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PubMed1998

Selenoprotein expression and brain development in preweanling selenium- and iodine-deficient rats.

Selenium deficiency causes further impairment of thyroid hormone metabolism in iodine-deficient rats and therefore could have a role in the aetiology of both myxoedematous and neurological cretinism in humans. Thyroidal type I iodothyronine deiodinase (ID-I), cytosolic glutathione peroxidase and phospholipid hydroperoxide glutathione peroxidase activities were increased in iodine-deficient adult rats and their offspring at 11 days of age. Thyroidal ID-I activity was unchanged and thyroidal cytosolic glutathione peroxidase activity was decreased by more than 75% by combined selenium and iodine deficiency in 11-day-old rats, indicating that, while the thyroid retained an ability to produce 3,3',5-triiodothyronine (T3), the gland was probably more susceptible to peroxidative damage caused by increased hydrogen peroxide concentrations driven by increased thyrotrophin. Thyroidal atrophy, common in myxoedematous cretinism, did not occur in iodine- or selenium and iodine-deficient rat pups. Iodine deficiency increased brain type II iodothyronine deiodinase activity 1.5-fold in 4-day-old rats and 3-fold in 11-day-old rats, regardless of selenium status. Thus rats were able to activate compensatory mechanisms in brain that would maintain T3 concentrations in selenium and iodine deficiencies. Surprisingly, however, selenium deficiency had a greater effect than iodine deficiency on markers of brain development in rat pups. Expression of the brain-derived neurotrophic factor (BDNF) mRNA was decreased in selenium deficiency in 4- and 11-day-old pups and in combined selenium and iodine deficiency in 4-day-old pups. Iodine deficiency caused an increase in BDNF expression in 11-day-old pups but had no effect on 4-day-old pups. Myelin basic protein mRNA expression in brain was decreased by combined selenium and iodine deficiency in 11-day-old rats.

Animals↗
PubMed1998

Selenium-based antihypertensives. Rationale and potential.

Selenium, long recognised as an important 'dietary antioxidant', is now known to be an essential component of the active sites of a number of enzymes, including the glutathione peroxidase selenoenzyme family which scavenge hydroperoxides to prevent cellular damage. Dietary selenium deficiency has been linked to diseases as diverse as cancer, heart disease, arthritis and AIDS, and epidemiological evidence is now emerging for the beneficial effects of selenium supplementation. Thus, the pharmacology, biology and biochemistry of selenium metabolism have become subjects of considerable interest, which are spurring efforts to develop synthetic selenium-containing compounds as potential therapeutic agents. Phenylaminoalkyl selenides were developed in the authors' laboratories as novel, selenium-based pharmacological agents. We demonstrated that these compounds exhibited dose-dependent antihypertensive activity in spontaneously hypertensive rats. Biochemical studies established that as a consequence of the redox properties of their selenium moieties, these phenylaminoalkyl selenides possessed the remarkable property of propagating a cycle of turnover-dependent local depletion of reduced ascorbate when processed by the key enzyme of catecholamine metabolism, dopamine-beta-monooxygenase. On the basis of inductively coupled plasma/mass spectroscopic analyses, corroborated by operant behaviour and locomotor activity investigations, an orally-active phenylaminoalkyl selenide with restricted CNS permeability was successfully developed. To our knowledge, this compound--4-hydroxy-alpha-methyl-phenyl-2-aminoethyl selenide--is the first orally active, selenium-based anti-hypertensive compound ever reported. In the future, we anticipate more widespread efforts to incorporate selenium into rationally designed pharmaceutical agents, with the goal of developing novel compounds which may be of therapeutic benefit toward a variety of human diseases.

Animals↗
PubMed2004

Apoptosis is a critical cellular event in cancer chemoprevention and chemotherapy by selenium compounds.

