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PubMed2006

Whole blood mercury and selenium concentrations in a selected Austrian population: does gender matter?

BACKGROUND: Data on mercury exposure of the Austrian population were inadequate. This study was performed to determine the causal factors underlying mercury exposure and selenium concentrations, and to estimate the gender-related health impacts. METHODOLOGY: Venous blood samples of 78 women and 81 men were drawn at the Austrian Red Cross, Vienna. Mercury contents in acid-digested whole blood samples were measured after amalgam enrichment by CV-AAS, and selenium by AAS (heated quartz-cell) after hydrid formation. RESULTS: The average total mercury blood content of Austrians was low (2.38+/-1.55 microgL(-1); N=152). Mercury and selenium concentrations were not different between the genders (P>0.05) but we observed discrepancies regarding the causal factors. Mercury levels in men were influenced not only by fish consumption but also by age, education level, and amalgam fillings, whereas in women, only the diet (fish/seafood, red wine consumption) determined blood mercury (P<0.05). Moreover, only the males indicated a depressive effect of dental amalgam on hematocrit (P<0.05). Regarding selenium, age and alcohol consumption led to lower concentrations in men, whereas a high-level education had the opposite effect; no determinant was found for women. For the whole study group, a significant effect of chronic disease on selenium levels could be detected (P<0.05). 18% of women and 13% of men showed marginal selenium deficiency (blood selenium<65 microgL(-1)). Selenium and mercury concentrations were not correlated. CONCLUSIONS: Our results indicate the need to evaluate and integrate gender-related findings in metal toxicology and trace element research, because different causal factors require different preventive measures to reduce mercury exposure and the risk of low selenium concentrations. Future research is needed on the gender- and age-related differences in fish/seafood consumption habits, the modifications of mercury toxicokinetics through sex hormones, the selenium supply in Austria, and the clinical relevance of a low selenium status.

Adolescent↗
PubMed1998

Role of glutathione and methylation in the biliary excretion of selenium. The paradoxical effect of sulfobromophthalein.

Biotransformation of selenite involves both reactions with GSH and methylations. Therefore, the role of GSH, methylation, and the hepatobiliary GSH transporter was investigated in the biliary excretion of selenium in rats injected with sodium [75Se]selenite (1-10 micromol/kg, i.v.). Biliary output of selenium exhibited an apparent capacity limitation with an approximately 3 nmol/kg x min maximal rate and a dose-related decline in the fractional excretion. HPLC analysis of bile indicated absence of selenite and presence of selenodiglutathione (GS-Se-SG) and/or its hydrolysis products as the major biliary selenite metabolites. Depletion of hepatic glutathione by D,L-buthionine-[S,R]-sulfoximine or diethyl maleate decreased selenium excretion into bile by 60 and 80%, respectively. In contrast, inhibitors of methylation, i.e. periodate-oxidised adenosine or ethionine doubled the rate of biliary selenium excretion. While indocyanine green--an inhibitor of hepatobiliary GSH transport--failed to influence biliary selenium output, sulfobromophthalein (BSP)--another inhibitor of this sort--dramatically enhanced it. This effect was found to be a function of the dose of both selenite and BSP. The degree of BSP-induced enhancement of the selenium excretion rate gradually increased with elevation of the selenite dose, approaching 20-fold at 10 micromol/kg selenite. In contrast, the stimulatory effect of BSP on biliary selenium output was maximal at 50-100 micromol/kg and gradually lessened with elevation of the BSP dose above 100 micromol/kg. In summary, this study revealed that the biliary excretion of selenium depended on availability of hepatic GSH, probably for formation of GS-Se-SG, the putative cholephilic selenite metabolite. Methylation counteracted selenium excretion into bile and thus may contribute to the apparent capacity limitation of biliary selenium excretion. Finally, selenium output into bile was insensitive to inhibitors of the hepatobiliary GSH transporter, and was enhanced, paradoxically, by BSP several-fold. The mechanism of this unexpected effect is explored in the adjoining article.

