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Effect of dietary selenium on the development of Fusarium-induced tibial dyschondroplasia in broiler chickens.

A trial was conducted to determine the effects of dietary level of selenium on the pathogenesis of Fusarium-induced tibial dyschondroplasia (FITD) in broiler chicks, and to assess the applicability of FITD as an animal model of Kashin-Beck disease of humans. Day-old female broilers were fed diets that were deficient in selenium (0.02 ppm Se), adequate in selenium (0.15 ppm Se), or generous in selenium (0.50 ppm Se). TDP-1, the toxic component of the fungus, was administered to 15 of 26 chicks in each dietary group starting at 1 week of age and continuing until the chicks were killed at 24-30 days of age. Plasma selenium levels and hepatic glutathione peroxidase activity were significantly lower in the selenium-deficient group than in other dietary groups; these parameters were not affected by treatment with TDP-1. The mortality rate of the TDP-1-treated selenium-generous group was significantly less than that in the other TDP-1-treated groups, but there were no differences in the incidence, severity, or character of the FITD lesions among the groups. Thus, the interaction of selenium and TDP-1 did not include an effect on FITD.

Amino Acids↗

Plasma selenium and glutathione peroxidase in relation to cancer, angina pectoris and short-term mortality in 68-year-old men.

Plasma selenium and plasma glutathione peroxidase were measured in 483 68-year-old men participating in a longitudinal population study, in which the probands were representatively selected. The prevalence of cancer and coronary heart disease was assessed by a structured interview. In plasma the concentration of selenium was 1.08 +/- 0.18 mumol X l-1 and the activity of glutathione peroxidase 540 +/- 90 mumol X l-1 X min-1. Plasma selenium was correlated to glutathione peroxidase activity (r = 0.49, p less than 0.001), but not significantly to plasma albumin levels (r = 0.18). Plasma selenium and glutathione peroxidase values in subjects with cancer or angina pectoris were not significantly different from those in subjects without these diseases. Plasma selenium concentration and glutathione peroxidase activity in the subjects who died within 1 year of screening were 89% and 88%, respectively, of the values among survivors (p less than 0.01). For the subjects who died during the second year after screening, these variables did not differ significantly from the values among survivors, 97% and 99%, respectively. Since the relation of low selenium and glutathione peroxidase to mortality was observed only for the first year, it was probably due to a disturbed nutritional state prior to death, rather than to a long-term negative influence of low plasma selenium on the mortality risk. Furthermore, the data have failed to demonstrate a relationship between selenium status and cancer or angina pectoris.

Aged↗

Selenium yeast.

Baker's yeast is able to assimilate carbon, nitrogen, phosphorus and sulphur sources together with a great number of minerals and trace elements into a palatable, nutritious product. The metabolism of yeast is precisely controlled during the production growth phase and thus it is possible to determine the composition of the product by controlling the raw materials. Because of existing deficiencies in the availability of certain trace elements, mainly selenium, in Finnish diets, we started testing the possibilities for enriching yeast with this essential trace element about five years ago. We have succeeded in developing a special yeast product with a selenium concentration of 500 mg/kg dry matter. Selenium was expected, because of its structural similarity to sulphur, to replace sulphur in the biosynthetic reactions of the yeast cell. We have recently studied the incorporation and distribution of selenium in yeast with radioactive selenium (75Se). Analysis of the protein fraction of selenium yeast has shown that selenium is present in all the major soluble proteins. Selenomethionine was identified as the major selenium-containing compound in the protein fraction as well as in the whole cell.

Amino Acids↗

Inhibitory effect of dietary selenium on carcinogenesis in rat glandular stomach induced by N-methyl-N'-nitro-N-nitrosoguanidine.