Epidemiological studies, preclinical investigations and clinical intervention trials support the role of selenium compounds as potent cancer chemopreventive agents; the dose and the form of selenium are critical factors in cancer prevention. Induction of apoptosis and inhibition of cell proliferation are considered important cellular events that can account for the cancer preventive effects of selenium. Toxicity should always be considered a determining factor in the selection of potential chemopreventive agents. Prior to induction of apoptosis, selenium compounds alter the expression and/or activities of a number of cell cycle regulatory proteins, signaling molecules, proteases, mitochondrial associated factors, transcriptional factors, tumor suppressor genes, polyamine and glutathione levels. Depending on the form, selenium compounds can target separate pathways but more efforts are needed to learn about disrupting different pathways converging to apoptosis. Numerous selenium compounds are known to inhibit carcinogenesis in several animal models but not all of these have been examined for their efficacy to induce apoptosis or vice versa in the corresponding target organ. Studies aimed at investigating the effects of selenium compounds on apoptosis in the target organ in vivo and in vitro are limited. On the basis of information provided in this review, we recommend that additional molecular markers should be added to those proposed in the Selenium and Vitamin E Cancer Prevention Trial (SELECT) on prostate cancer. Apart from the selenium compounds reviewed here, several novel synthetic organoselenium compounds need to be examined both in vitro and in vivo for their potential to induce apoptosis; such an investigation may provide better and mechanism-based cancer chemoprevention as well as chemotherapeutic agents.

Animals↗
PubMed1985

Selenium treatment in rheumatoid arthritis.

A low selenium level has been reported in rheumatoid arthritis and juvenile chronic arthritis. Selenium is an essential part of the enzyme glutathione peroxidase, which catabolizes peroxides, compounds which are suggested to be of pathogenetic importance in rheumatic diseases. To assess a possible antirheumatic effect of selenium, 40 patients with active RA were included in a 6-month double-blind clinical study of selenium versus placebo. The patients in the selenium group were given daily supplements of 256 micrograms selenium in selenium-enriched yeast. Although concentrations of selenium in serum and erythrocytes increased considerably, no significant antirheumatic effect of selenium could be demonstrated.

Arthritis, Rheumatoid↗
PubMed1980

Toxicology of selenium: a review.

The concentration of selenium in soil, water, or minerals is site specific. World or regional averages are of little practical value. In one report from the front range area of Colorado, average selenium concentrations in bodies of standing water were from 0.3 to 15.8 micrograms Se per liter of water. In some aquatic organisms there is a strong correlation between the Se content of the water ant that of the body tissues; in others no such correlation obtains. Some organisms bioaccumulate Se by factors as high as 1300 to 3800. In most fish the amount of Se in the flesh seems to depend on the amount in the food taken in; there are exceptions, however. Aquatic organisms from seleniferous regions bioconcentrate selenium so as to reach total body levels of 60 micrograms Se per gram or up to 100 micrograms Se per gram of liver. There seems to be no evidence for "biomagnification" of selenium by aquatic organisms. Selenium exerts a strong protective action against the poisoning effects of many heavy metals (lead, cadmium, arsenic, and mercury, for example) and of some organic toxicants (paraquat, for example) in birds, mammals, and man. Data on man are sketchy. Selenium is released into the environment from the burning of coal. No identifiable hazard to man or to plants and animals useful to man can, at this time, be attributed to this source. Selenium is poisonous to man and animal in large amounts. It is a necessary micronutrient for many animals in small amounts; it may also be a needed micronutrient for man, but the data are sparse. The usual American diet contains adequate selenium for human health. Occupational selenium poisoning is mostly accidental and rare.

Animals↗
PubMed1981

Effect of high but nontoxic dietary intake of copper and selenium on metabolism in calves.

