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Protective role of supplemental vitamin E and selenium on lipid peroxidation, vitamin E, vitamin A, and some mineral concentrations of Japanese quails reared under heat stress.

This study was conducted to determine the effects of vitamin E and selenium (Se) on lipid peroxidation (MDA), serum and liver concentration of antioxidant vitamins, and some minerals of Japanese quails reared under heat stress (34 degrees C). One hundred twenty 10-d-old Japanese qualis (60 males, 60 females) were randomly assigned to 4 treatment groups, 3 replicates of 10 birds each. The experiment was designed in a 2x2 factorial arrangement using two levels of vitamin E (125 and 250 mg/kg of diet) and two levels of selenium (0.1 and 0.2 mg/kg of diet). Greater dietary vitamin E and selenium inclusions resulted in a greater (p = 0.001) serum vitamin E and vitamin A, but lower (p = 0.001) MDA concentrations. Liver vitamin E and vitamin A concentrations increased (p = 0.001) and MDA concentrations decreased (p = 0.001) when both dietary vitamin E and selenium increased. No interactions between vitamin E and selenium were detected (p > or = 0.11) for any parameters. Increasing both dietary vitamin E and selenium caused an increase in serum concentrations of Fe and Zn (p = 0.001), but a decrease in serum concentration of Cu (p = 0.001). Results of the present study showed that dietary vitamin E and selenium have synergistic effects and that supplementing a combination of dietary vitamin E (250 mg/kg of diet) and selenium (0.2 mg/kg of diet) offers a good management practice to reduce heat stress-related depression in performance of Japanese quails.

Animals↗

Selenium levels in human plasma and hair in northern Poland.

The aim of this study was to (1) estimate the concentration of selenium in the plasma of 146 residents (65 men and 81 women) and in the hair of 34 persons from the Gdańsk region in northern Poland, aged 19-70 and (2) compare the obtained results with data corresponding to healthy populations living in different European countries. Selenium in plasma was determined by atomic absorption spectrometry using the hydride generation method. The mean selenium concentration in plasma of the investigated persons was 73.3 +/- 14.1 microg/L, 76.7 +/- 13.2 microg/L in men, and 70.4 +/- 14.7 microg/L in women. No age - dependent differences in plasma selenium were found in the investigated population. In 20% of the investigated persons, the selenium level in plasma was lower than 60 microg/L. The mean selenium concentration in hair was 0.30 +/- 0.11 microg/g. A positive, statistically significant correlation between selenium concentrations in the plasma and hair of the investigated persons was found. The obtained results indicate that the selenium level in significant part of this population is suboptimal and should be elevated by supplementation with this element.

Adult↗

Gender difference regarding selenium penetration into the mouse brain.

A sex difference in the penetration of selenium into the brain was observed using lipopolysaccharide (LPS)-injected mice. The selenium concentration increased in the brains of sodium selenite-injected LPS-treated female mice, but not males. The selenium concentration peaked when selenite was injected 3 h after the injection of LPS into female mice. In addition, selenium in the brain increased when a dosage of 30 micromol/kg and more of selenite was injected into LPS-treated female mice. Also, the selenium concentration in the brain increased and peaked 2-3 h after selenite injection; 24 h later, the level was similar to the Se-only group. The penetration of selenium into the brain was inhibited by pretreatment with aminoguanidine, an inhibitor of nitric oxide synthetase. From the present results, selenium more easily penetrated into the brains of female mice compared to males after LPS treatment, and nitric oxide may have affected the penetration. However, the sex difference mechanism for selenium penetration needs further investigation.

Animals↗

Effect of selenium on lipids, lipid peroxidation, and sulfhydryl group in neuroendocrine centers of rats.