The influence of dietary selenium on the incidence of stomach carcinoma induced by N-methyl-N'-nitro-N-nitrosoguanidine was studied in 108 rats that survived for over 10 wk. The incidence of glandular stomach cancer in the high-selenium (4.0 ppm) diet group (20 carcinomas in 54 rats) was lower than in the low-selenium (0.1 ppm) diet group (33 carcinomas in 54 rats). The selenium level and glutathione peroxidase activity in the blood, liver, and stomach mucosa were significantly higher in the high-selenium diet group than in the low-selenium diet group. Glutathione peroxidase activity as well as the concentration of selenium in the glandular stomach was increased significantly in the high-selenium diet group.

Adenocarcinoma↗

Swedish views on selenium.

For a long time selenium was known only for its toxic characteristics. During the last few decades selenium deficiency has been recognized as an important agricultural problem in Sweden. On average, grains and pastures only contain one tenth of the amount of selenium considered necessary to avoid symptoms of deficiency. However, the incidence of muscle degeneration among the animals has been low, probably due to imported animal feed. Since 1980 selenium has been added to animal feed, but only minor changes in the selenium content of Swedish food stuffs have been recorded. Some studies have shown that the average Swedish dietary intake of selenium is 10-70 micrograms/day. The lowest levels were found in vegan diets, based on locally-grown products. Swedish studies have found depressed glutathione peroxidase (GSH-Px) levels in patients with various skin disorders, including acne; myotonic dystrophy and rheumatic arthritis. Clinical trials with selenium supplementation have given positive results in some of these disorders as well as in some patients with disabling muscular and joint pains. Today there is a large sale of selenium tablets sometimes with additional vitamin E. The marketing of these tablets, however, is often based on unsubstantiated claims.

Animal Feed↗

Effect of selenium in combination with cis-diamminedichloroplatinum(II) in the treatment of murine fibrosarcoma.

cis-Diamminedichloroplatinum(II) (cis-DDP) is a well-known anticancer agent the use of which is limited by its toxicity. Since it has been demonstrated that selenium is able to combine with metals like cadmium and mercury and to reduce their toxicity, we decided to investigate whether it could reduce the toxicity of platinum. We treated fibrosarcoma-bearing mice with a combination of cis-DDP and selenium. The dose of 2 or 4 micrograms selenium/g animal weight had no effect on tumor growth. The i.p. injection of 16 micrograms cis-DDP/g led to early death of animals. The i.p. treatment of tumor-bearing animals with 2 or 4 micrograms of selenium reduced the early mortality induced by cis-DDP at a dose of 16 micrograms/g. Therefore, the addition of selenium allowed the administration of high doses of cis-DDP, which resulted in an improved antitumor effect. Clonogenic assays following drug exposure showed that selenium had no direct effect on tumor cells and did not modify the antitumor activity of cis-DDP. Electron microscopy showed reduced changes in renal cells when selenium was added to the cis-DDP treatment. Microanalysis showed no accumulation of either selenium or platinum within renal cells. These results suggest that the addition of selenium decreases the nephrotoxicity of cis-DDP.

Animals↗

Dietary selenium and levels of L-ascorbic acid in the plasma, livers, and lungs of polychlorinated biphenyls-treated rats.

Administration of polychlorinated biphenyls (PCB) (500 mg Aroclor, 1254/kg body weight) intraperitoneally significantly increased the levels of L-ascorbic acid in the plasma and livers, but not in the lungs of one-month-old male rats maintained on a basal low selenium diet with or without 2.0 ppm selenium (as sodium selenite) supplementation for 19 weeks prior to PCB treatment. The levels of L-ascorbic acid were not significantly altered by dietary selenium. In another experiment, 40 days or 15-month-old male rats were fed the same basal selenium diet with or without 1.0 ppm selenium for 1 month prior to PCB treatment. The plasma levels of ascorbic acid were found to increase significantly by PCB treatment, but not by the status of dietary selenium or by animal age. As expected, the activity of selenium dependent glutathione peroxidase was markedly decreased in the plasma, livers, and lungs of rats fed the low selenium diet. However, the enzyme activity was not significantly altered by PCB treatment in plasma, livers, and lungs of animals in both dietary groups.

