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PubMed2001

The protective role of selenium on genetic damage and on cancer.

Collectively, results from epidemiologic studies, laboratory bioassays, and human clinical intervention trials clearly support a protective role of selenium against cancer development. Several hypotheses have been proposed to explain these observations. Increased genomic instability, either inherent or induced by exogenous agents (mutagens or carcinogens), has been considered as a primary event leading to neoplastic transformation. This report deals specifically with the evidence for a role of selenium in the inhibition of carcinogen-induced covalent DNA adduct formation and retardation of oxidative damage to DNA, lipids and proteins, and for modulating cellular and molecular events that are critical in cell growth inhibition and in the multi-step carcinogenesis process. At present, the bulk of our knowledge on the role of selenium on genetic stability is based primarily on animal data and from studies conducted in in vitro systems. Studies performed in vitro showed that the dose and form of selenium compounds are critical factors with regard to cellular responses. Inorganic (at doses up to 10microM) and organic selenium compounds (at doses equal to or greater than 10microM) elicit distinctly different cellular responses. The recommended daily allowance (RDA) is 50-70 microgramSe per day for healthy adults; with 40 microgramSe as minimum requirement. Less than 11 microgramSe will definitely put people at risk of deficiency that would be expected to cause genetic damage. Daily doses of 100-200 microgramSe inhibited genetic damage and cancer development in humans. About 400 microgramSe per day is considered an upper limit. Clearly, doses above the RDA are needed to inhibit genetic damage and cancer. However, it has been hypothesized that the intake of excessive doses of selenium may cause oxidative damage, leading to genomic instability. The use of a cocktail consisting of selenium, and other vitamins and minerals appears to be a promising approach to inhibit genetic damage and the development of cancer. It is the author's recommendation that development of mechanism-based hypotheses that can be tested in pilot studies in different populations prior to a large-scale clinical trial in humans, is of paramount importance in order to better understand the role of selenium on genetic stability and cancer.

Animals↗
PubMed2001

Serum selenium concentration in a representative sample of the Canarian population.

The concentration of serum selenium in 395 individuals (187 males + 218 females) living in the Canary Islands, Spain was determined by hydride generation atomic absorption spectrometry. The mean selenium concentration was 74.7 +/- 25.2 microg/l ranging between 7.86 and 182.3 microg/l. Twenty-two adults (7.2% of the total) had serum selenium concentrations under 45 microg/l. It is widely accepted that below this selenium serum concentration (45 microg/l) there is an increased risk of cardiovascular disease and cancer. Our results fall within data recently published in other Spanish and European regions and are much lower than data observed in USA or seleniferous regions. The estimated Se intakes of our population were lower than the Recommended Dietary Allowances for American people. Individuals from Lanzarote had a mean Se concentration significantly higher than individuals from the other islands. This could be attributed to differences in Se content of soil and/or differences in dietary habits of the populations. Serum selenium concentration did not vary with the sex of the subjects. Individuals younger than 14 years old had a serum selenium concentration significantly lower than the rest of the individuals. No relationship with socio-economic status, educational level, smoking habits, physical exercise or beer consumption was found. However, individuals who consume wine more than three times a week showed higher selenium concentrations than individuals with lower consumption. Also, individuals with consumption above seven units of spirit drinks a week had the highest mean selenium concentration.

Adolescent↗
PubMed2002

Selenium concentrations in serum of individuals with liver diseases (cirrhosis or hepatitis): relationship with some nutritional and biochemical markers.

Serum concentrations were measured in individuals (n = 50) with liver diseases (cirrhosis and hepatitis) by hydride generation atomic absorption spectrometry in a cross-sectional study. Mean serum selenium levels determined in patients with cirrhosis (n = 12) or with hepatitis (n = 38) were significantly lower (P<0.01) than those measured in control groups mainly due to a decreased liver function. Mean serum selenium concentrations were significantly lower in cirrhotic individuals when compared with patients with hepatitis (P<0.05). Therefore, the severity of the live injury is a factor conditioning the impairment in the selenium body status observed in individuals with hepatopathies. In hepatic patients serum total cholesterol levels showed a significant correlation with serum selenium concentrations (r=0.912, P<0.05) demonstrating the important role of selenium as an antioxidant agent; similarly, gamma-glutamic-transferase levels were significantly correlated with the serum selenium levels (r=-0.803, P<0.05) indicating that when the intensity of the hepatic injury increases (enhancement in serum GGT levels) concomitantly the serum selenium levels decrease significantly. No significant relationships between serum selenium levels and sex or age of patients were observed.

