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PubMed2004

A report of high-dose selenium supplementation: response and toxicities.

Concerns about the toxicity of selenium has limited the doses used in chemoprevention. Based on previous studies, intakes of 400 microg/day and plasma selenium of 1000 ng/ml (Dietary Reference Intakes, Academy Press, New York, 2000, p. 384) were established as the no observed adverse effect level (NOAEL). This investigation summarizes the plasma response and toxicity reports from 24 men with biopsy-proven prostate cancer who were randomized to either 1600 or 3200 microg/day of selenized yeast as part of a controlled clinical trial testing selenium as a chemopreventive agent for prostate cancer progression. Subjects were on these doses for averages of almost 12 months. Plasma selenium levels were monitored throughout the course of follow-up. Symptoms of selenium toxicity were assessed by patient interview with specific questions regarding breath, hair and nail changes. Several liver and kidney function tests and hematology were measured at 6-month intervals. 8 subjects were randomized to the 1600 microg/day and 16 to the 3200 microg/day group. The mean plasma selenium levels achieved with supplementation were 492.2 ng/ml (SD = 188.3) and 639.7 ng/ml (SD = 490.7) for the 1600 and 3200 microg/ day doses, respectively. The 3200 microg/day group reported more selenium-related side effects. Blood chemistry and hematology results were all within normal limits for both treatment groups. More subjects on 3200 microg/day reported symptoms of selenium toxicity; however, these reports did not correspond to peaks in plasma selenium levels. We observed no obvious selenium-related serious toxicities. As selenium is used in more chemoprevention and therapeutic settings, additional information on selenium species, sequestration of selenium in specific organs, excretion, and toxicities is needed.

Aged↗
PubMed2004

Making sense of sex and supplements: differences in the anticarcinogenic effects of selenium in men and women.

The role of the essential trace mineral selenium in human health and disease is currently a subject of intense interest. In particular, the possible cancer preventive effects of dietary selenium supplementation are now being investigated in several large, randomized trials. The association between selenium status, genotoxic damage, and cancer risk remains enigmatic because epidemiologic studies have failed to consistently link low selenium status with increased cancer risk in men and women. In this paper, we considered the evidence that there are sex-based differences in the anticarcinogenic effects of selenium in humans. We focused our review on prospective human studies in which the relationship between selenium status and cancer risk in men and women was directly compared. Results from cohort studies conducted in seven countries (Belgium, China, Finland, Japan, Netherlands, Norway, and United States) were used to assess the strength of association between low selenium status and the incidence of all cancers, sex-specific cancers, and cancers at particular anatomic sites. In general, the available data support the hypothesis that cancer risk in men is more profoundly influenced by selenium status than cancer risk in women. Factors contributing to the apparent difference in the effects of selenium on cancer incidence in men and women may include sex-based differences in the metabolism and/or tissue distribution of selenium, as well as sex- or gender-related factors that influence tumor biology. Studies are needed to further define the dose-response relationship between selenium and cancer risk in men and women. A more complete understanding of the mechanisms by which selenium modulates cancer initiation and progression is needed to optimize dietary selenium supplementation as a practical cancer preventive strategy. Ultimately, achieving the ambitious goal of cancer prevention may require sex- and gender-specific approaches.

Anticarcinogenic Agents↗
PubMed2005

Molecular chemoprevention by selenium: a genomic approach.