Animals↗
PubMed2003

Sex, age, geographical location, smoking, and alcohol consumption influence serum selenium concentrations in the USA: third National Health and Nutrition Examination Survey, 1988-1994.

Selenium has been reported to reduce the risk for heart diseases and cancer. We examined the association of sex, age, geographical location, serum cotinine concentrations, a measure of smoking intensity, and alcohol consumption with serum selenium concentrations in the third National Health and Nutrition Examination Survey (NHANES III), 1988-1994. Study sample consisted of 14,619 apparently healthy individuals (male: 7,102; female: 7,517) aged 14 to >90 years. Sex, age, geographical location, serum cotinine concentrations, and alcohol consumption significantly influenced serum selenium concentrations (P < 0.05). The mean (+/- standard error) serum selenium concentration in men (124.5 +/- 0.20 ng/mL) was significantly higher than in women (122.0 +/- 0.20 ng/mL) (P < 0.0001). Men in the 31-50 y age group had the highest mean serum selenium concentration. In the same age group, women had the lowest mean serum selenium concentration. In both sexes, participants living in the Midwest and West had significantly higher serum selenium concentrations than those living in South and Northeast geographical locations. Serum cotinine was negatively associated with serum selenium concentrations in both men (beta = -0.0108; P < 0.0001 for trend) and women (beta = -0.0097; P < 0.0001 for trend). Alcohol consumption is positively associated with serum selenium in women (beta = 0.0462; P = 0.0044 for trend) but not in men (beta = 0.0015; P = 0.8496 for trend). Although, sex, age, geographical location, smoking, and alcohol intake influenced serum selenium concentrations, clinically low serum selenium concentrations are not common in the USA.

Adolescent↗
PubMed2004

Selenium content of Spanish infant formulae and human milk: influence of protein matrix, interactions with other trace elements and estimation of dietary intake by infants.

The selenium content of infant formulae varies as a result of differences in the amount of intrinsic selenium compounds. Manufacturers have been gradually changing the protein profile of infant formulae to reflect human milk contents more closely. Because of these variations in infant formula composition and their potential impact on selenium content, this trace element was analysed with regard to the different protein sources. The aims of this study were to determine the selenium content in infant formulae sold commercially in Spain, to estimate a daily dietary intake for infants fed on formulae and to compare with the selenium provided by Spanish breast milk samples used as a reference. We have also identified certain trace elements added to formulae which interact with selenium according to the type and protein matrix of the infant formulae. Selenium concentration was determined by inductively coupled plasma atomic emission spectrometry (ICP-AES) with a hydride generator. The selenium concentrations in human milk and infant formulae determined in this study are similar to those found by other researchers in different countries. The daily selenium intake from the formulae studied was estimated according to the recommended doses from the manufacturers. The theoretical selenium intake of nursed infants has been studied in relation to the Recommended Dietary Allowance (RDA: 10 microg Se/day) and the specific recommendations for infant formula nutrient contents (10-35 microg Se/L) set by the Expert Panel of life Sciences Research Office (LSRO) of the American Society for Nutritional Sciences. According to our results, on an overall view, infants fed on the studied infant formulae have an intake between basal and normative requirements. This might be considered as providing an adequate selenium supply. However, the intake of setenium provided by several formulae included in this research did not reach the RDA for the first month of neonate life.

Animals↗
PubMed1995

The necessity of selenium substitution in total parenteral nutrition and artificial alimentation.

For the trace element selenium, in contrast to zinc, iron, copper, chromium, manganese and iodine, there is still no clear official recommendation with regard to routine substitution in artificial nutrition. An overview of the manifestations of selenium deficiency in humans during the period 1979-1995 shows that nutritive deficiencies are exclusively TPN-induced or the result of severe malnutrition. The pathology of TPN-induced selenium deficiency and the analytic assessment of selenium status are described. Patients undergoing long-term parenteral nutrition or suffering from an increased loss of intestinal secretions have to be characterized as being especially at risk for clinical selenium deficiency. The relationship of the serum selenium kinetics in pediatric and adult patients to the depletion of body compartments during the course of short-term and prolonged TPN is discussed. Because of the importance of the selenoproteins, the regularly occurring depletion during selenium-free TPN and the borderline supply of selenium in Germany the routine substitution of selenium in TPN is strongly recommended. The pharmaceutical industry should be encouraged to develop a trace element solution that includes selenium, so that the nutritive requirement of patients on TPN can be satisfied. Adequate intravenous dosage recommendations are based on maintenance of glutathione peroxidase homeostasis. The routine supplementation dosage may not meet the selenium requirements of intensive care patients under conditions of increased metabolic demands on their anti-oxidative system.