Adult↗
PubMed2002

Selenium in soils, spermatophytes and bryophytes around a Zn-Pb smelter, New South Wales, Australia.

Selenium concentrations and its spatial distribution in soils, spermatophytes and bryophytes (mosses) around the Cockle Creek Zn-Pb smelter, New South Wales were studied from May to November 2000. Selenium was determined by ICP-MS on soils digested in nitric and hydrochloric acid (HNO3:HCl = 3:1), and plant samples digested in distilled concentrated nitric acid. At distances greater than 3 km, selenium in soils, spermatophytes and bryophytes converge to uniform values, which are considered to represent the background value. Mean selenium in soils around the smelter is two times higher than the background value. Mean concentration of selenium in plants around the smelter is three times greater than that for background plants. Selenium from 'in site' bryophyte is twice that found in the background bryophyte. The transfer coefficients of selenium between plants and soils are low, especially at a distance less than 1 km from the smelter. However, mosses show the reverse trend. This study indicates that the Zn-Pb smelter is one of the anthropogenic point sources of selenium pollution in the Lake Macquarie district.

Bryopsida↗
PubMed2002

Selenium toxicity: cause and effects in aquatic birds.

There are several manners in which selenium may express its toxicity: (1) an important mechanism appears to involve the formation of CH(3)Se(minus sign) which either enters a redox cycle and generates superoxide and oxidative stress, or forms free radicals that bind to and inhibit important enzymes and proteins. (2) Excess selenium as selenocysteine results in inhibition of selenium methylation metabolism. As a consequence, concentrations of hydrogen selenide, an intermediate metabolite, accumulate in animals and are hepatotoxic, possibly causing other selenium-related adverse effects. (3) It is also possible that the presence of excess selenium analogs of sulfur-containing enzymes and structural proteins play a role in avian teratogenesis. L-selenomethionine is the most likely major dietary form of selenium encountered by aquatic birds, with lesser amounts of L-selenocysteine ingested from aquatic animal foods. The literature is suggestive that L-selenomethionine is not any more toxic to adult birds than other animals. L-Selenomethionine accumulates in tissue protein of adult birds and in the protein of egg white as would be expected to occur in animals. There is no suggestion from the literature that the levels of L-selenomethionine that would be expected to accumulate in eggs in the absence of environmental concentration of selenium pose harm to the developing embryo. For several species of aquatic birds, levels of Se as selenomethionine in the egg above 3 ppm on a wet weight basis result in reduced hatchability and deformed embryos. The toxicity of L-selenomethionine injected directly into eggs is greater than that found from the entry of L-selenomethionine into the egg from the normal adult diet. This suggests that there is unusual if not abnormal metabolism of L-selenomethionine in the embryo not seen when L-selenomethionine is present in egg white protein where it likely serves as a source of selenium for glutathione peroxidase synthesis in the developing aquatic chick.

Animals↗
PubMed1996

Selenium deficiency and thyroid fibrosis. A key role for macrophages and transforming growth factor beta (TGF-beta).

Free radical damage and fibrosis caused by selenium deficiency are thought to be involved in the pathogenesis of myxoedematous cretinism. So far, no pathway explains the link between selenium deficiency and tissue fibrosis. Pharmacological doses of iodine induce necrosis in iodine-deficient thyroids. Necrosis is much increased if the glands are also selenium-deficient, which then evolve to fibrosis. This rat model was reproduced to explore the role of selenium deficiency in defective tissue repair. At first, proliferation indexes of epithelial cells and fibroblasts were comparable between selenium-deficient and control groups. Then, in selenium-deficient thyroids the inflammatory reaction was more marked being mainly composed of macrophages. The proliferation index of the epithelial cells decreased, while that of the fibroblasts increased. These thyroids evolved to fibrosis. TGF-beta immunostaining was prominent in the macrophages of selenium-deficient rats. Anti TGF-beta antibodies restored the proliferation indexes, and blocked the evolution to fibrosis. In selenium deficiency, an active fibrotic process occurs in the thyroid, in which the inflammatory reaction and an excess of TGF-beta play a key role.