Basic research and clinical chemoprevention trials support the protective role of selenium in cancer prevention but the mechanisms based on the molecular level remain to be fully defined. This mini-review focuses only on the elucidation of the molecular mechanisms of cancer prevention by selenium using the genomics approach; target organs discussed here are breast, prostate, colon and lung. The results described here support the utility of microarray technology in delineating the molecular mechanisms of cancer prevention by selenium. These results are based on studies employing human and rodent cell lines and tissues from animal models ranging from normal to frank cancer. The dose and the form of selenium are determining factors in cancer chemoprevention. The results of the microarray analysis reviewed here indicate that selenium, independent of its form and the target organ examined, alters several genes in a manner that can account for cancer prevention. Selenium can up regulate genes related to phase II detoxification enzymes, certain selenium-binding proteins and select apoptotic genes, while down regulating those related to phase I activating enzymes and cell proliferation. Independent of tissue type, selenium arrests cells in G1 phase of cell cycle, inhibits CYCLIN A, CYCLIN D1, CDC25A, CDK4, PCNA and E2F gene expressions while induces the expressions of P19, P21, P53, GST, SOD, NQO1, GADD153 and certain CASPASES. In addition to those described above, genes such as OPN, which is mainly involved in metastasis and recently reported to be down regulated by selenium, should be considered as potential molecular marker in clinical chemoprevention trials. Collectively, literature data indicate that some of these genes that were altered by selenium are also involved in the development of human cancers described in this review. It appears that androgen receptor status may influence the effect of selenium on gene expression profile in prostate cancer; whether estrogen receptor may influence the effect of selenium on gene expression in breast cancer requires further studies. Knowledge from gene array data in combination with proteomics approaches, using homogenous population of cell types with the aid of laser capture microdissection, may provide an individualized dimension of information on cancer risk and potential targets for its prevention. The molecular (genetic) biomarkers presented in this review will provide the foundation for future studies of the chemopreventive properties of structurally varied selenium compounds.

Animals↗
PubMed2002

Selenium intakes, absorption, retention, and status in adolescent girls.

OBJECTIVES: To assess selenium intakes, absorption, retention, and status in healthy adolescent girls and the effect of calcium supplementation on selenium parameters. DESIGN: Annual 2-week study conducted each year for 3 consecutive years in which yearly selenium intakes, absorption, and retention and blood selenium status were measured. SETTING: A metabolic unit in a large metropolitan hospital located in Columbus, Ohio--a low selenium region of the United States. SUBJECTS: Healthy white girls aged 11 to 14 years (n=16) enrolled in a calcium balance study and randomly assigned to receive a placebo of methylcellulose (n=9) or a calcium supplement containing 1,000 mg supplemental calcium as calcium citrate malate (n=7). INTERVENTIONS: Each subject consumed a diet with approximately 100 microg selenium/day during the yearly 2-week balance studies. RESULTS: Selenium status measurements (serum and erythrocyte selenium and glutathione peroxidase activity) were all within normal ranges for adults during the study. Apparent selenium absorption averaged 71%, 76%, and 74% for years 1, 2, and 3 of the study, respectively, and did not vary significantly (P>.05). Average daily selenium retention did not differ among the years of the study (P>.05) and indicated that the usual selenium intake was approximately 100 microg daily. Measurements of selenium status and retention did not differ between calcium-supplemented and placebo groups. CONCLUSIONS: An intake of approximately 100 microg selenium/day is the typical intake of the mineral among the subjects and appeared adequate to maintain selenium status in these healthy adolescent girls; in addition, calcium supplementation of 1,000 mg daily does not have a negative impact on selenium parameters.

Adolescent↗
PubMed2000

Effect of supplementation with organic selenium on mercury status as measured by mercury in pubic hair.

The purpose of this study was to evaluate the effect of four months of yeast-based selenium supplementation on selenium and mercury status in subjects with low serum selenium. The study was carried out in Rakvere, Estonia. Pubic hair mercury, serum selenium and blood selenium concentrations in 23 subjects (serum selenium < 90 micrograms/l) were investigated before and after selenium supplementation. Thirteen subjects were randomized into the selenium supplementation group and ten into the placebo group. The selenium supplementation group received daily 100 micrograms of selenomethionine. Selenium supplementation reduced pubic hair mercury level by 34% (p = 0.005) and elevated serum selenium by 73% and blood selenium by 59% in the supplemented group (p < 0.001 for both). The study indicates that mercury accumulation in pubic hair can be reduced by dietary supplementation with small daily amounts of organic selenium in a short range of time.

Dietary Supplements↗
PubMed2002

Relationship of dietary intake of fish and non-fish selenium to serum lipids in Japanese rural coastal community.