Enteral Nutrition↗
PubMed2004

Selenium biotransformations in an insect ecosystem: effects of insects on phytoremediation.

Phytoremediation of selenium-contaminated soils may be influenced by higher trophic levels including insects. We examined how selenium affects the behavior, survival, and development of the wasp parasitoid Cotesia marginiventris, parasitizing its natural host, the beet armyworm Spodoptera exigua, feeding on alfalfa, Medicago sativa, irrigated with water containing selenate. X-ray absorption spectroscopy was used to quantify the selenium chemical forms in each trophic level. Alfalfa partially transformed selenate to organoselenium. S. exigua contained only organoselenium, both directly absorbed from M. sativa and transformed from selenate. C. marginiventris cocoons collected shortly after larval emergence contained only organoselenium derived from the host. The surprising finding of trimethylselenonium-like species in adult parasitoids and the cocoons from which they emerged suggests that adults and pharates can detoxify excess selenium through methylation and volatilization. Adult parasitoids do not discriminate against selenium-containing alfalfa, even though alfalfa generates selenium volatiles. Parasitoids raised on selenium-fed larvae emerged later and pupae weighed less than their selenium-free counterparts. We conclude therefore that C. marginiventris can be used to control S. exigua damage to M. sativa being used to remove selenium from soils. Moreover, the presence of such insects may improve phytoremediation by increasing biotransformation of inorganic selenium and release of volatile selenium species.

Animals↗
PubMed2000

Toenail selenium and breast cancer-a case-control study in Finland.

OBJECTIVE: Low levels of selenium have been associated with a higher risk of cardiovascular diseases and cancer in humans. Since 1984, selenium supplementation through fertilizers has been employed in Finland to increase the very low concentration of selenium in the nation's food supply. As a result, the selenium concentration of Finnish foods became one of the highest in Europe. A decade after selenium supplementation began, the association between toenail selenium and the risk of breast cancer was examined. DESIGN: Case-control study. SETTING: Eastern Finland. SUBJECTS: 289 pre- and postmenopausal breast cancer cases and 433 community controls. The diagnosis was unknown at the time the toenail samples were collected. RESULTS: The mean toenail selenium concentration was 0.80 mg/kg in premenopausal cases and 0.84 mg/kg in premenopausal controls: and 0. 77 mg/kg in postmenopausal cases and 0.80 mg/kg in postmenopausal controls. The odds ratio (OR) comparing the highest with the lowest quintiles of toenail selenium concentration was 1.1 (95% CI 0.4-3.2) in premenopausal women and 0.7 (95% CI 0.3-1.5) in postmenopausal women. The intake of retinol, beta-carotene, vitamin E and vitamin C did not change the association between toenail selenium and breast cancer. CONCLUSIONS: A decade after selenium supplementation, selenium seems not to be an important factor in the etiology of breast cancer, neither in premenopausal nor postmenopausal women. SPONSORSHIP: This work was supported by the EVO funds from the Kuopio University Hospital and by research grants from the Academy of Finland, Yrjö Jahnsson Foundation and Juho Vainio Foundation. European Journal of Clinical Nutrition (2000) 54, 98-103

Adult↗
PubMed1999

Parenteral selenium supplementation in extremely low birth weight infants: inadequate dosage but no correlation with hypothyroidism.

