Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Selenium”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,117 records · Page 62Linked to original sources

Zinc, copper and selenium in reproduction.

Of the nine biological trace elements, zinc, copper and selenium are important in reproduction in males and females. Zinc content is high in the adult testis, and the prostate has a higher concentration of zinc than any other organ of the body. Zinc deficiency first impairs angiotensin converting enzyme (ACE) activity, and this in turn leads to depletion of testosterone and inhibition of spermatogenesis. Defects in spermatozoa are frequently observed in the zinc-deficient rat. Zinc is thought to help to extend the functional life span of the ejaculated spermatozoa. Zinc deficiency in the female can lead to such problems as impaired synthesis/secretion of (FSH) and (LH), abnormal ovarian development, disruption of the estrous cycle, frequent abortion, a prolonged gestation period, teratogenicity, stillbirths, difficulty in parturition, pre-eclampsia, toxemia and low birth weights of infants. The level of testosterone in the male has been suggested to play a role in the severity of copper deficiency. Copper-deficient female rats are protected against mortality due to copper deficiency, and the protection has been suggested to be provided by estrogens, since estrogens alter the subcellular distribution of copper in the liver and increase plasma copper levels by inducing ceruloplasmin synthesis. The selenium content of male gonads increases during pubertal maturation. Selenium is localized in the mitochondrial capsule protein (MCP) of the midpiece. Maximal incorporation in MCP occurs at steps 7 and 12 of spermatogenesis and uptake decreases by step 15. Selenium deficiency in females results in infertility, abortions and retention of the placenta. The newborns from a selenium-deficient mother suffer from muscular weakness, but the concentration of selenium during pregnancy does not have any effect on the weight of the baby or length of pregnancy. The selenium requirements of a pregnant and lactating mother are increased as a result of selenium transport to the fetus via the placenta and to the infant via breast milk.

Animals↗

Serum selenium and colonic neoplastic risk.

BACKGROUND: Selenium deficiency has been associated with cancer risk in several organs. This association was investigated in neoplasia of the colorectum. DESIGN: A case-control study is reported with two patient series, colorectal cancer and colorectal adenomatous polyps, and a control group found to be free of colorectal neoplasia. Diagnosis was determined by colonoscopy and histologic review of suspected neoplasms. Serum drawn at the time of colonoscopy was subsequently assayed for selenium content, and quartiles based on selenium were defined. Crude and adjusted odds ratios with 95 percent confidence intervals for adenoma related to selenium were calculated, controlling for known or suspected risk factors including gender, age, race, body mass index, family history, tobacco use, alcohol consumption, serum beta carotene, serum alpha tocopherol, and serum ferritin. RESULTS: There were 138 controls who had no neoplastic disease, 139 adenoma patients, and 25 cancer patients. For adenoma, comparing higher quartiles of selenium to the first (lowest selenium), the adjusted odds ratio for the second quartile was 1.7 (95 percent confidence interval, 0.8-3.7), the third quartile was 1.4 (0.7-3.2), and the fourth (highest selenium) quartile was 1.8 (0.9-4). The odds ratios for cancer patients were 0.8 for the second quartile, 1 for the third quartile, and 1.7 for the fourth quartile. CONCLUSION: No trend could be detected toward a protective effect of higher levels of serum selenium for colonic benign or malignant tumors.

Adenoma↗

Selenium. Mechanistic aspects of anticarcinogenic action.

Selenium is increasingly recognized as a versatile anticarcinogenic agent. Its protective functions cannot be solely attributed to the action of glutathione peroxidase. Instead, selenium appears to operate by several mechanisms, depending on dosage and chemical form of selenium and the nature of the carcinogenic stress. In a major protective function, selenium is proposed to prevent the malignant transformation of cells by acting as a "redox switch" in the activation-inactivation of cellular growth factors and other functional proteins through the catalysis of oxidation-reduction reactions of critical SH groups of SS bonds. The growth-modulatory effects of selenium are dependent on the levels of intracellular GSH and the oxygen supply. In general, growth inhibition is achieved by the Se-mediated stimulation of cellular respiration. Selenium appears to inhibit the replication of tumor viruses and the activation of oncogenes by similar mechanisms. However, it may also alter carcinogen metabolism and protect DNA against carcinogen-induced damage. In additional functions of relevance to its anticarcinogenic activity, selenium acts as an acceptor of biogenic methyl groups, and is involved in the detoxification of metals and of certain xenobiotics. In its interactions with transformed cells at higher concentrations, it may induce effects ranging from metabolic and phenotypical changes, and partial renormalization to selective cytotoxicity owing to reversible or irreversible inhibition of protein and DNA synthesis. Selenium also has immunopotentiating properties. It is required for optimal macrophage and NK cell function. Its protective effects are influenced by synergistic and antagonistic dietary and environmental factors. The latter include a variety of toxic heavy metals and xenobiotic compounds, but they are also influenced by essential elements, such as zinc. The exposure to antagonistic factors must be minimized for the full expression of its anticarcinogenic potential.