Animals↗
PubMed2000

Selenium and cancer: some nutritional aspects.

The level of selenium in cancer patients is lower than that in control subjects. However, low selenium levels in body fluids can be due to the malnutrition observed in these patients. There is evidence from epidemiologic studies that high dietary selenium intakes and high selenium status in people are associated with lower cancer mortality. However, contradictory information has been found in some prospective studies. The presence of other nutrients in selenium-rich foods can influence the role of the selenium in cancer etiology. Therefore, there are selenium antagonistic elements that inhibit the anticarcinogenic effects of selenium and other antioxidant micronutrients such as ascorbic acid, retinol, beta-carotene, alpha-tocopherol, and some other elements have a synergistic effect on the prevention of cancer.

Animals↗
PubMed1996

An evaluation of urinary measures of iodine and selenium status.

The aim of this study was to establish methodology for a survey of the iodine and selenium status of New Zealand residents, more specifically to investigate the correlation between fasting or random casual urine samples and 24 hour urines for iodine and selenium excretion. Sixty-two (31 M, 31 F) adults collected casual, fasting and 24 hour urine samples for analysis of iodide, selenium and creatinine. Plasma and serum samples were collected for analysis of selenium and glutathione peroxidase activity. Results indicated that fasting urine samples, but not casual urines, may give a reasonable estimate of urinary output of iodine and selenium on a population basis, but that 24 hour urines are necessary for diagnosis of iodine deficiency in an individual and for research purposes. The results for iodine also give no support for expressing iodine as the iodide-creatinine ratio, although there was some indication that the selenium-creatinine ratio might be useful. Significant correlations between total daily excretion of selenium and iodine and also for urinary concentrations of the two trace elements in fasting and in 24 hour urine specimens may reflect a relationship of selenium and iodine to body size which may have implications for dietary requirements of these trace elements. Alternatively the correlations may reflect a relationship between dietary intake of the two trace elements in a country in which food concentrations are low, and this needs further investigation.

Adolescent↗
PubMed1997

Maternal selenium status influences the concentration and binding pattern of zinc in human milk.

To study the health effects of high dietary maternal selenium intake breast milk, blood and toe-nails were collected from 143 women (20-24 days of lactation) living in Venezuelan states of Yaracuy and Portuguesa. Depending on the regional selenium intake level three regions were defined within the total range of 90-980 microgram per day. The samples were analyzed by means of INAA for the determination of trace elements, including selenium and zinc. The significant inverse correlation between Se and Zn in breast milk found in former studies was confirmed. Investigation of the Zn-binding pattern in milk whey was carried out by an on-line combination HPLC (SEC) for protein separation and ICP-AES for element detection. Six Zn-binding compounds including citrate were detected. A highly significant negative correlation was found between the citrate, which is the main low-molecular Zn-binding compound, and the maternal daily selenium intake. We determined that the decrease in zinc concentration is due to a decrease in the citrate level, which depends on the selenium concentration in breast milk. The selenium concentration in breast milk is, in turn, proportional to the dietary intake. In addition, significant changes in the UV- and Zn-profiles were observed in the milk whey with the highest selenium content, indicating that above a certain maternal intake level substantial changes in the composition of mammary secretory cells occur. This effect can be of interest for estimation of the safe dietary intake level of selenium.

Adult↗
PubMed2006

Use of selenium in chemoprevention of bladder cancer.