The effects of various doses of sodium selenite (0.05, 0.1, and 0.2 mg/kg body weight, i.p.) were studied on the content of phospholipids, cholesterol, esterified fatty acids (EFA), gangliosides, thiobarbituric acid reactive substance (TBARS), and sulfhydryl group in neuroendocrine centers of male Wistar rats for 7 d. The lowest dose of Se (0.05 mg/kg) did not alter the above parameters significantly in neuroendocrine centers. The content of phospholipids was depleted significantly in the pituitary and depletion in the pineal was 80.22% with a 0.1-mg/kg dose of Se, but this dose elevated its level significantly in the hypothalamus. Conversely, a 0.2-mg/kg dose of selenium elevated the level of phospholipids significantly in the pituitary and hypothalamus, the elevation in the pineal was 70%. Selenium, 0.1 mg/kg, elevated the level of cholesterol in the pituitary but depleted its level in the pineal (56.8%) and hypothalamus (13.60%). Selenium, 0.2 mg/kg, elevated the level of cholesterol significantly in the hypothalamus but its level was not significant in the pituitary and pineal. The depletion of esterified fatty acid in the pituitary and pineal with doses of 0.1 and 0.2 mg/kg was significant in the pituitary, whereas its depletion in the pineal was 85.4% and 69.26%, respectively. Selenium, 0.1 and 0.2 mg/kg, depleted the level of gangliosides significantly and dose dependently in the pituitary but has elevated its level significantly and dose dependently in the hypothalamus. Its depletion in the pineal was 87.1% and 67.8% with the 0.1- and 0.2-mg/kg dose of selenium, respectively. Selenium, 0.1 mg/kg, increased the content of TBARS significantly in neuroendocrine centers and its elevation in the pineal was 703.8%. Selenium, 0.2 mg/kg, elevated its level in the pituitary and it was 126.9% in the pineal, but this dose depleted its level significantly in the hypothalamus. The content of the sulfhydryl group with a 0.1-mg/kg dose of selenite was depleted significantly in neuroendocrine centers and it was 55.9% in the pineal. Selenium, 0.2 mg/kg, depleted the level of the sulfhydryl group more significantly in the pituitary and pineal, but its elevation in hypothalamus was significant.

Animals↗

Adverse health effects of selenium in humans.

Epidemiologic studies and case reports have shown that chronic exposure to selenium compounds is associated with several adverse health effects in humans. An early toxic effect of selenium is on endocrine function, particularly on the synthesis of thyroid hormones following dietary exposure of around 300 micrograms Se/d, and on the metabolism of growth hormone and insulin-like growth factor-1. Other adverse effects of selenium exposure can be the impairment of natural killer cells activity and at higher levels, hepatotoxicity and gastrointestinal disturbances. Dermatologic effects, such as nail and hair loss and dermatitis, occur after exposure to high levels of environmental selenium. Assessing the toxicity and morbidity after long-term exposure to environmental selenium is difficult: neurotoxicity, particularly the degeneration of motor neurons leading to increased risk of amyotrophic lateral sclerosis, might occur after chronic exposure to both organic and inorganic selenium compounds. The results of laboratory investigations and cohort studies suggest that selenium species exhibit a bivalent effect in cancer, either increasing or decreasing risk. Current environmental selenium exposure limits appear to be inadequate for averting adverse health effects.

Biomarkers↗

Effects of a selenium deficient diet on thyroid function of normal and perchlorate treated rats.

Pregnant rats were submitted to a selenium-deficient diet immediately after mating; it was continued for 4 weeks after delivery. The pups were sacrificed at 3 and 4 weeks of age. Perchlorate, an antithyroid agent inhibiting iodide trapping in the thyroid, was administered via the drinking water to half of the rats. Rats submitted to a normal laboratory diet and to the experimental diet supplemented with selenium were used as controls. The effects of selenium deficiency were an increase in the number of growth abnormalities, growth retardation, and decreased seleno-dependent glutathione peroxidase (GSH-Px) activity in plasma and in various organs. These effects were relieved by selenium supplementation in the diet. Perchlorate treatment induced the classic picture of primary hypothyroidism. Selenium deficiency increased thyroid hormone levels in perchlorate-treated rats and in controls drinking tap water. In the latter group, it also decreased TSH plasma concentration and thyroid weight. These effects were partially reversed by Se supplementation. In vitro experiments, performed on adult rats, revealed increased radioiodide uptake and organification in glands from the rats submitted to the selenium-free diet. Plasma T3 half-life was similar in control and Se-deficient rats. These data suggest a higher efficiency of thyroid hormone synthesis in the thyroids of selenium-deficient rats, despite a lower thyroid stimulation as evaluated by serum TSH. They are compatible with the hypothesis that decreased selenium supply, leading to a decreased GSH-Px in the thyroid, increases hydrogen peroxide steady state level and thus thyroid peroxidase activity and thyroid hormone synthesis.