Several studies have suggested that dietary selenium deficiency may be associated with an increased risk of coronary heart disease (CHD). In the present study, 55 men and 71 women were selected from participants in a health examination in a rural coastal community in Japan. The mean dietary selenium intake calculated from the simple food frequency questionnaire (SFFQ) was 127.5 micrograms/day. Fish was the major source of dietary selenium and it contributed to 68.7% of the daily total. HDL cholesterol was higher in the middle selenium intake group and in the high selenium intake group than in the low selenium intake group in all subjects and for males, and a significant difference was found between the middle selenium intake group and the low selenium intake group. The atherogenic index was significantly higher in the low selenium intake group than in the middle selenium intake group and in the high selenium intake group in males. GPx activity, total cholesterol and triacylglycerols did not show any significant differences among the three different selenium intake groups. Dietary intake of non-fish Se had a positive correlation with HDL cholesterol, and an inverse correlation with the atherogenic index in all subjects and for females. On the other hand, dietary intake of fish-Se had no relationship with any serum lipids. Non-fish Se is an important factor in selenium status for the prevention of CHD.

Aged↗
PubMed2004

Elements in autopsy liver tissue samples from Greenlandic Inuit and Danes. V. Selenium measured by X-ray fluorescence spectrometry.

The content of selenium in normal liver tissue samples from Greenlandic Inuit was measured and the results compared with those obtained in normal liver tissue samples from Danes. Normal liver tissue samples were obtained at autopsy from 50 Greenlandic Inuit (27 men, 23 women) with a median age of 61 years (range 23-83) and from 74 Danes (44 men, 30 women) with a median age of 60 years (range 15-87). Total liver selenium content was measured by X-ray fluorescence spectrometry. The content of selenium (median) was in Inuit 26.6 micromol/kg dry liver (5-95 percentile: 15.2-49.4) and in Danes 17.7 micromol/kg dry liver (5-95 percentile: < 3.8-36.5) (p < 0.0001). Liver selenium content displayed no significant gender difference, either in Inuit or Danes. In Inuit men, there was a negative correlation between liver selenium content and age (rs = -0.39, p < 0.05), whereas Danish men displayed a positive correlation between liver selenium content and age (rs = 0.37, p = 0.02). There was no correlation in Inuit or Danish women. In Inuit, the median hepatic selenium index (liver selenium content divided by age) was 0.48 and in Danes 0.33 (p = 0.001). There was an inverse correlation between hepatic selenium index and age both in Inuit (rs = -0.77, p < 0.0001) and in Danes (rs = -0.47, p < 0.0001). In conclusion, Inuit had a higher liver content of selenium and a higher hepatic selenium index compared with Danes. The more favourable selenium status is due to a higher nutritional selenium intake with fish and meat from sea mammals.

Adolescent↗
PubMed2002

Selenium status and associated factors in a British National Diet and Nutrition Survey: young people aged 4-18 y.

OBJECTIVE: Assessment of selenium status to provide normative reference values, and investigation of associated socio-demographic factors, in a national sample of British young people aged 4-18 y. SETTING: National Diet and Nutrition Survey-a nationwide cross-sectional sample of young people aged 4-18 y living in mainland Britain in 1997. METHODS: Selenium status was measured, mainly in fasting blood samples, by plasma selenium concentration in 1127 participants, by red blood cell (RBC) selenium concentration in 1112, and by whole-blood glutathione peroxidase (GPx) activity in 658. RESULTS: No evidence of severe selenium deficiency or toxicity was observed. Plasma selenium concentration was directly correlated with RBC selenium concentration, and both were associated directly, although less strongly, with GPx activity. Plasma and RBC selenium concentrations increased significantly with age, with RBC concentrations significantly higher in older girls than boys. Region of domicile exhibited a significant relationship. Associations also occurred with parental occupational social class, selenium concentrations being higher in more socially advantaged children. Black and Indian children had considerably higher concentrations than Caucasian children. Concentrations, especially of plasma selenium, were significantly lower in children either (or both) of whose parents were smokers, although, unexpectedly, there was no evidence that children who themselves smoked had lower levels. CONCLUSIONS: The observed associations between selenium status indices and age, gender, social class, parental smoking and ethnic group indicate a complex network of biological factors which determine selenium concentrations in blood components, and which thus need to be controlled for when using these indices to assess selenium status in young people. SPONSORSHIP: The survey was commissioned jointly by the Department of Health and the Ministry of Agriculture, Fisheries and Food, whose responsibility has since been transferred to the Food Standards Agency. Support for the further analysis presented in this paper was provided by the Department of Health.