Sixteen male Holstein calves in a 2 X 2 factorial design with four animals per treatment were fed 0 and 100 ppm supplemental copper from copper carbonate and 0 and 1 ppm added selenium from sodium selenite for 15 days in a practical diet containing .1 ppm selenium and 15 ppm copper. On day 13, calves received an oral dose of selenium-75 and were sacrificed 48 h later. Feed consumption, serum glutamic oxaloacetic transaminase, creatine phosphokinase, and stable copper in blood and urine were unaffected by diets. Stable copper in pancreas, spleen, kidney, muscle, and spinal cord along with selenium-75 in lung, pancreas, liver, heart, and muscle also were unaffected. In calves fed high selenium, selenium-75 was lower in blood, kidney, and spinal cord, and more was excreted in the urine, indicating less retention. Urine was the major excretory pathway of excess selenium-75. Liverstable copper was greater for high copper diets. Stable copper in the lung was higher in calves fed high selenium-high copper than in either control or calves fed high copper. Stable copper was greater in heart tissue in both groups fed high selenium than in controls and slightly higher than the group fed high copper.

Animal Feed↗
PubMed1984

Effect of vitamin E and selenium supplementation on incidence of clinical mastitis and duration of clinical symptoms.

Incidence of clinical mastitis and duration of clinical symptoms for complete lactations were evaluated for 80 cows randomly assigned to one of four groups: vitamin E supplemented- and selenium injected, selenium injected, vitamin E supplemented, and controls. Vitamin E supplementation and selenium injection were during the dry period. Log-linear analysis of incidence data revealed a significant 37% reduction of clinical mastitis by vitamin E. Incidence was not affected by selenium alone, nor was there any evidence for interaction of vitamin E with selenium on incidence. However, duration of clinical symptoms (calendar months clinical/quarter lactating) was reduced by 46% for the selenium group, 44% for the vitamin E group, and 62% for the vitamin E-selenium group as compared to controls. We conclude that dairy cow diets deficient of vitamin E may elevate incidence of clinical mastitis. Selenium deficiency may result in greater duration of clinical symptoms, and selenium may interact with vitamin E. Coliform bacteria and species of streptococcus other than Streptococcus agalactiae were isolated from 70% of the clinical cases.

Animals↗
PubMed1985

Distribution of supplemental selenium in the serum, hair, colostrum, and fetus of parturient dairy cows.

A selenium supplementation study was conducted with Holstein cows to evaluate amounts and methods of administration, namely, oral supplementation (1 vs. 2 mg/head/d, last 60 d of gestation) and intramuscular injection (50 mg at 40 and 20 d prepartum vs. 50 mg at 60, 40, and 20 d prepartum). Blood was collected every 10 d, starting 60 d prepartum and extending 20 d postpartum for cows, and at birth to 20 d for calves. Hair samples of cows were obtained at 60 to 40 and 20 d prepartum, and of the calves at birth. Colostrum samples were obtained for assay. Oral (2 mg/d) and both injection treatments resulted in increased selenium in serum of cows, but selenium in serum of calves at birth was greater only for those whose dams received selenium by injection. Selenium in hair of cows was increased by both injection treatments as well as by the oral treatment of 2 mg/d. Selenium in hair of calves was increased by all methods of administering selenium to the dams. Selenium in colostrum was not affected by any treatment. Thus, pregnant dairy cattle respond to selenium supplementations of a daily oral intake of 2 mg/head/d, the last 60 d of gestation, or by injection of 50 mg each on d 40 and 20 prepartum.

Animals↗
PubMed1986

Tolerance of the preruminant calf for selenium in milk replacer.

Calves were fed skim milk powder-based milk replacer containing either .2, 1, 3, 5, or 10 ppm selenium (added as sodium selenate) in the dry matter from 3 to 45 d of age to estimate the lowest amount of dietary selenium that would reduce calf performance and feed utilization. Only at the highest selenium (10 ppm) did calves show reduced average daily gain and feed efficiency and lower blood packed cell volume. Apparent digestibility of dry matter, nitrogen, and lipid, and plasma creatine phosphokinase activity were not affected by any of the selenium intakes. In general, selenium in blood, bile, duodenal mucosa, liver, kidney, and muscle reflected selenium intakes with liver and kidney reaching the highest selenium concentrations. Postmortem examinations of calves revealed no gross abnormalities for any of the selenium treatments. The preruminant calf is very tolerant of high inorganic selenium concentrations in skim milk powder-based milk replacer.