Animals↗

Blood selenium concentrations in cows and heifers on 253 cow-calf operations in 18 states.

This study was conducted to determine the geographic distribution of selenium deficiency among beef cows and heifers in selected states. Whole blood selenium concentrations were determined for cows and heifers on 253 cow-calf operations in 18 states. Overall, 7.8% of the samples were severely deficient, and another 10.4% of the samples were considered marginally deficient for selenium. Blood selenium concentrations varied by geographic region. Cattle from the southeastern states were more commonly considered severely or marginally deficient (18.6% and 23.8%, respectively) than cattle from other regions. Herds from the southeastern states were also more commonly considered severely or marginally deficient (14.9% and 20.9%, respectively) than herds from other regions. Blood selenium concentration also varied by whether selenium had been supplemented to the herd. We conclude that blood selenium levels for cattle vary by geographic region and selenium supplementation of the herd.

Animals↗

Regulation of essential nutrient additions to animal diets (selenium -- a model case).

Responsibility for regulation of essential nutrient additions to animal diets has been assumed by the Food and Drug Administration (FDA) through internal interpretation of the Federal Food, Drug and Cosmetic Act. Thus, these substances are regulated as food additives or through qualification for the generally recognized as safe (GRAS) list. Although essential nutrients, such as selenium, are not optional additives to animal diets that are demonstrably deficient (if animal health and welfare are of concern), supplementation with unapproved nutrients places one in violation of FDA interpretation of law. Selenium was established as a dietary essential in 1957, and practical problems with a deficiency of this nutrient were recognized soon after. Research was begun in 1967 specifically to gain FDA approval for selenium as a dietary supplement. Approval was granted for selenium supplements to swine and certain poultry diets in 1974. At that time, FDA staff members reported that the inability to supplement these diets with selenium had caused annual losses of over $82 million. Annual losses to the beef cattle, dairy cattle and sheep industry were estimated in 1975 at nearly $545 million. In a coordinated effort (initiated in 1975) involving scientists at nine United States universities and the FDA, data were gathered leading to approval in 1979 of selenium supplements for ruminants. The cost of the effort to meet regulatory requirements for selenium has been estimated at more than $1 million. Since this nutrient is not a proprietary product, this effort has been made largely at public expense. The inability to supplement selenium-deficient diets prior to FDA approval has cost hundreds of millions of dollars.

Animal Nutritional Physiological Phenomena↗

Distribution of selenium and glutathione peroxidase in plasma compared in healthy subjects and rheumatoid arthritis patients.

The distribution of selenium and glutathione peroxidase activity in plasma was compared in samples from healthy adult controls and patients with rheumatoid arthritis. Plasma was separated by gel filtration, and selenium was measured in the eluted fractions by means of graphite furnace atomic absorption spectrometry with Zeeman background correction. Most of the selenium in plasma of healthy controls was seen in proteins that migrated close to immunoglobulin G, and that had an apparent molecular weight at the peak of 174 kDa. One major peak of glutathione peroxidase activity with an apparent molecular weight of 99 kDa was unmatched by any significant peak in selenium content. Thus, there was only limited correspondence between the elution patterns of selenium and glutathione peroxidase activity. Also, in patients with active rheumatoid arthritis, selenium was distributed amongst plasma proteins with a wide range of molecular weights. The major selenium peak was less pronounced in patients, but the amount of selenium in other parts of the chromatogram was not different from that in controls. Further work is necessary to define the occurrence of different selenoproteins in plasma in patients and in healthy subjects.

Aged↗

Cell cycle specific effects of selenium on the lens epithelium studied in vivo by the direct chemical approach.