Animals↗

Inhibitory effects of selenium on the growth of L1210 leukemic cells.

Selenium has been shown to inhibit L1210 cells both in vitro and in vivo. The death of L1210 cells in vitro as indicated by trypan blue exclusion was dependent upon the form and concentration of selenium tested. Incubation of L1210 cells in buffer containing selenium at 1 microgram/ml for 1 hr prior to inoculation into mice significantly retarded the ability of the cells to propagate in vivo. Sodium selenite injected i.p. increased the longevity of mice inoculated with L1210 cells. Administration of 40 microgram selenium as sodium selenite daily for 7 days resulted in a 65% increase in longevity of mice inoculated with 10(5) L1210 cells. Injections of sodium selenite at doses of 40 microgram/day or less for 7 days did not significantly alter growth, liver weight, or red and white blood cell counts. The efficacy of selenium therapy was dependent upon the total number of tumor cells given in the initial inoculum. Selenium administration as sodium selenite was shown to be more effective in increasing the longevity of L1210-inoculated mice than was treatment with sodium selenate, selenocystine, or selenomethionine. Sodium selenite treatment at 20, 30, or 40 microgram/day in mice inoculated with 10(2) cells resulted in 50, 80, and 90% cures, respectively. Supplementation of the drinking water with 3 ppm selenium as sodium selenite increased the longevity of L1210-inoculated mice by approximately 30%. Combined therapy with selenium (30 microgram/day) and methotrexate resulted in a significantly longer life span of L1210-treated mice than resulted from either compound administered separately.

Animals↗

Biochemical and clinical effects of selenium on dimethylhydrazine-induced colon cancer in rats.

The biochemical and clinical effects of selenium (Na2SeO3) on 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in male Sprague-Dawley rats are presented. A 4-ppm selenium supplement to the drinking water was provided before, during, and after 20 weekly injections of 20 mg DMH per kg body weight. Immediately after the 20th DMH injection, part of the rats were sacrificed. The incidences of colon tumors in groups provided selenium before DMH, before and during DMH, and only during DMH treatment were reduced to 39, 43, and 36%, respectively. The incidence in the DMH only control was 63%. Other rats in all treated and control groups were maintained up to 5 months post-DMH treatment. At 10-week intervals throughout the study, selected blood and tissue components were analyzed. The following hematological changes correlated with DMH treatment. (a) Serum glutamic oxalacetic transaminase increased 2-fold (normal, 66 +/- 14 g/dl). (b) Serum alkaline phosphatase increased 24% (normal, 166 +/- 56 units/liter). (c) Serum protein decreased 14% (normal, 6.77 +/- 0.48 g/dl). (d) White blood count increased 2- to 3-fold (normal, 7.7 +/- 2.7 X 10(3)/cu mm). And (e) hemoglobin decreased 67% (normal, 18.1 +/- 1.3 g/dl). The magnitude of these changes varies with each selenium treatment group and with each 10-week analysis period. Provision of 4 ppm selenium doubled both liver and blood selenium levels compared to unsupplemented controls. The effects of selenium and DMH treatments on glutathione peroxidase and beta-glucuronidase activities and on sialic acid are presented. Possible mechanisms by which selenium protects against DMH-induced neoplasia are discussed.

1,2-Dimethylhydrazine↗

[Selenium content in cattle hair in areas with incidence of nutrition-induced muscular dystrophy].