Animal Feed↗
PubMed1990

Relationships among vitamin E, selenium, and bovine blood neutrophils.

Effects of vitamin E and selenium supplementation on in vitro phagocytosis and intracellular kill of bacteria by bovine neutrophils were investigated. Diets were not supplemented with vitamin E and selenium during the dry period and first 21 d of lactation. Cows were then assigned to one of four treatment diets for 30 d. Treatment diets were either unsupplemented or supplemented with vitamin E, selenium, or both vitamin E and selenium, in a 2 x 2 factorial arrangement. Peripheral blood neutrophils were isolated from each cow on lactation d 51. Vitamin E supplementation of diets increased intracellular kill of Staphylococcus aureus and Escherichia coli by neutrophils. Intracellular kill of S. aureus was greater in neutrophils isolated from selenium supplemented cows than in neutrophils from cows without supplemental selenium. Intracellular kill of E. coli did not differ between neutrophils from selenium supplemented and selenium unsupplemented cows. Ability of neutrophils to phagocytize either S. aureus or E. coli was independent of vitamin E and selenium.

Animals↗
PubMed1978

Mercury metabolism in Japanese quail. I. The effect of dietary mercury and selenium on their tissue distribution.

Immature and adult coturnix quail were fed isolated soybean protein diets to which methylmercuric chloride or mercuric chloride were added with or without supplemental selenium for seven days. Samples of brain, blood, liver, and kidney were analyzed for total mercury and selenium via atomic absorption spectrophotometry. Selenium addition had no effect on the mercury concentration in kidney, brain, or blood but did tend to increase the concentration of mercury in the livers of the methylmercuric chloride-treated birds. Selenium in the presence of methylmercury increased the selenium concentration of liver and kidney but had little effect on the selenium concentration of brain or blood. Methylmercuric chloride supplementation resulted in increased selenium concentration in the blood of the selenium supplemented group. All other tissue selenium levels were unaffected by the addition of mercury.

Animals↗
PubMed2004

Ecologic study of serum selenium and upper gastrointestinal cancers in Iran.

AIM: Both observational and experimental studies have shown that higher selenium status reduces the risk of upper gastrointestinal cancers in selenium deficient populations. Recent cancer registry data have shown very different rates of esophageal cancer (EC) and gastric cancer (GC) in four Provinces of Iran, namely Ardabil, Mazandaran, Golestan, and Kerman. The aim of this study was to have a preliminary assessment of the hypothesis that high rates of EC in Golestan and high rates of GC in Ardabil may be partly attributable to selenium deficiency. METHODS: We measured serum selenium in 300 healthy adults from Ardabil (n = 100), Mazandaran (n = 50), Golestan (n = 100), and Kerman (n = 50), using inductively coupled plasma, with dynamic reaction cell, mass spectrometry (ICP-DRC-MS) at the US Centers for Disease Control (Atlanta, Georgia). RESULTS: The median serum selenium concentrations were very different in the four Provinces. The medians (IQR) for selenium in Ardabil, Mazandarn, Golestan, and Kerman were 82 (75-94), 123 (111-132), 155 (141-173), and 119 (110-128) microg/L, respectively (P<0.001). The results of linear regression showed that the Province variable, by itself, explained 76% of the variance in log selenium (r2 = 0.76). The proportion of the populations with a serum selenium more than 90 microg/L (the concentration at which serum selenoproteins are saturated) was 100% in Golestan, Kerman, and Mazandaran but only 29% in Ardabil. CONCLUSION: Our findings suggest that selenium deficiency is not a major contributor to the high incidence of EC seen in northeastern Iran, but it may play a role in the high incidence of GC in Ardabil Province.