OBJECTIVE: Selenium is an essential trace element, known to be important in thyroid metabolism. We speculated that parenteral selenium supplementation is inadequate in preterm infants and may contribute to the development of hypothyroidism. STUDY DESIGN: Serum selenium and thyroid function were evaluated on day 10 of life in extremely low birth weight infants. Selenium intake provided by parenteral nutrition was prospectively evaluated. RESULTS: Selenium intake was close to the recommended 2 micrograms/kg per day. Serum selenium values were 0.54 +/- 0.13 microM (mean +/- SD, n = 29). Selenium serum levels were low in 26 of 29 infants. In infants with subnormal serum selenium levels, free T4 was transiently low in 10 of 26 infants but was normal in 16 of 26 infants. No significant correlation was found between serum selenium levels and hypothyroidism. CONCLUSION: Current selenium supplementation guidelines may be inadequate in extremely low birth weight infants. However, selenium deficiency does not seem to play a major role in neonatal hypothyroidism.

Birth Weight↗
PubMed1989

Inhibition of type I and type II iodothyronine deiodinase activity in rat liver, kidney and brain produced by selenium deficiency.

Selenium deficiency for periods of 5 or 6 weeks in rats produced an inhibition of tri-iodothyronine (T3) production from added thyroxine (T4) in brain, liver and kidney homogenate. This inhibition was reflected in plasma T4 and T3 concentrations, which were respectively increased and decreased in selenium-deficient animals. Although plasma T4 levels increased in selenium-deficient animals, this did not produce the normal feedback inhibition on thyrotropin release from the pituitary. Selenium deficiency was confirmed in the animals by decreased selenium-dependent glutathione peroxidase (Se-GSH-Px) activity in all of these tissues. Administration of selenium, as a single intraperitoneal injection of 200 micrograms of selenium (as Na2SeO3)/kg body weight completely reversed the effects of selenium deficiency on thyroid-hormone metabolism and partly restored the activity of Se-GSH-Px. Selenium administration at 10 micrograms/kg body weight had no significant effect on thyroid-hormone metabolism or on Se-GSH-Px activity in any of the tissues studied. The characteristic changes in plasma thyroid-hormone levels that occurred in selenium deficiency appeared not to be due to non-specific stress factors, since food restriction to 75% of normal intake or vitamin E deficiency produced no significant changes in plasma T4 or T3 concentration. These data are consistent with the view that the Type I and Type II iodothyronine deiodinase enzymes are seleno-enzymes or require selenium-containing cofactors for activity.

Animals↗
PubMed1998

Effects of selenium deficiency on diaphragmatic function after resistive loading.

Diaphragmatic fatigue has been associated with increased production of reactive oxygen species. Among the defenses against reactive oxygen species is the glutathione redox system. The selenium-dependent enzyme glutathione peroxidase is an important component of this system. Thus, we hypothesized that selenium deficiency would lower glutathione peroxidase activity and render the diaphragm more susceptible to a mild exertional protocol. Sprague-Dawley rats were fed a selenium-deficient or control diet for 12 weeks then divided into four experimental groups: (1) unloaded, basic diet with selenium supplementation (control); (2) unloaded, selenium-deficient diet; (3) loaded, basic diet with selenium supplementation; and (4) loaded, selenium-deficient diet. Diaphragmatic in vitro contractile properties, glutathione peroxidase activity and glutathione content were measured. During inspiratory resistive loading, the animals breathed against an inspiratory resistor at 70% of maximal airway pressure until the target pressure was not achieved for five consecutive breaths. Selenium deficiency resulted in a significant decrease in diaphragmatic glutathione peroxidase activity, without changes in total glutathione content. Neither selenium deficiency nor inspiratory resistive loading alone impaired diaphragmatic contractility. Selenium deficiency in conjunction with inspiratory resistive loading resulted in a significant decrease in diaphragmatic twitch and tetanic force, with a downward shift in the force/frequency curve. These data suggest that selenium deficiency lowers diaphragmatic glutathione peroxidase activity, and when these animals are subjected to the oxidative stress of resistive loading, there is an impairment in muscle function. We conclude that a functional glutathione peroxidase is necessary to protect the diaphragm against the effects of resistive loading.

Animals↗
PubMed2003

Cell death caused by selenium deficiency and protective effect of antioxidants.