The anticarcinogenic potential of selenium was first identified nearly 40 years ago in geographical studies that reported lower death rates for cancer in regions with high levels of selenium. Cancer of the bladder was one of the body sites found to share this inverse association. Although many subsequent studies have been done on selenium and cancer, only a few have specifically assessed the relation with bladder cancer. However, the high recurrence rate and ability to monitor bladder urothelial-cell carcinoma make selenium a good candidate for chemoprevention. Evidence suggests that selenium is a biologically plausible, safe, and efficacious potential chemoprevention agent for bladder cancer. Large tertiary chemoprevention trials are needed to further investigate the role of selenium in the prevention of bladder cancer. Future studies should assess the best dose and form of selenium, and whether the protective effect of selenium differs between the sexes.

Antioxidants↗
PubMed1998

Selenium and liver cirrhosis.

Effects of selenium deficiency, induced by thioacetamide, were investigated in rats. Thioacetamide (0.3 g/L) given in drinking water, as expected, caused a significant loss of selenium from the liver. It was accompanied by liver cirrhosis and a significant increase in the liver weight as well as liver to body weight ratio. A significant loss of selenium from spleen was also accompanied by an increase in its weight. Weights of lungs, testis and kidney, however, were not affected by thioacetamide and there was no change in their selenium content. Plasma levels of selenium were significantly reduced in the thioacetamide treated group. All these changes were confirmed to be due to selenium deficiency caused by thioacetamide, as supplementation with selenium reversed these changes. The mode of action of selenium is unknown but may involve anti-oxidant defense mechanisms.

Animals↗
PubMed2002

Serum selenium and the risk of cervical cancer among women in the United States.

OBJECTIVE: To explore the relationship between serum selenium and cervical cancer. METHODS: We conducted a case-control study of cervical cancer in five areas around Birmingham, AL; Chicago, IL; Denver, CO; Miami, FL; and Philadelphia, PA. Community controls were selected by random-digit dialing and were matched to invasive cervical cancer cases by age, race/ethnicity, and telephone exchange. Serum selenium was determined by neutron activation analysis. Logistic regression analysis controlling for known risk factors of cervical cancer, including human papillomavirus (HPV) type-16 measured serologically, was performed on 227 invasive cases, 127 in-situ cases, and 526 controls. RESULTS: Values of serum selenium ranged from 67.5 to 185.0 ng/ml. Adjusted odds ratios for invasive cervical cancer by quintile were: 1.0 (highest selenium), 1.1, 1.0, 0.8, and 1.0 (lowest selenium), p for trend = 0.82. Similar patterns were observed for Stage I invasive, and Stages II-IV invasive cases, suggesting severity of disease did not influence the null results. Although no associations were seen among current or never smokers, a protective effect of selenium was suggested among former smokers. Effect modification was not evident for other variables examined. CONCLUSIONS: This study does not support a relationship between serum selenium and invasive cervical cancer at typical serum selenium levels in the US.

Adult↗
PubMed2003

Selenium serum concentrations in malnourished Ecuadorian children: a case-control study.

Little is known about the selenium status of children living in the Andean regions of South America, which commonly have volcanic soil with low selenium content. Human selenium deficiency has been hypothesized to have a negative impact on immune function and to increase the risk of infection. The objective of this study was to evaluate the serum selenium concentrations of severely malnourished children living in urban and rural Andean Ecuador, and to compare them to a control group of normally nourished children from the same communities. Forty-three children, aged six to 36 months, with marasmus or kwashiorkor and 30 control children were enrolled from July to November 1993 in Quito, Ecuador. Serum selenium concentrations were lower in the children with marasmus (0.91 +/- 0.28 microM/L, n = 21) and kwashiorkor (0.37 +/- 0.15 microM/L, n = 22) than in those who were normally nourished (1.77 +/- 0.75 microM/L, n = 30, p < 0.001 for each difference). The serum selenium concentrations in children with kwashiorkor were significantly lower than those in children with marasmus (p < 0.001). All 22 of the children with kwashiorkor, 15 of the 21 children with marasmus, and five of the 30 normal children had serum levels < 1.08 microM/L (8.5 micrograms/dL) (chi 2 = 38.4, p < 0.00000001). In the Andean regions of Ecuador, selenium deficiency is prevalent in children with protein and caloric deficiency. Furthermore, 17% of Ecuadorian children with normal weight-for age-Z score are selenium-deficient.