Animals↗

Selenium status of healthy Turkish children.

Selenium concentrations, in blood plasma, red blood cells, hair of 61 healthy children, ages 0-14 yr, were determined using hydride generation atomic absorption spectrometry. Starting from late lactation period, selenium concentrations in all these matrices were found to be increasing with age. A good correlation was found between erythrocyte and plasma, hair and plasma, and hair and erythrocyte selenium concentrations. Although plasma, erythrocyte, and hair selenium concentrations of girls seemed to be higher than that of boys (only in erythrocytes), selenium concentrations of girls were found to be significantly (p < 0.002) higher than that of boys, 71 +/- 9 ng/mL, vs 65 +/- 10 ng/mL, respectively. Selenium status of Turkish children is found to be lower than that found in the literature; marginal selenium deficiency could be important in the development of some selenium deficiency related diseases. There is a need for extension of this study to healthy children from different regions in Turkey and to different disease states.

Adolescent↗

Selenium in serum and whole blood in patients with surgical interventions.

Selenium values of serum and whole blood were determined for two groups of patients undergoing large surgical interventions (e.g., gastrectomy) and receiving a total parenteral nutrition (TPN). All patients showed low selenium values at the beginning of TPN. The first group received a supplementation of selenium, and it was established that selenium levels normalized after 6-7 d. The balances of selenium turned out to be positive in all cases. The second group, which was not administered selenium supplementation, showed significantly lower values of selenium. It can, therefore, be concluded that a substitution of selenium prior to large surgical interventions following TPN clearly helps patients combat the increase in the oxidant stress reactions.

Aged↗

The daily dietary selenium intake of West German adults.

The selenium content of food consumed in the Federal Republic of Germany (FRG) was determined for the estimation of the dietary selenium intake of West German adults. The daily dietary selenium intake of men is 47 micrograms (micrograms) and that of women 38 micrograms, corresponding to 0.67 microgram/kg body weight per day for both men and women. Animal protein is the main source of dietary selenium, accounting for 65.5% of the total selenium intake. Pork contributes 25.1% to the total Se intake, reflecting the current consumption and the selenium supplementation of feedstock rather than the availability of selenium from natural dietary sources. The selenium intake of adults in West Germany is only slightly higher than in New Zealand, Finland, and Italy, nearly equal to that in Belgium and France, and distinctly lower than in Great Britain, the USA, Canada, and Japan.

Adult↗

[Selenium substitution in acute myocardial infarct].

BACKGROUND: Previous examinations have demonstrated decreased selenium levels in serum and full blood in patients with myocardial infarction. PATIENTS AND METHOD: 28 patients received a selenium treatment additional to the usual treatment of myocardial infarction. 19 patients with myocardial infarction with no supplementary selenium treatment served as a control group. Selenium levels in serum, full blood and urine were measured and the complications of the myocardial infarction documanted. RESULTS: There was a significant increase of serum and full blood selenium and glutathione peroxidase levels under i.v. selenium therapy in the acute phase of myocardial infarction (first to third day). Left heart failure more rarely occurred in the selenium group (20%) than in control patients (57%). Acute tachycardial cardiac rhythm disturbances such as ventricular extrasystoles and couplets diminished in both groups; ventricular extrasystoles decreased in the selenium group. CONCLUSIONS: Selen should be substituted in patients with acute myocardial infarction and decreased selen levels. It would be useful to carry out a prospective double-blind study.

Administration, Oral↗

[Selenium in phenylketonuria patients. Effects of sodium selenite administration].