Selenium is an essential trace element and it is well known that selenium is necessary for cell culture. However, the mechanism underlying the role of selenium in cellular proliferation and survival is still unknown. The present study using Jurkat cells showed that selenium deficiency in a serum-free medium decreased the selenium-dependent enzyme activity (glutathione peroxidases and thioredoxin reductase) within cells and cell viability. To understand the mechanism of this effect of selenium, we examined the effect of other antioxidants, which act by different mechanisms. Vitamin E, a lipid-soluble radical-scavenging antioxidant, completely blocked selenium deficiency-induced cell death, although alpha-tocopherol (biologically the most active form of vitamin E) could not preserve selenium-dependent enzyme activity. Other antioxidants, such as different isoforms and derivatives of vitamin E, BO-653 and deferoxamine mesylate, also exerted an inhibitory effect. However, the water-soluble antioxidants, such as ascorbic acid, N-acetyl cysteine, and glutathione, displayed no such effect. Dichlorodihydrofluorescein (DCF) assay revealed that cellular reactive oxygen species (ROS) increased before cell death, and sodium selenite and alpha-tocopherol inhibited ROS increase in a dose-dependent manner. The generation of lipid hydroperoxides was observed by fluorescence probe diphenyl-1-pyrenylphosphine (DPPP) and HPLC chemiluminescence only in selenium-deficient cells. These results suggest that the ROS, especially lipid hydroperoxides, are involved in the cell death caused by selenium deficiency and that selenium and vitamin E cooperate in the defense against oxidative stress upon cells by detoxifying and inhibiting the formation of lipid hydroperoxides.

Antioxidants↗
PubMedDate not supplied

Tissue level, distribution, and total body selenium content in healthy and diseased humans in Poland.

The authors obtained tissue samples taken at autopsy from 46 healthy individuals killed in accidents and from 75 corpses of victims of various diseases to analyze selenium levels. The per-weight-unit basis of selenium levels (all expressed as ng/gm wet tissue) in tissues decreased in the following order: kidney (469) > liver > spleen > pancreas > heart > brain > lung > bone > skeletal muscle (51). The highest proportion of body selenium was found in skeletal muscles (27.5%); much less selenium was found in bones (16%) and blood (10%). In the tissues of cancer corpses, the selenium levels were much lower than levels in controls. The lowest selenium levels were found in the livers of alcoholics. Tissue selenium levels found in the study were significantly lower than levels reported in Japan, United States, Canada, and other countries. The low selenium levels in the tissues of Polish residents result from inadequate selenium levels in the soil. The authors used selenium levels in tissues to calculate the amount of selenium in humans in Poland (i.e., approximately 5.2 mg). This level was similar to levels found in New Zealand (i.e., 3.0-6.1 mg), but it was lower than the mean level found in Germany (i.e., 6.6 mg) and in the United States (i.e., 13.0-20.3 mg).

Accidents↗
PubMed2005

Total selenium concentrations in canine and feline foods commercially available in New Zealand.

AIMS: To determine the total selenium concentrations in petfoods commercially available in New Zealand and to establish whether these meet the current minimum recommended requirements of selenium in foods for cats and dogs. METHODS: Samples (n=89) from petfoods commercially available in New Zealand were analysed for total selenium concentration using a fluorometric method. Data, expressed on a dry matter (DM) basis, were analysed according to petfood type (dog or cat, and wet or dry), predominant flavour (chicken, seafood, chicken and seafood, beef, meat mix, other), manufacturer and country of manufacture. RESULTS: Fifty percent of petfoods purchased for this study were manufactured in Australia, and the remainder were produced in the United States of America (USA), New Zealand or Thailand. Mean total selenium concentrations were similar (0.61-0.80 mg/kg DM) in petfoods produced in Australia, New Zealand and the USA, but higher (mean 3.77 mg/kg DM; p<0.05) in petfoods produced in Thailand. Petfoods produced in Australia, New Zealand and the USA contained a variety of predominant flavours, whereas petfoods from Thailand contained only seafood flavour. Seafood-based flavours had the highest selenium concentrations in both cat and dog foods. Wet and dry dog foods had similar concentrations of selenium to dry cat foods, but wet cat foods had higher and more variable concentrations of selenium than these others (p<0.05). The mean selenium concentrations in cat and dog foods were 1.14 and 0.40 mg/kg DM, respectively, and there were no significant differences between manufacturers. CONCLUSIONS: Selenium concentrations in commercial petfoods sold in New Zealand appeared to meet recommended dietary requirements, although the range of concentrations was highly variable. Whether these recommendations are adequate for the maintenance of optimal health in cats and dogs has yet to be determined. CLINICAL RELEVANCE: Overt selenium deficiency disorders are unlikely in dogs and cats in New Zealand fed commercial petfoods unless the bioavailability of selenium in particular petfoods is low.