Case-Control Studies↗
PubMed2001

Centrilobular endothelial cell injury by diquat in the selenium-deficient rat liver.

Low doses of diquat cause massive liver necrosis and death of selenium-deficient rats within a few hours. Protection against this injury by selenium correlates with the presence of selenoprotein P, an extracellular selenoprotein that associates with endothelial cells. Selenium-deficient rats were injected with diquat (10 mg/kg) and their livers were removed for light and electron microscopy at times up to 120 minutes after injection. Selenium-replete animals were studied before and 120 minutes after the same dose of diquat. With selenium deficiency, diquat caused injury to centrilobular endothelial cells. This injury was evident 20 minutes after diquat injection and progressed to cell loss at 60 minutes after diquat injection. At 120 minutes, endothelial cells were virtually absent from the centrilobular regions and hepatocytes in those areas were undergoing necrosis. Portal and midzonal areas remained normal in selenium-deficient livers, as did the entire liver lobule of selenium-replete rats. These findings indicate that the initial liver lesion in selenium-deficient rats given diquat is injury of the endothelial cells in the centrilobular region. After detachment of the endothelial cells, centrilobular hepatocytes undergo necrosis. We postulate that selenoprotein P protects the centrilobular endothelial cells against injury by oxidant molecules that result from diquat administration.

Animals↗
PubMed2006

Relationship between plasma selenium concentrations and lower genital tract levels of HIV-1 RNA and interleukin type 1beta.

OBJECTIVE: To examine the relationship between selenium nutritional status and intermediates of human immunodeficiency virus (HIV)-1 transmission. DESIGN: Prospective cohort study. SETTING: A study clinic at Muhimbili National Hospital, Dar es Salaam, Tanzania. SUBJECTS: A total of 340 HIV-1-infected pregnant women with gestational ages 12-27 weeks. METHODS: Women's plasma selenium concentrations were determined at enrollment and modeled as tertiles (tertile 1: <114 microg/l (reference); tertile 2: 114-131 microg/l; tertile 3: >131 microg/l). Cervicovaginal lavage specimens were obtained at 36 weeks of gestation to determine HIV-1 RNA and interleukin-1beta (IL-1beta) levels. In subgroup analyses, 123 women with genital tract infections at enrollment were excluded. RESULTS: Plasma selenium concentrations >or=114 microg/l were related to increased risk of lower-genital shedding of HIV-1 RNA. Excluding women with genital tract infections strengthened the associations (relative risk (RR) tertile 2: 1.46, 95% confidence interval (CI)=1.10, 1.92; RR tertile 3: 1.39, 95% CI=1.05, 1.84). There was evidence for an association between plasma selenium concentrations >or=114 microg/l and increased HIV-1 RNA levels among the entire cohort and after excluding women with genital tract infections. There was no association between plasma selenium and IL-1beta concentrations. CONCLUSIONS: High selenium status may lead to increased risk of genital HIV-1 shedding, but data from other studies indicate that the evidence is mixed. Results from ongoing selenium trials are awaited to clarify the impact of selenium on HIV-1-related transmission endpoints. SPONSORSHIP: National Institute of Child Health and Human Development (NICHD R01 32257) and the Fogarty International Center (NIH D43 TW00004).

Adult↗
PubMed2004

Growth inhibition and induction of apoptosis in mesothelioma cells by selenium and dependence on selenoprotein SEP15 genotype.