Adolescent↗
PubMed1993

Selenium status of infants is influenced by supplementation of formula or maternal diets.

Plasma selenium of infants fed proprietary formula was significantly less than that in infants fed human milk. Addition of selenite to the formula (0.253 mumol Se/L) increased plasma selenium and activities of glutathione peroxidase (GPx) and total peroxidase (Px). However, erythrocyte selenium decreased significantly during the 12-wk study in infants receiving human milk or formula with or without supplemental selenite. Infants fed human milk from women receiving 0 or 200 micrograms supplemental selenium as selenomethionine or selenium-enriched yeast had plasma selenium that paralleled changes in their selenium intake. Plasma GPx and Px activities were unrelated to human milk selenium intake. Milk from women given either selenium supplement prevented the decline in infant erythrocyte selenium. Results of these studies suggest that the method of feeding modifies the infant's apparent selenium status and that the molecular form of selenium provided and/or its interaction with other milk constituents are determinants of infant selenium status.

Anthropometry↗
PubMed2006

Selenium and coronary heart disease: a meta-analysis.

BACKGROUND: It is hypothesized that low selenium concentrations are associated with an increased risk of cardiovascular disease and that selenium supplements prevent coronary heart disease. OBJECTIVE: The objective was to perform a meta-analysis on the association of selenium biomarkers with coronary heart disease endpoints in observational studies and on the efficacy of selenium supplements in preventing coronary heart disease endpoints in randomized trials. DESIGN: The MEDLINE and the Cochrane Library databases were searched for studies conducted from 1966 through 2005. Relative risks were pooled by using an inverse-variance weighted random-effects model. RESULTS: Twenty-five observational studies (14 cohort and 11 case-control studies) that measured blood or toenail selenium concentrations and 6 randomized trials that evaluated supplements containing selenium met our inclusion criteria. The pooled relative risk in a comparison of the highest with the lowest selenium concentration categories was 0.85 (95% CI: 0.74, 0.99) in cohort studies and 0.43 (0.29, 0.66) in case-control studies. In observational studies, a 50% increase in selenium concentrations was associated with a 24% (7%, 38%) reduction in coronary heart disease risk. In randomized trials, the pooled relative risk in a comparison of supplements containing selenium with placebo was 0.89 (0.68, 1.17). CONCLUSIONS: Selenium concentrations were inversely associated with coronary heart disease risk in observational studies. Because observational studies have provided misleading evidence for other antioxidants, the validity of this association is uncertain. Few randomized trials have addressed the cardiovascular efficacy of selenium supplementation, and their findings are still inconclusive. Evidence from large ongoing trials is needed to establish low selenium concentrations as a cardiovascular disease risk factor. Currently, selenium supplements should not be recommended for cardiovascular disease prevention.

Biomarkers↗
PubMed1987

Influence of dietary fat and selenium in initiation and promotion of aflatoxin B1-induced preneoplastic foci in rat liver.

