0.003). The strongest association of plasma selenium level and cancer was found in cancer breast (70.50 ng/ml) and gastrointestinal tract (73.05 ng/ml) cancer. Selenium level decreased with the progress of disease and recurrence of disease. No significant association between histopathological diagnosis and selenium level was observed. Anaemia and hypoproteinemia was also not found to be related with selenium level.

Adult↗