Adult↗
PubMed2005

Effect of long-term administration of arsenic (III) and bromine with and without selenium and iodine supplementation on the element level in the thyroid of rat.

The aim of this study was to evaluate the influence of arsenic and bromine exposure with or without iodine and selenium supplementation on the element level in the thyroid of rats. Four major groups of Wistar female rats were fed with respective diets: group A - standard diet, group B - iodine rich diet (10 mg I/kg food), group C - selenium rich diet (1 mg Se/kg) and group D - iodine and selenium rich diet (as in group B and C). Each group was divided into four subgroups per 7 animals each receiving either NaAsO(2) ip (6.5 mg.kg(-1) twice a week for two weeks and 3.25 mg.kg(-1) for six weeks) or KBr in drinking water (58.8 mg.l(-1)) for 8 weeks or combined administration of both substances. Remaining subgroup served as controls. After 8 weeks thyroid glands were analyzed by ICP-MS for As, Br, Se, and I content. The exposition of rat to arsenic or bromine causes the accumulation of these elements in the thyroid gland ( approximately 18 ppm of As, approximately 90 ppm of Br) and significantly affects iodine and selenium concentration in the thyroid. In iodine and/or selenium supplemented rats the bromine intake into the thyroid was lowered to approximately 50% of the level in unsupplemented animals. Also selenium thyroid level elevated due to KBr administration was lowered by iodine supplementation in the diet. The accumulation of arsenic in the thyroid was not influenced by selenium or iodine supplementation; however, As(III) administration increased iodine thyroid level and suppressed selenium thyroid level in selenium or iodine supplemented group of animals.

Animals↗
PubMed1975

Mechanisms of action of selenium and vitamin E in protection of biological membranes.

Opinions vary as to the mode of action of vitamin E and selenium. Some argue that they act as nonspecific biological antioxidants. Others propose that the functions of the two substances are distinct and that vitamin E acts as a true vitamin in addition to functioning as a lipid-soluble antioxidant. Support for the "Biological Antioxidant Theory" is largely circumstantial. However, lipoperoxides have been detected in adipose tissues of vitamin E-deficient animals, and increased rates of in vitro peroxidation have been demonstrated in homogenates of several tissues of selenium and vitamin E-deficient animals. The basis of the antioxygenic role of selenium in these systems was elucidated by the discovery of Rotruck et al. (1973) that selenium is a component of rat erythrocyte glutathione peroxidase. Further studies in this laboratory have demonstrated the important role of glutathione peroxidase in protection against the vitamin E- and selenium-deficiency disease of chicks, exudative diathesis, which results from increased capillary permeability. Also shown were the activities of both dietary selenium and vitamin E in prevention of ascorbate-induced peroxidation in mitochondrial and microsomal preparations from chick liver. Recent results demonstrate that both selenium and vitamin E are required to protect hepatic mitochondria and microsomes from peroxidative degradation. Dietary requirements of the chick for both nutrients for this function have been determined: approximately 0.06 ppm selenium in the presence of adequate vitamin E; 30-50 IU vitamin E per kg in the presence of adequate selenium.

Aging↗
PubMed2001

[Retention of selenium volatility using lime in coal combustion].

For understanding the volatility of selenium, the effect of the contents of exchangeable cations of coal on it, and the retention of selenium using CaO in coal combustion, the sequential chemistry extraction, the fixed bed and circulating fluidized bed (CFB) combustion, X-ray diffraction (XRD) and atomic fluorescence spectrometry (AFS) were undertaken. The results showed that the volatility of selenium was more than 97% in coal combustion at 815 degrees C, and the volatility of selenium was affected by the content of exchangeable cations of coal in low-middle temperature. It was identified that lime can restrain the volatility of selenium. In fixed bed combustion of coal, the retention rates of selenium volatility were between 11.6% and 50.7% using lime. In circulating fluidized bed combustion of coal, partitioning of selenium changed very much in ash of different size fraction between without lime and with lime. Comparing with combustion without lime, the content of selenium in ash from chimney was less than fourth times and that in leaching water from chimney decreased by two orders of magnitude using lime. Retention of selenium volatility using lime is so effective in coal combustion, especially in CFB combustion of coal.