In the South Bohemian Region which is an area of enzootic incidence of nutritional muscle dystrophy selenium content in the fur of dairy cows and young cattle was determined. In the breeds in which the "white muscle disease" appeared in the past years in young cattle, lambs and calves the lowest mean selenium values in the fur dry matter found were: 0.18 +/- 0.07, 0.19 +/- 0.06, and 0.21 +/- 0.08 ppm, with repeated findings of mere 0.09 ppm Se. 60 to 100 per cent samples from these farms showed selenium values below the 0.25 ppm level. The fur of heifers which recovered from nutritional muscle dystrophy and were treated 10 days prior to sampling with a selenium preparation in injection form (Selevit inf. SPOFA) contained 0.29 ppm selenium (+/- 0.11). In other breeds 0.30 +/- 0.07 to 3.33 +/- 0.16 ppm selenium was found in the fur of cows and young cattle. The initial field essay of selenium content in cattle fur indicated a relation of low selenium values to the frequency of clinical forms of nutritional muscle dystrophy in domestic ruminants.

Animals↗

Safety, efficacy, and effects on copper metabolism of intrareticularly placed selenium boluses in beef heifer calves.

Intrareticularly placed sustained-release selenium boluses were administered to 1 group of selenium-deficient heifer calves (n = 16), and a second group (n = 16) was left as nontreated controls. Age range for all calves was 83 to 156 days. These boluses release 3 mg of selenium each day, as sodium selenite. Measurements of blood selenium concentration, plasma copper concentration, hepatic copper concentration, and body weight were made over a 188-day study. The treated group of calves had significantly higher mean blood selenium concentration at posttreatment days 68 (P < 0.0001), 112 (P < 0.0001), and 188 (P < 0.005) than did the control group. Mean blood selenium concentration in the treated calves was > 0.10 micrograms/ml for 188 days. These boluses were observed to be clinically safe; signs of selenium toxicosis were not detected and untoward effects were not seen in the selenium-treated calves. There were no differences between control and treatment groups with respect to mean hepatic copper concentration or mean plasma copper concentration. There were no observed differences between the control and treatment groups with respect to weight gain during the study.

Animals↗

Studies on vitamin E and selenium deficiency in young pigs. I. Hematological and biochemical changes.

Pigs which were deficient in vitamin E and/or selenium had the following parameters weekly determined from six to 13 weeks of age: Packed cell volume, hemoglobin concentration, red cell and white cell counts, red cell indices, reticulocyte count, serum iron, serum total iron binding capacity, myeloid: erythroid ratio, serum glutamic-oxaloacetic transaminase and creatine phosphokinase activities and body weight. Except for the myeloid:erythroid ratio and serum creatine phosphokinase activity, these parameters were not found to be significantly affected by either vitamin E deficiency, selenium deficiency or deficiency of both. The myeloid:erythroid ratio was increased (p less than 0.01) in association with selenium deficiency, which tends to indicate decreased erythropoiesis but was not reflected in the peripheral red cell picture. Evidence of dyserythropoiesis was not found to be a significant feature in serial bone marrow aspiration biopsies of vitamin E and/or selenium deficient pigs. Even if the serum glutamic-oxaloacetic transaminase activities were not found to be significantly affected by either vitamin E deficiency, selenium deficiency or deficiency in both as compared to replete animals, a few animals, especially in the group deficient in both vitamin E and selenium, presented quite marked transient increases of serum glutamic-oxaloacetic transaminase activity which was interpreted to reflect the occurrence of acute episodes of hepatosis dietetica. Serum creatine phosphokinase activities were found to be increased in association with vitamin E deficiency (p less than 0.01), selenium deficiency (less than 0.05) and the interaction was also significant (p less than 0.01). It was concluded that the serum creatine phosphokinase activity increases reflect the occurrence of subclinical muscular dystrophy and that vitamin E and selenium deficiencies have marked additive effects in the induction of skeletal muscular dystrophy.

Animals↗

Studies on vitamin E and selenium deficiency in young pigs. IV. Effect on coagulation system.