Malignant mesotheliomas (MMs) are aggressive tumors derived from mesothelial cells lining the lungs, pericardium and peritoneum, and are often associated with occupational asbestos exposure. Suppression subtractive hybridization was used to identify genes differentially expressed in MM cells compared to normal mesothelial cells. A gene, SEP15, encoding a 15-kDa selenium-containing protein was isolated using this approach and was subsequently shown to be downregulated in approximately 60% of MM cell lines and tumor specimens. A SEP15 polymorphic variant, 1125A, resides in the SECIS recognition element in the 3'-UTR and may influence the efficiency of Sec incorporation into the protein during translation. Since previous studies have implicated a potential role of the trace element selenium as a chemopreventive agent in animal models and in several types of human cancer, we investigated the effect of selenium on MM cells and its dependence on SEP15 genotype. Selenium was shown to inhibit cell growth and induce apoptosis in a dose-dependent manner in MM cells but had minimal effect on normal mesothelial cells. However, MM cells with downregulated SEP15 or the 1125A variant were somewhat less responsive to the growth inhibitory and apoptotic effects of selenium than MM cells expressing wild-type protein. RNAi-based knockdown studies demonstrated that SEP15 inhibition makes sensitive MM cells more resistant to selenium. These data imply that selenium may be useful as a chemopreventive agent in individuals at high risk of MM due to asbestos exposure, although those with the 1125A polymorphism may be less responsive to the protective benefits of dietary selenium supplementation.

Apoptosis↗
PubMed1987

Effect of vitamin E- and selenium-deficiency on rat liver chemiluminescence.

The role of vitamin E and selenium as protective agents against oxidative stress was evaluated by measuring liver chemiluminescence in situ. Weanling rats fed a vitamin E- and selenium-deficient diet showed liver chemiluminescence that was increased 60 and 100% over control values at 16 and 18 days respectively after weaning. At day 21, the double deficiency led to hepatic necrosis, as observed by optical and electron microscopy, and increased serum levels of lactate dehydrogenase and alanine aminotransferase. Single deficiencies, in either vitamin E or selenium, did not produce liver necrosis but increased liver chemiluminescence. Vitamin E deficiency led to a 23 and 50% increase in liver emission at days 18 and 20 respectively; selenium deficiency produced a 64% increase at day 16. The activity of liver selenium-glutathione peroxidase diminished to 13% of the control value in the rats fed doubly deficient and selenium-deficient diets. Activities of superoxide dismutase, catalase and non-selenium-glutathione peroxidase were not modified by the different diets. These results suggest that oxy-radical generation may play a major role in hepatic necrosis in vitamin E- and selenium-deficiency.

Animals↗
PubMed2003

Protective effects of the antioxidant selenium on quinolinic acid-induced neurotoxicity in rats: in vitro and in vivo studies.

Quinolinic acid (QUIN), a well known excitotoxin that produces a pharmacological model of Huntington's disease in rats and primates, has been shown to evoke degenerative events in nerve tissue via NMDA receptor (NMDAr) overactivation and oxidative stress. In this study, the antioxidant selenium (as sodium selenite) was tested against different markers of QUIN-induced neurotoxicity under both in vitro and in vivo conditions. In the in vitro experiments, a concentration-dependent effect of selenium was evaluated on the regional peroxidative action of QUIN as an index of oxidative toxicity in rat brain synaptosomes. In the in vivo experiments, selenium (0.625 mg per kg per day, i.p.) was administered to rats for 5 days, and 2 h later animals received a single unilateral striatal injection of QUIN (240 nmol/ micro L). Rats were killed 2 h after the induction of lesions with QUIN to measure lipid peroxidation and glutathione peroxidase (GPx) activity in striatal tissue. In other groups, the rotation behavior, GABA content, morphologic alterations, and the corresponding ratio of neuronal damage were all evaluated as additional markers of QUIN-induced striatal toxicity 7 days after the intrastriatal injection of QUIN. Selenium decreased the peroxidative action of QUIN in synaptosomes both from whole rat brain and from the striatum and hippocampus, but not in the cortex. A protective concentration-dependent effect of selenium was observed in QUIN-exposed synaptosomes from whole brain and hippocampus. Selenium pre-treatment decreased the in vivo lipid peroxidation and increased the GPx activity in QUIN-treated rats. Selenium also significantly attenuated the QUIN-induced circling behavior, the striatal GABA depletion, the ratio of neuronal damage, and partially prevented the morphologic alterations in rats. These data suggest that major features of QUIN-induced neurotoxicity are partially mediated by free radical formation and oxidative stress, and that selenium partially protects against QUIN toxicity.

Animals↗