PATIENTS AND METHOD: 17 patients (8 female, 9 male; age 8.2 +/- 3.7 years) with phenylketonuria under phenylalanin restricted diet were investigated prior to and after 3 months of selenium substitution (sodium selenite, 115 micrograms Se/m2 BSA/d). Different parameters in blood were determined: selenium, glutathione peroxidase (Gpx) activity, thyroid hormones, blood cell count, lymphocytic antigen expression, muscle function and -enzymes, cardiac ultrasound. RESULTS: The main significant results of selenium substitution are: increased plasma-selenium, blood cell selenium, plasma-Gpx activity and left ventricular cardiac index as well as decreased plasma thyroxin, free thyroxin, reverse triiodthyronin, total cholesterol, mean erythrocyte and thrombocyte volume and lymphocytic CD2 expression. CONCLUSION: The data indicate metabolic and functional signs of selenium deficiency in patients with phenylketonuria without selenium substitution. We conclude that, despite of lacking clinical symptoms, a selenium supply in phenylketonuria patients under diet is necessary and should be performed with usefull peroral sodium selenite (115 micrograms Se/m2 BSA/d) initially, followed by a dosage between 30 and 60 micrograms Se/m2 BSA/d).

Antioxidants↗

[Selenium administration in children with SIRS].

PATIENTS AND METHOD: At the Clinic for Paediatric Surgery of the University of Dresden, in a time period ranging from 5/1994 to 12/1996, all patients aged between 1 and 16 years with severe inflammatory surgical diseases or extended scalded skin, were given an adjuvant selenium substitution. As control group, all patients with the same diagnosis and age treated during the months 1/1997 to 12/1998, did not receive this adjuvant selenium substitution. All these patients fulfilled the criteria of "Systemic Inflammatory Response Syndrome" (SIRS). The selenium-therapy group consisted of 34 patients and the control group without substitution consisted of 31 patients. The following laboratory parameters were measured on the 1st, 2nd, 3rd, 6th and last treatment day: white blood cell count, interleukin 6, C-reactive protein, fibrinogen, malondialdehyde, activity of glutathione peroxidase in plasma and level of selenium in plasma and whole blood. RESULTS: The initially high interleukin 6 rates declined significantly in both groups from the 2nd day on. The acute phase proteins, i.e. the C-reactive protein and fibrinogen, normalized in both groups after the 3rd day of treatment. The initial low rates of selenium in plasma and blood gained more rapidly a normal level in the therapy group than in the control group. On the 1st day of therapy the glutathione peroxidase activity in plasma was in both groups at the inferior limit of norm range and remained at this level in the control group for the whole observation period. In the selenium-substitution group on the contrary, these initial low values raised to the double as an expression of an elevated cell membrane protection. The initial significant elevated malondialdehyde rates in both groups, expressing a raised lipidperoxidation, fell down to a normal level in the selenium-substitution group, whereas they remained at their initial high level in the control group during the whole observation period. CONCLUSION: The substitution of selenium in children with SIRS is a supportive therapy.

Adolescent↗

Toxicity and chemical form of selenium in the liver of mice orally administered selenocystine for 90 days.

The subacute oral toxicity of selenocystine and chemical form of selenium in the liver following exposure to this compound were assessed in ICR male mice. Animals were dosed 6 days/week for 30, 60 or 90 days with 0, 5, 10 or 15 mg/kg per day. Body weight gain decreased with dosage. The activities of aspartate aminotransferase and alanine aminotransferase in plasma were significantly elevated at the highest dose level after 60 days and at the two higher dose levels after 90 days of exposure. However, the level of selenium content in the liver was the same at the two higher dosages at both 60 and 90 days of exposure. The subcellular distribution of selenium in the liver from mice treated with selenocystine showed that the major part of the total selenium content, 68.3-72.1%, existed in the cytosolic fraction. Sephadex G-150 chromatograms of liver cytosol of the animals administered selenocystine revealed three selenium-containing fractions which involve glutathione peroxidase (molecular weight 80,000) high molecular (molecular weight 55,000-60,000) and low molecular (molecular weight < 10,000) substances. Selenium content and acid-volatile selenium content in the high molecular weight fraction increased with exposure time to selenocystine. Thus, in a subacute toxicity study selenocystine given for 90 days caused hepatic damage in mice, depending on the acid-volatile selenium content in the liver cytosol.

Administration, Oral↗

Inhibitory effects of selenium on the growth of DU-145 human prostate carcinoma cells in vitro.