We attempted to separate S phase from post-S phase effects of selenium upon the lens epithelium by exposing the lens in vivo to selenium either during S phase synthesis of DNA or immediately after completion of DNA synthesis. Incorporation of 3H-thymidine into lens epithelial cell DNA is complete within about 3 hours after intraperitoneally injecting this substrate. Young rats were given selenium either 5 hours before injecting 3H-thymidine (selenium present at the time of labeled-DNA synthesis) or 5 hours after 3H-thymidine (selenium present immediately after completion of S phase). By measuring changes in the distribution of 3H-DNA between the epithelium and lens body for 14 days after injection we estimated migration times and rates of differentiation of the labeled cell population. When selenium was present during DNA synthesis, DNA labeling was decreased by 70%, net migration time (movement from the germinative zone to the equator) was markedly prolonged and the rate of differentiation was slightly accelerated. Selenium had little affect on these parameters if first present immediately after S phase. We conclude that selenium insult to the lens epithelium is largely confined to germinative epithelial cells in S or pre-S phases of the cell cycle.

Animals↗

Low selenium level in severe rheumatoid arthritis.

Serum selenium concentrations were measured in 87 patients with rheumatoid arthritis. The serum selenium levels of the whole group of patients was significantly reduced (70.2 +/- 13.3 micrograms/l, p less than 0.001) when compared with the reference material (79.8 +/- 10.6 micrograms/l). However, the reduction was not equally pronounced in three groups of patients representing different courses of the disease. One group with an active, disabling disease of long duration had a very reduced serum selenium level (63.7 +/- 14.1 micrograms/l, p less than 0.001). Another group, with a protracted but mild disease had a slightly reduced level (74.1 +/- 10.8 micrograms/l, p less than 0.01), and a group with mild disease of short duration had a slightly but not significantly reduced selenium level (75.9 +/- 10.8 micrograms/l, p less than 0.1). Significant correlation was found between serum selenium and the number of joints with limitation of motion, number of joints with active arthritis, haemoglobin concentration and IgG concentration. No correlation was found between serum selenium and disease duration, morning stiffness, ESR, C-reactive protein, rheumatoid factor titre, serum albumin, IgM and IgA. Selenium is part of the enzyme glutathione peroxidase that catabolizes peroxides which are suggested to be actively involved in inflammation. A low selenium level may thus be a further factor in the pathogenesis of rheumatoid arthritis.

Adult↗

Selenium deficiency and thyroid function in acute renal failure.

The lethality of acute renal failure exceeds 50% due to multiorgan dysfunction. In such critically ill patients a reduction of thyroid hormone concentrations without clinical symptoms or laboratory evidence of hypothyroidism frequently occurs. Selenium has recently been shown to play a major role in thyroid hormone metabolism. The aim of this study was to investigate the possible influence of selenium on thyroid hormone metabolism in acute renal failure. Changes in thyroid metabolism were related to the severity of multiorgan failure and to the clinical course. Thyroxine (T4), tri-iodothyronine (T3), free-T4, free-T3, thyrotropin (TSH), serum creatinine, and plasma selenium concentrations in 28 patients (mean age 60 +/- 13) with acute renal failure and multiple-organ dysfunction syndrome were determined initially, and every 3 days after hospital admission. The plasma selenium concentration was found to be reduced compared to normal controls (32 +/- 14 vs. 70-120 micrograms/L). T4 (56 +/- 15 nmol/L, normal range 64-148), T3 (1.31 +/- 0.38 nmol/L, normal range 1.42-2.46), free-T3 (3.1 +/- 1.0 pmol/L, normal range 4.7-9.0), and free-T4 (10.8 +/- 4.0 pmol/L, normal range 10.3-25.8) values were low in 50-70% of the patients at the time of presentation. Plasma TSH concentrations were within the normal range (0.59 +/- 0.79 mU/L, normal range 0.25-3.1), and no clinical symptoms of hypothyroidism were observed. T4 concentration was higher in patients who survived acute renal failure compared to nonsurvivors (62 +/- 22 vs. 51 +/- 16 nmol/L, p < 0.05). Plasma selenium concentration was lower in patients with a severe organ dysfunction syndrome (36 +/- 10 vs. 29 +/- 19 micrograms/L) and correlated with the number of organ failures in these patients (r = -0.247, p < 0.05). T4 and free-T4 values paralleled decreasing selenium concentrations (r = 0.35, p < 0.05). Thyroid hormone levels were reduced in patients with acute renal failure without an increase in TSH. An increase in T4 concentrations became apparent during treatment and may be related to a favorable outcome in acute renal failure. Thyroid hormone concentrations paralleled plasma selenium levels, indicating a possible influence of selenium on thyroid function in acute renal failure.