Calcium Compounds↗
PubMed2001

Plasma selenium level before diagnosis and the risk of prostate cancer development.

PURPOSE: Epidemiological studies and a randomized intervention trial suggest that the risk of prostate cancer may be reduced by selenium intake. We investigated whether plasma selenium level before diagnosis correlated with the risk of later developing prostate cancer. MATERIALS AND METHODS: A case control study was performed on men from the Baltimore Longitudinal Study of Aging registry, including 52 with known prostate cancer and 96 age matched controls with no detectable prostatic disease. Plasma selenium was measured at an average time plus or minus standard deviation of 3.83 +/- 1.85 years before the diagnosis of prostate cancer by graphite furnace atomic absorption spectrophotometry. Adjusted odds ratio and 95% confidence interval were computed with logistic regression. RESULTS: After correcting for years before diagnosis, body mass index, and smoking and alcohol use history, higher selenium was associated with a lower risk of prostate cancer. Compared with the lowest quartile of selenium (range 8.2 to 10.7 microg./dl.), the odds ratios of the second (10.8 to 11.8), third (11.9 to 13.2) and fourth (13.3 to 18.2) quartiles were 0.15 (95% confidence interval 0.05 to 0.50), 0.21 (0.07 to 0.68) and 0.24 (0.08 to 0.77, respectively, p =0.01). Furthermore, plasma selenium decreased significantly with patient age (p <0.001). CONCLUSIONS: Low plasma selenium is associated with a 4 to 5-fold increased risk of prostate cancer. These results support the hypothesis that supplemental selenium may reduce the risk of prostate cancer. Because plasma selenium decreases with patient age, supplementation may be particularly beneficial to older men.

Aged↗
PubMed1975

Interrelationships of selenium with other trace elements.

Biological interactions between selenium and a number of other elements occur that render selenium much less toxic than when it is present alone. These elements are arsenic, mercury, cadmium, and copper. Furthermore, the presence of selenium reduces the toxicity of mercury and cadmium. These are general biological interactions and have been found to occur in a number of animal species under a variety of conditions. It has been shown that the reaction products of selenium with mercury and cadmium are less toxic than an equal amount of selenium fed alone to chicks. The presence of arsenic shifts the excretion of selenium to the bile. There is no conclusive evidence that the presence of other elements reduces the absorption or retention of selenium. It is possible that some of the interactions are caused by the formation of a compound by selenium and other elements which has less affinity for active groups on biologically active compounds.--Hill, C.H. Interrelationships of selenium with other trace elements.

Animals↗
PubMedDate not supplied

[Selenium tolerance of yeasts].

Selenium tolerance of yeasts widely varies: the growth of some yeasts can be inhibited by a selenium concentration as low as 10(-4) M, whereas others can grow in the presence of 10(-1) M selenium. Homogeneous yeast taxa are characterized by a certain level of selenium tolerance, and heterogeneous taxa show a variable level of tolerance to selenium. In general, ascomycetous yeasts are more tolerant to selenium than basidiomycetous yeasts. Among the ascomycetous yeasts, the genera Dekkera and Schizosaccharomyces exhibited the lowest and the species Candida maltosa, Hanseniaspora valbyensis, Kluyveromyces marxianus, and Yarrowia lipolytica the highest tolerance to selenium. Among the basidiomycetous yeasts, the genera Bullera, Cryptococcus, and Holtermannia showed the lowest and the species Cryptococcus curvatus, Cr. humicola, and Trichosporon spp. the highest tolerance to selenium. The selenium tolerance of yeasts depends on the composition of the growth medium, in particular, on the presence of sulfate, sulfur-containing amino acids, and glutamine in the medium.

Adaptation, Physiological↗