Animal Feed↗
PubMed1990

Effect of dietary selenium on the induction of altered hepatic foci and hepatic tumors by the peroxisome proliferator ciprofibrate.

The purpose of this study was to determine if the dietary antioxidant selenium could inhibit hepatocarcinogenesis induced by peroxisome proliferators, which are hypothesized to induce tumors by increased production of hydrogen peroxide or other reactive oxygen species. Rats were fed diets containing the peroxisome proliferator ciprofibrate and one of three concentrations (0.04, 0.2, or 1.0 ppm) of selenium for 6 or 21 months. The incidence of hepatic tumors and the number and volume of gamma-glutamyl transpeptidase-positive, ATPase-negative, glucose-6-phosphatase-negative, and glucose-6-phosphatase-positive foci at 21 months were lower in rats fed higher levels of selenium (no foci or tumors were seen at 6 mo). Indices of oxidative damage in the liver (thiobarbituric acid reactants, conjugated dienes, and lipid-soluble fluorescence products), however, were not decreased in rats fed the high-selenium diet. Therefore, selenium was protective against ciprofibrate-induced hepatocarcinogenesis, but not by reducing the degree of oxidative damage. The liver selenium and glutathione concentrations, and liver selenium-dependent glutathione peroxidase activity, increased as dietary selenium increased. Therefore, inhibition of carcinogenesis by selenium was correlated with increased levels of glutathione and glutathione peroxidase, but these did not inhibit the indices of oxidative damage. Peroxisomal beta-oxidation also increased with the dietary selenium content; it therefore does not appear to be a factor in the inhibition of hepatocarcinogenesis in rats fed higher levels of selenium.

Analysis of Variance↗
PubMed1999

Metabolism of selenite in men with widely varying selenium status.

OBJECTIVE: This study was undertaken to investigate the metabolism of selenite in men with life-long intakes of deficient, adequate and excess selenium. METHODS: Stable isotopes of selenium were infused for five hours into Chinese men living in deficient, adequate or excessive selenium areas, and 24-hour urine and blood samples were collected daily for the next seven days. Stable isotopic selenium excretion was determined in urine and in whole plasma and plasma fractions. RESULTS: Even though there was a positive correlation of selenium intake with the urinary excretion of this element, this relationship was not linear over the entire range (deficient, adequate, excessive) of selenium intake. When the urine excretion was normalized internally within each group, a sharp increase in the slope of this relationship was found when long-term intake increased to adequate amounts, but the slope reached a plateau when the daily intake exceeded the adequate group. The plasma selenoprotein P fraction was labeled initially, but the incorporation in the glutathione peroxidase fraction subsequently increased by a small amount. A two-month dietary restriction of selenium of the subjects from the excess area did not result in a reduction of urinary excretion of infused selenite. CONCLUSION: A complex relationship exists between long-term intake of selenium and selenium status, and subjects living in the excess area are more saturated with selenium than anticipated. More than two months of depletion are required to affect urinary excretion of selenium.

Adult↗
PubMed2001

Selenium and the brain: a review.