An evaluation of the coagulation system has been conducted in vitamin E and/or selenium deficient swine. The partial thromboplastin time, plasma fibrinogen concentration, platelet lipid peroxides, as well as the fibrinogen/fibrin degradation products were not found to be significantly affected by either vitamin E deficiency, selenium deficiency, or deficiency of both. With selenium deficiency, the prothrombin time was shortened (p less than 0.05). The platelet count and platelet turnover were greatly decreased by both vitamin E (p less than 0.001) and selenium deficiency (p less than 0.005). Further-more, the survival of platelets labelled with 75Se-selenomethionine and the per cent isotope incorporated into platelets were reduced (p less than 0.05 and p less than 0.005) in association with vitamin E deficiency, but not with selenium deficiency. These results were interpreted as evidence of a platelet production defect and possibly a platelet function defect in vitamin E deficient animals. Selenium deficiency were also associated with decreased (p less than 0.05) survival of fibrinogen labelled with 75Se-selenomethionine and increased (p less than 0.05) turnover of fibrinogen. From these fibrinogen kinetic findings, it was considered that chronic low grade disseminated intravascular coagulation possibly occurs in selenium deficient animals, probably in relation to the development of hepatosis dietetica or widespread microvascular damage. However, other possibilities such as increased fibrinogenolysis in relation with hepatosis dietetica or an intrinsic fibrinogen defect due to selenium deficiency also need to be taken into consideration and have not been ruled out in the present study.

Animals↗

[Level of zinc, copper, selenium and nickel in serum of patients treated for chronic renal failure with hemodialysis--influence of erythropoietin therapy].

52 patients with chronic renal failure treated with haemodialysis and 21 healthy subjects were observed. All patients were divided in 2 groups: 1. erythropoietin treated patients (+EPO), 2. patients not treated with erythropoietin (-EPO). In all patients immediately before dialysis and after dialysis the blood samples were withdrawn for estimation of creatinine, haemoglobin concentration, haematocrit value and zinc, copper, selenium, and nickel concentration. In healthy subjects such measurements we made only once. In all patients serum zinc, selenium and nickel concentrations were significantly lower than in normals. Copper concentration was insignificantly higher in normals than in patients with CRF. No significant differences were found in serum concentration of zinc, copper, selenium and nickel between +EPO and -EPO. During haemodialysis a decrease of serum zinc, copper and selenium levels in all examined group was seen. No significant changes between serum, zinc, selenium, copper and nickel concentration between patients treated with erythropoietin and without erythropoietin. Conclusions 1. Serum zinc, selenium and nickel concentration were significantly lower in patients treated with haemodialysis than in normals. 2. Serum concentration of zinc, copper and selenium decreased during haemodialysis. 3. Probably erythropoietin therapy does not influence serum zinc, selenium, copper and nickel levels in patients with chronic renal failure.

Adult↗

Predictors of toenail selenium levels in men and women.

Potential predictors of toenail selenium levels were studied in 1211 men and 1248 women aged 55-69 years. These subjects were randomly selected cohort members without prevalent cancer (other than skin) participating in a prospective study on diet and cancer in the Netherlands. Information on the considered potential predictors (gender, age, smoking, intake of dietary selenium and alcohol, Quetelet index) was collected together with toenail specimens in 1986. The average toenail selenium concentration was significantly (P < 0.001) lower in men than in women: 0.547 +/- 0.126 microgram/g (mean +/- SD) and 0.575 +/- 0.109 microgram/g, respectively. The gender difference remained significant after adjustment for the other variables in multiple regression analyses. Age was not associated with toenail selenium levels in men or women. An inverse association was observed with current smoking but not with past smoking. The average toenail selenium values for male current smokers were 0.513 +/- 0.106 microgram/g (mean +/- SD) versus 0.571 +/- 0.133 microgram/g for male never- or ex-smokers (P < 0.001). For women these values were 0.548 +/- 0.101 and 0.581 +/- 0.109 microgram/g, respectively (P < 0.001). Dietary selenium intake was positively associated with toenail selenium levels in multivariate analyses (P < 0.001), but the association was weak (partial r = 0.09). Alcohol intake and Quetelet index were not significant independent predictors of toenail selenium. The observed associations had similar directions in men and women but were stronger in men.