Aflatoxin B1-induced hepatic gamma-glutamyl transpeptidase-positive foci were quantified in rats fed different levels of fat and selenium during either initiation or early promotion. Male Sprague-Dawley rats were divided into 12 groups. One of six experimental diets were fed to groups 1-6 prior to and during aflatoxin B1 exposure (initiation, weeks 1-4.5) and to groups 7-12 during weeks 4.5-15 (promotion). The six experimental diets contained 2 or 20% corn oil, each with either less than 0.02, 0.15 or 2.5 (or 1.9) p.p.m. selenium. When not fed the experimental diets, rats were fed a modified AIN-76A diet. In groups 1-6, 0.03% phenobarbital was added as a promoter to the AIN-76A diet. Individual and interactive effects of selenium and fat were dependent on the stage of carcinogenesis. High dietary fat fed with either less than 0.02 or 0.15 p.p.m. selenium during initiation resulted in a significant increase in the number and size of foci when compared with low fat groups. In rats fed 20% fat and 2.5 p.p.m. selenium during initiation, preneoplastic development was reduced below all low fat groups. In contrast, selenium status but not dietary fat level influenced focal formation during promotion. Rats fed less than 0.02 p.p.m. selenium had a significantly greater percentage of liver section occupied by foci than rats fed either 0.15 or 1.9 p.p.m. selenium. Feeding 1.9 p.p.m. selenium during promotion did not afford greater protection above the 0.15 p.p.m. level. Hepatic glutathione peroxidase activity at week 15 was significantly diminished in animals fed less than 0.02 p.p.m. selenium during promotion. Feeding 1.9 p.p.m. selenium when compared with 0.15 p.p.m. did not result in a consistent increase in enzyme activity. Although differences were observed in growth due to dietary treatment, there were no significant correlations between preneoplastic foci and body weight, food consumption or food efficiency. These findings indicate an interaction between dietary fat and selenium during initiation, but not during early promotion. Furthermore, dietary selenium and fat may function by different mechanisms at different stages of carcinogenesis.

Aflatoxin B1↗
PubMed1997

Dietary Iodine and selenium interact to affect thyroid hormone metabolism of rats.

The interaction of dietary selenium and iodine on the activities of the selenoenzymes, selenium-dependent glutathione peroxidase (GSH-Px), and type I deiodinase (DI-I), and the thyroid hormones thyroxine (T4) and triiodothyronine (T3) were studied. Male weanling Sprague-Dawley rats were fed an AIN-93G diet for 6 wk with modified selenium and iodine concentration as follows: three levels each of iodine and selenium (0.03, 0.2 added and 1.0 added mg iodine/kg diet, and 0.05, 0.18 added and 1.0 added mg selenium/kg diet) were used in a 3 x 3 factorial design. Renal, but not hepatic, DI-I activity was lower in rats with low selenium intake than in controls. Circulating T3 concentration was not affected by the dietary levels of iodine or selenium. Unlike in liver, kidney and erythrocytes, thyroidal GSH-Px activity was not lower than in controls in rats with low selenium intake, but was significantly higher when iodine intake was low. Significant interactions of iodine and selenium on serum T4 and thyroidal GSH-Px activity were observed. Serum T4 was maintained at control levels when both dietary iodine and selenium were low, but not when iodine alone, or selenium alone, was low. Activity of thyroidal GSH-Px was lowest in rats fed a diet containing high iodine and low selenium. The results suggest that high iodine intake, when selenium is deficient, may permit thyroid tissue damage as a result of low thyroidal GSH-Px activity during thyroid stimulation. A moderately low selenium intake normalized circulating T4 concentration in the presence of iodine deficiency.

Animals↗
PubMed2001

Selenium and zinc status are suboptimal in a sample of older New Zealand women in a community-based study.

The importance of selenium and zinc in the immune functioning of the aged is widely recognized. Seniors in New Zealand are at particularly high risk of low selenium status because of the low selenium soil environment. The zinc status of the New Zealand elderly has never been assessed. In this cross-sectional study, the biochemical selenium, zinc and lipid levels, physical functional capacity and dietary intakes of 103 randomly selected free-living New Zealand women (mean age +/- SD, 75 +/- 3 y) were assessed. Among nonusers of selenium supplements (n = 80), 80% [95% confidence interval (CI): 70; 88%] had plasma selenium levels (0.85 +/- 0.23 micromol/L) below 1.00 micromol/L [ approximately 10% below mean plasma selenium necessary for full expression of glutathione peroxidase (GPx) activity in New Zealand subjects]. Plasma selenium was strongly correlated with GPx: r = 0.56; P < 0.0001. For nonusers of zinc supplements (n = 88), serum zinc concentrations were 12.4 +/- 1.4 micromol/L, with 12% (95% CI: 6; 21%) having levels below the cut-off value (10.7 micromol/L). Estimated mean daily selenium and zinc intakes were 34 +/- 10 microg and 8.7 +/- 2.0 mg, respectively. Subjects in the highest tertile of a functional capacity index had higher biochemical zinc and selenium values than those in the lowest tertile (P < 0.05). The correlation between plasma selenium and GPx indicates that selenium intake in these women is still insufficient for full expression of GPx activity. Lower serum zinc levels also appear to be prevalent. Because a suboptimal trace element status may be more common among those with a poor physical functioning, promotion of the consumption of nutrient dense foods or supplements to improve selenium and zinc status of elderly women in New Zealand may be beneficial.