Similar to other tissues selenium from selenomethionine is deposited in the brain at higher concentrations than selenium in other forms. Vitamin E has a greater effect than selenium in reducing lipid peroxidation in various brain regions. Selenium does not have as great effect on glutathione peroxidase (GPX) activity in the brain as in most other organs. Prolonged selenium and iodine deficiencies will compromise thyroid hormone homeostatus in the brain and this is due to changes in deiodinases activities and lipid peroxidation. Even though selenium deficiency results in reduced GPX activity and selenium content in the brain, there is no reduction in thioredoxin reductase activity or selenoprotein W levels. Selenoprotein P is taken up in greater amounts by the brain but not by other organs in selenium deficient animals, suggesting a critical function of this selenoprotein in this organ. Selenium will influence compounds with hormonal activity (and neurotransmitters) in the brain, and this is postulated to be the reason selenium affects moods in humans and behavior in animals. Even though selenium counteracts the neurotoxicity of mercury, cadmium, lead and vanadium, it causes them to accumulate in the brain, presumably in a nontoxic complex.

Animals↗
PubMed1985

Dietary selenium, glutathione peroxidase activity, and toxicity of 2,3,7,8-tetrachloro-dibenzo-p-dioxin.

TCDD has been shown to inhibit selenium-dependent glutathione peroxidase activity. The role of selenium in TCDD toxicity is not known. We have therefore examined the effect of TCDD administration on hepatic glutathione peroxidase, aryl hydrocarbon hydroxylase, glutathione reductase, and glutathione S-transferase activities, glutathione content, and lipid peroxidation in rats fed 0, 0.10, and 2.0 ppm dietary selenium. TCDD treatment significantly inhibited selenium-dependent glutathione peroxidase in animals on diets containing 0.10 and 2.0 ppm selenium. The selenium-dependent glutathione peroxidase activities in rats on 0.10 and 2.0 ppm dietary selenium were 8.3-and 4.7-fold greater than in animals fed a diet containing 0 ppm selenium. TCDD administration enhanced hepatic microsomal lipid peroxidation by factors of 4.0, 4.9, and 9.8 in animals fed diets containing 0, 0.10, and 2.0 ppm selenium, respectively. The administration of a lethal dose of TCDD to rats fed diets containing 0, 0.10, and 2.0 ppm selenium resulted in 0, 46, and 7% survival, respectively, after 66 d. Aryl hydrocarbon hydroxylase, glutathione S-transferase, and glutathione reductase activities were induced by TCDD. The results indicate that optimum dietary selenium provides partial protection from the toxic effects of TCDD.

Animals↗
PubMed1983

Effect of dietary selenium levels on 7,12-dimethylbenzanthracene-induced mouse mammary tumorigenesis.

The effect of dietary selenium levels on 7,12-dimethylbenzanthracene (DMBA)-induced mammary tumors was examined in mice fed a semi-purified diet (20% casein, 50% sucrose, 5% corn oil). (C57BLxDBA/2f)F1 (BD2F1) female mice were fed diets containing 0.2, 0.5, 1.0 and 2.0 p.p.m. selenium starting at 7 weeks of age. The mammary tumor incidence was 56, 30, 25 and 16%, respectively, after the mice were on the diet for 9 months. In a second experiment, BALB/cV female mice were fed diets containing 0.2 and 2.0 p.p.m. selenium. After 9 months on the diet, the mammary tumor incidence was 39 and 7%, respectively. Both strains of mice grew equally well on the 0.2 and 2.0 p.p.m. selenium diets indicating that the highest dietary selenium level was compatible with normal growth. The selenium concentration and selenium dependent-glutathione peroxidase (GSH-Px) activity of mammary glands from control BD2F1 mice fed 0.2, 1.0 and 2.0 p.p.m. dietary selenium was examined at 8, 9 and 10 months of age. As in previous experiments in adult BALB/c mice, the concentration of mammary gland selenium, but not GSH-Px activity, increased with increasing levels of dietary selenium. These results document that nutritional levels of dietary selenium (0.5 p.p.m. Se) as well as non-toxic higher levels (2.0 p.p.m. Se) inhibit DMBA-induced mammary tumorigenesis.

9,10-Dimethyl-1,2-benzanthracene↗