Age Factors↗

Effect of selenium on lipids and some lipid metabolising enzymes in DMBA induced mammary tumor rats.

Current evidences clearly point out that an increase in lipid peroxidation influences lipid metabolism in cancer patients. Several investigations recognize selenium as a potent antioxidant, as well as an anticarcinogen, in both animal and human systems. Selenium was administered to Wistar rats bearing mammary tumor induced by 7,12-dimethylbenz(a)anthracene (DMBA) to study alterations in the concentration of lipid profiles and in the activities of some lipid metabolising enzymes. Control and tumor-bearing rats administered with selenium, were fed 5 mg sodium selenite/kg diet from the day of tumor induction. Plasma total lipids, total cholesterol, free fatty acids, triglycerides, phospholipids, VLDL and LDL cholesterol were significantly lower in selenium-treated rats bearing tumors, whereas, plasma ester cholesterol and HDL cholesterol were significantly greater due to selenium administration in DMBA induced-tumor rats. Total lipase and lecithin: cholesterol acyltransferase registered greater activities in plasma of selenium administered rats with tumor, while the activity of preheparin lipoprotein lipases in plasma of rats bearing tumors was lower due to selenium administration. These observations clearly indicate the effect of selenium in correcting the abnormalities of lipid metabolism in tumor-induced rats.

9,10-Dimethyl-1,2-benzanthracene↗

[Selenium in blood serum and in tumors of patients with benign and malignant bone neoplasms].

The content of selenium in the serum and bones was compared in persons having no neoplasms and in patients with malignant and benign bone tumors. The mean level of selenium in the healthy femoral bone was 81 micrograms/kg, with more predominant accumulation in the epiphysis than in the metaphysis and diaphysis and with higher concentrations in the periosteum than in the cambial layer. The normal mean bone/serum selenium ratio was 0.74. This index varied 0.8 to 5.1 in patients with benign tumors and 2.3 to 10.0 in those with malignant tumors. Benign tumors were characterized by significant multiple variations of tumor selenium levels depending on the type of an abnormality with maximally observed values in giant-cell tumor. In patients with various osteosarcomas, the mean selenium content was decreased to 71% in the serum and increased up to 300% in the tumor. The examination of the impact of the type of non-adjuvant therapy on serum selenium levels in patients with bone tumors indicated a negative selenium effect in the application of radiation therapy and a positive selenium effect in the transfusion of bone marrow suspension and in the use of platidium or SAR-regimen therapy.

Adult↗

The changing selenium status of New Zealand residents.

OBJECTIVE: The aim of this paper was to compile all the studies of selenium status carried out in Otago and in other areas of New Zealand in order to follow the history of selenium status in New Zealand residents over the last 20 years. DESIGN: Since 1970 baseline blood samples have been collected from several groups of healthy adult subjects, either for the assessment of Se status or to determine baseline Se levels as part of a number of other studies. A comparison has been made of selenium concentrations recorded in recent published and unpublished studies with earlier studies by the Otago research group, and also those by other groups in New Zealand. SETTING: Otago and other New Zealand centres. RESULTS: Blood selenium concentrations of Otago residents were consistently low from 1972 until 1988 at around 0.77 mumol/l, apart from a temporary increase in 1985, and then rose to reach 1.03 mumol/l in 1991 and 1.19 mumol/l in 1992-3. Blood selenium status reflected changes in the importation of Australian wheat. Correlations between selenium and glutathione peroxidase in whole blood and plasma were consistently high prior to 1989, but were no longer significant from 1990. CONCLUSIONS: The lack of a correlation between selenium and glutathione peroxidase in bloods collected after 1990 indicates that at least for glutathione peroxidase, the selenium intake of New Zealanders is now close to that required for saturation. Whether this is sufficient to meet the requirements for other functional selenoproteins or for a possible cancer prevention effect remains to be determined.

Adult↗