Acute Kidney Injury↗

Selenium: clinical significance and analytical concepts.

Selenium is an essential trace element in humans and animals. Its only established function in humans is the antioxidant activity of glutathione peroxidase, a selenoenzyme. Severe prolonged deficiency may cause a fatal cardiomyopathy. Iatrogenic causes of selenium deficiency include parenteral and enteral nutrition. Low plasma selenium is also found in malabsorption, cystic fibrosis, rheumatoid arthritis, neoplasia, and other varied clinical disorders. Death has resulted from a single massive ingestion of selenium, while chronic excessive intake causes skin, nail, and hair pathology. Extreme geographical variation in population blood and urine selenium levels and a marked age-specific variation in population reference intervals are important factors in understanding selenium nutrition. Nutritional requirements, biological availability, and metabolism are discussed in relation to geographical, age, and method variability. Sampling, processing procedures, and methods for selenium quantitation are reviewed. Selenium content in different biological matrices and reference values for pediatric, adult, and obstetric populations are provided.

Animals↗

Dietary habits and selenium intake of residents in mountain and coastal communities in Japan.

We used a Simple Food Frequency Questionnaire (SFFQ) in combination with other dietary approaches to estimate the selenium intake from different food groups based on the average long-term diet, in two rural communities in Japan, one in a mountain area and the other in a coastal area. The intake frequencies of rice and wheat products were significantly different in the two districts. The intake frequencies of fish, meat, and eggs, which are rich in selenium, were not significantly different. The mean dietary selenium intake, estimated from the SFFQ and the 24-h recall method, was 82.7 microg/d (n=234) (range 19.2-180.1 microg/d) in the mountain community. The mean dietary selenium intake estimated from the SFFQ and average value of the normal portion size was 118.0 microg/d (n=123) (range 22.6-255.3 microg/d) in the coastal community. These estimated mean values exceeded the Japanese RDA, although the range of daily selenium intake was large. In the mountain community, fish made the largest contribution to dietary selenium intake (48.2% of daily total), followed by eggs (24.3%), and meat (17.0%). In the coastal community, fish accounted for 57.7% of daily total selenium intake, followed by meat (17.5%), and eggs (16.1%). In both districts, the total contribution of rice and wheat products was around 10%. It was found that the contribution of fish to dietary selenium intake was high and the contribution of cereals was low among Japanese.

Adult↗

Selenium and sulfur in antioxidant protective systems: relationships with vitamin E and malaria.

The metabolic relationships among the antioxidant nutrients selenium, sulfur, and vitamin E are particularly close. Selenium and vitamin E have long been known to spare one another in certain nutritional diseases of animals, and selenium has been considered to have a key antioxidant defense function as a component of glutathione peroxidase. However, the antioxidant role of glutathione peroxidase has been questioned and new proteins containing selenium have been identified: phospholipid hydroperoxide glutathione peroxidase, selenoprotein P, and iodothyronine deiodinase. Glutathione peroxidase activity independent of selenium resides in the glutathione S-transferases. Glutathione participates in both enzymatic and nonenzymatic antioxidant defense systems. Some low-molecular weight selenium compounds (e.g., ebselen) exhibit glutathione peroxidase-like action. Certain low molecular weight thiols decompose peroxides nonenzymatically (e.g., the ovothiols). Murine malaria appears to be a useful experimental model for investigating interrelationships of selenium and vitamin E. Vitamin E deficiency protects against the parasite, especially when the mice are concurrently fed peroxidizable fat such as fish or linseed oils. Selenium deficiency, on the other hand, has little or no protective effect against the parasite. Any practical utility of pro-oxidant diets in combating human malaria remains to be determined.