The growth of DU-145 human prostate carcinoma cells is reduced to 50% of control by 1 X 10(-6) M to 2 X 10(-6) M selenium and to 2% of control at 10(-4)M selenium. These cells show greater sensitivity to inhibition of growth or DNA synthesis by selenium than human W1-38 and HeLa cells and mouse mammary tumor cells. It has been shown that selenium inhibits carcinogenesis and reduces the incidence of chemical carcinogen and virus-induced tumors of a variety of organs in animals. Selenium may also inhibit the growth of certain tumor cells of non-human origin. To our knowledge, this is the first study on the effects of selenium on the growth of human tumor cells. From extrapolation, it is deduced that selenium serum levels in humans living in high selenium areas may be as high as 10(-6) M and could be effective in inhibiting the growth of tumor cells in vivo. These findings have implications in the prevention and intervention of prostate cancer in man.

Animals↗

Selenium and drug metabolism--I. Multiple modulations of mouse liver enzymes.

Male albino mice were raised on diets containing less than 10 ppb selenium (Se-) or supplemented with 0.5 ppm selenium (Se+) for 6 months. In the (Se-) group total liver selenium was less than 10% of the control, liver selenium-dependent glutathione peroxidase (GSH-Px) less than 2%. The specific activities of catalase and superoxide dismutase showed essentially no differences between the dietary groups. Several phase I-related specific enzyme activities were measured in liver microsomes. No significant differences between the two animal groups were found for cytochrome P-450 and b 5 content, NADH-cytochrome b 5 reductase, as well as for aniline hydroxylation and aminopyrine dealkylation rates. In (Se-) microsomes, NADPH-cytochrome P-450 reductase activity was about half that found in (Se+) microsomes. An increase in microsomes from (Se-) mice was found for 7-ethoxycoumarine deethylation rate (460%), cytochrome P-450 hydroperoxidase activity (170%), and heme oxygenase (276%). The N-oxidation rate of the flavin-containing monooxygenase decreased by 35%, the N-demethylation rate by 50% in (Se-) animals. Stopped-flow measurements of the reduction rates of microsomal pigments did not support evidence for limitations in microsomal electron supply during selenium deficiency. Among the phase II reactions examined, sulfotransferase activity towards 4-nitrophenol was 47% of the controls in Se-deficient liver cytosols while UDP-glucuronyl transferase activity towards this substrate increased to 215%. Glutathione-S-transferase activity was much higher in (Se-) livers than in (Se+): 310% with 1,2-dichloro-4-nitrobenzene, 255% with 1-chloro-2,4-dinitrobenzene and 120% with ethacrynic acid as substrate. The data indicate that in addition to GSH-Px many other enzyme activities in mouse liver are affected by prolonged dietary selenium deficiency. These effects might be useful in assessing the severity of selenium deficiency. A microsomal selenium-dependent metabolic modulator is discussed as a possible mechanism.

Cytochrome P-450 Enzyme System↗

The impact of selenium supplementation on mood.

The possibility that a subclinical deficiency of the trace element selenium might exist in a sample of the British population was examined by giving a selenium supplement for 5 weeks. Using a double-blind cross-over design, 50 subjects received either a placebo or 100 mcg selenium on a daily basis. On three occasions they filled in the Profile of Moods States. A food frequency questionnaire was used to estimate the intake of selenium in the diet. Intake was associated with a general elevation of mood and in particular, a decrease in anxiety. The change in mood when taking the active tablet was correlated with the level of selenium in the diet, which was estimated from a food frequency questionnaire. The lower the level of selenium in the diet the more reports of anxiety, depression, and tiredness, decreased following 5 weeks of selenium therapy. The results are discussed in terms of the low level of selenium in the food chain in some parts of the world.

Adolescent↗

Decreased glutathione peroxidase activity in mice in response to nafenopin is caused by changes in selenium metabolism.

The activity of selenium-dependent glutathione peroxidase is known to be reduced in the liver of both rats and mice after exposure to nafenopin, as well as other peroxisome proliferators. The mechanism for this down-regulation is not known, but might involve changes in incorporation of selenium into selenoproteins. In this paper we show that both incorporation of selenium into selenoproteins and the level of selenium in liver is reduced in mice treated with nafenopin. The activity of selenium dependent glutathione peroxidase (GPx), as well as incorporation of selenium into its 23 kD subunit were found to be decreased. Contrary to what might have been expected, the decreased GPx activity was detected concomitantly with a slight increase in mRNA levels after 10 days of treatment, while a small decrease in mRNA levels was detected in treated animals after 26 weeks, together with the decrease in GPx-activity. Incorporation of selenium into liver fatty acid binding protein (L-FABP) was also decreased, even though large increases in protein and mRNA levels were detected. Taken together these data suggest that the decrease in GPx-activity in response to nafenopin is due to post-transcriptional mechanisms, involving changes in selenium metabolism.