Antioxidants↗

Effect of selenium and mercury on survival of chick embryos.

Factorial experiments were arranged in a completely randomized or randomized block design. The factors included: selenium and day of injection; mercury and day of injection; selenium and mercury; and selenium, mercury and day of injection. Each treatment factor consisted of several levels, selenium ranged from 0.00 p.p.m. to 0.05 p.p.m., mercury from 0.00 p.p.m. to 0.30 p.p.m. and injection was performed on day-3, 9, and 15 of incubation. Babcock-300, and White Leghorn x New Hampshire cross eggs were obtained from 13-15 month old hens. Mercury was injected into the air cell at 4 or 24 hours after selenium injection. Analysis of variance on arcsine transformed data showed that selenium significantly decreased survival at all 3 injection times (P less than 0.01). Survival was significantly greater with increasing age at injection (P less than 0.01). Survival of embryos significantly decreased (P less than 0.01) with increasing levels of mercury from 0.00 p.p.m. to 0.20 p.p.m. injected into eggs on day-3 of incubation. Survival of embryos injected at later stages was less than that of controls but not significantly less. Injection of low levels of selenium, 0.01 p.p.m. or 0.02 p.p.m., to mercury treated eggs tended to improve the survival of embryos as compared to treatment with mercury alone, although individual differences were not significant. At higher levels, selenium accentuated the toxicity of mercury.

Animals↗

Death receptor 5 regulation during selenium-mediated apoptosis in human prostate cancer cells.

Selenium is an essential micronutrient that is currently being tested for prostate cancer chemoprevention. In spite of its significant promise as a chemopreventive agent, the molecular mechanisms of selenium-mediated effects remain to be elucidated. Recent evidence suggests that selenium may mediate its chemopreventive effects by inducing apoptosis in human prostate cancer cells. Here we report that selenium-mediated apoptosis appears to involve membrane death receptor, DR5-dependent pathway in human prostate cancer cells. Selenium specifically upregulated DR5 expression but not that of DR4. Selenium upregulation of DR5 was coupled with caspase 8 activation and Bid cleavage thereby suggesting the existence of a potential cross-talk between the DR5 and the mitochondrial pathways. Thus, our results suggest that DR5 is specifically regulated by selenium and its activation may play an important role in selenium-mediated chemoprevention.

Antioxidants↗

Dietary selenium and copper intake by resident undergraduate students of the University of Ghana.

OBJECTIVES: To determine and evaluate dietary intake of selenium and copper by resident undergraduate students of the University of Ghana. DESIGN: Prospective/comparative study. SETTING: The university of Ghana, Legon, Accra. SUBJECT: One hundred and fifty undergraduate resident students in five out of seven halls of residence of the University of Ghana. MAIN OUTCOME MEASURES: Pre-tested structure questionnaires were administered to informed students to obtain personal data, intake of selenium, copper and/or multimineral supplements and foods consumed as well as frequency of consumption. A twenty four hour food intake on two non-consecutive days, were used to determine food intake. Selenium and copper levels in the foods identified were determined using Atomic Absorption Spectrophotometer (AAS) and compared to the respective RDAs to assess intake adequacy/inadequacy. RESULTS: None of the students interviewed took in selenium or copper supplements, although 2% took in multi-mineral supplements, which contained insignificant levels of selenium and/or copper. In the case of copper, 7.3% (11/150) met 75-100% of the RDA, while 1.3% (2/150) met the RDA in the case of selenium. As many as 15.3% (23/150; in the case of copper) and 83% (123/150; in the case of selenium) did not meet the required intakes. However, 77% (116/150) had excess intake of copper while 15.7% (25/150) took excess selenium. CONCLUSION: Due to the importance of these micronutrients and in the face of poor nutritional status, as judged by the few that met the required RDAs as well as excess, there is a need to carry out blood analyses to determine whether the dietary pattern has been translated systemically. If indicated, the University authorities must consider mounting nutritional education to ensure that those deficient take in the required levels while those consuming excess are made to cut down on their intakes, since both deficient and excess status have physiological consequences.

Adult↗