Animals↗

Congestive cardiomyopathy and the selenium content of serum.

A deficiency of selenium is suspected to be involved in the pathogenesis of congestive cardiomyopathy. Therefore the serum selenium content of 20 patients with proven congestive cardiomyopathy was measured and compared to that of a healthy control group. The serum selenium content of the patients with cardiomyopathy was found to be different from that of the healthy control group. The mean value of selenium in serum for the control group was 80.1 micrograms Se/1 (SD +/- 13.2) within a range of 53 and 117 micrograms Se/1. From the 20 patients with congestive cardiomyopathy six patients showed selenium concentrations in the normal value range of the control group; in the serum of 14 patients a distinct lower selenium content was found (mean value 47.8 micrograms Se/1 (SD +/- 16.2)) within a range of 23 and 70 micrograms Se/1. A positive correlation was found between serum selenium content and the left ventricular ejection fraction. Our results suggest that a deficiency of selenium may be present in a number of patients with congestive cardiomyopathy.

Adult↗

Decreased serum selenium in alcoholics--a consequence of liver dysfunction.

The serum concentration of selenium was decreased by 17 and 48% in non-cirrhotic and cirrhotic alcoholics, respectively, as compared to healthy controls. In these alcoholics the serum selenium correlated positively with the serum albumin and plasma prothrombin time and inversely with the serum bilirubin, alkaline phosphatase and gamma-glutamyl transpeptidase. Abstinence from ethanol for two weeks was without effect on the serum selenium level in non-cirrhotic alcoholics and acute alcohol intake did not change the serum selenium concentration in non-alcoholic volunteers. In patients with primary biliary cirrhosis the serum concentration of selenium was similar to that in the alcoholic cirrhotics. In patients with hypoalbuminaemia of renal origin the serum selenium was normal. In conclusion our results show that the deterioration of liver function, irrespective of its aetiology, leads to the decrease in serum selenium levels. Whether a defect in removal of lipoperoxides is associated with this decrease in serum selenium concentration remains to be decided by further studies.

Adult↗

Blood and liver selenium concentrations in patients with liver diseases.

To study the relation between blood and liver selenium levels in hepatic disorders we measured the selenium concentrations of whole blood, serum and liver tissue obtained at laparoscopy in 17 patients with different kinds of liver diseases. As compared to healthy controls the mean concentration of selenium was decreased by 24% (p less than 0.001) in the whole blood of the patients (n = 15). Similarly, the mean concentration of selenium in serum was 35% lower in the patients than in the controls (p less than 0.001). As compared to the control samples obtained at autopsy the selenium content of liver was decreased by 13% (p less than 0.05) in the patients. Significant positive correlations were found between the selenium content of the liver and the whole blood (r = 0.62, p less than 0.05) as well as also between liver and serum (r = 0.52, p less than 0.05) selenium concentrations. In conclusion, the present study suggests that in patients with liver disorders the selenium concentrations are decreased not only in the blood but also in the liver tissue. Whether this means a decreased activity of hepatic glutathione peroxidase and, further, an increased possibility of oxidative cell injury, remains open.

Adult↗

The nutritional selenium status of healthy Greeks.

The nutritional selenium status of apparently healthy Greeks has been assessed by measuring fluorimetrically the selenium content of whole blood, morning urine, hair and finger nails. The means and standard deviations were 165 +/- 33, 25 +/- 7 ng Se ml-1, 416 +/- 86, and 536 +/- 91 ng Se g-1, respectively. No significant difference was found between the selenium content of whole blood, hair and finger nails, but, for morning urine, there was a significant difference between males and females. The young and the elderly have less selenium in these biological materials than other Greeks. Whole blood selenium correlates significantly with morning urine, hair, and finger nail selenium, as does hair and nail selenium of male, female and male + female Greeks. The results are compared with those in the literature and possible explanations for the observations are presented. It is concluded that the selenium status of Greeks is satisfactory.

Adolescent↗