Aged↗
PubMed2004

Dietary and biochemical selenium status of urban 6- to 24-month-old South Island New Zealand children and their postpartum mothers.

A community-based, cross-sectional survey was conducted in the South Island of New Zealand to assess the dietary and biochemical selenium status of children (n = 136) and their mothers (n = 302), and to assess factors influencing selenium status. Serum and plasma samples from children and their mothers were analyzed for selenium using graphite furnace atomic absorption spectrometry. Dietary selenium intakes were analyzed from 3-d weighed diet records, and food sources of selenium were quantified. Mean dietary selenium intakes in infants (6-11.9 mo), toddlers (12-24 mo), and mothers were below recommended levels. Toddlers had higher selenium intakes than infants (13.7 +/- 8.4 and 7.9 +/- 6.2 microg/d, respectively, P = 0.0001) and the selenium density of their diets was also higher [3.2 +/- 1.7 and 2.4 +/- 1.7 microg/(MJ . d), respectively, P = 0.003]. Household smoking was associated with lower serum selenium concentrations in infants and toddlers (P = 0.02). South Island women who were currently pregnant had lower plasma selenium concentrations (0.74 +/- 0.15 micromol/L) than nonpregnant lactating and nonpregnant nonlactating women (0.94 +/- 0.16 and 0.93 +/- 0.16 micromol/L, respectively, P = 0.0001). Clearly, pregnant women, infants and toddlers are at risk of suboptimal selenium status, and further research is warranted to assess potential effects in these groups. The finding of an association between household smoking and lower selenium concentrations in children should be investigated further. Dietary interventions are recommended to improve dietary selenium intakes in South Island children and their mothers.

Cross-Sectional Studies↗
PubMed2006

Mechanisms of selenium down-regulation of androgen receptor signaling in prostate cancer.

Prevention trials showed that selenium reduced prostate cancer incidence by 50%, establishing selenium as a promising chemopreventive agent for prostate cancer. Selenium inhibited human prostate cancer cell growth, blocked cell cycle progression at multiple transition points, and induced apoptotic cell death. Previous studies showed a novel mechanism of selenium anticancer action in which selenium markedly reduces androgen signaling and androgen receptor (AR)-mediated gene expression, including prostate-specific antigen (PSA), in human prostate cancer cells. The molecular mechanisms of selenium-mediated down-regulation of AR signaling are not clear. In this study, a systemic approach was taken to examine the modification of androgen signaling by selenium in human prostate cancer cells. In addition to reduced AR mRNA expression, selenium was found to initially increase the stability of AR mRNA within 6 hours while decreasing the stability of AR mRNA after 8 hours. Selenium increased AR protein degradation and reduced AR nuclear localization. Scatchard analysis indicated that selenium did not affect ligand binding to AR in LNCaP cells. Chromatin immunoprecipitation analyses showed that DHT increased the recruitment of AR and coactivators, such as SRC-1 and TIF-2, to the promoter of the PSA gene, and that recruitment was greatly diminished in the presence of 5 micromol/L selenium. On the other hand, selenium enhanced the recruitment of corepressors, such as SMRT, to the promoter of the PSA gene. Taken together, these results suggest that selenium disrupts AR signaling at multiple stages, including AR mRNA expression, mRNA stability, protein degradation, nuclear translocation, and recruitment of coregulators.

Anticarcinogenic Agents↗
PubMed1998

The effect of subclinical selenium toxicosis on pregnant beef cattle.

A field investigation conducted by the South Dakota Animal Disease Research and Diagnostic Laboratory suggested that subclinical selenium toxicosis in pregnant cows may have contributed to an outbreak of aborted/stillborn calves in a high-selenium region of South Dakota. This study was undertaken to evaluate the relationship between abortion and subclinical selenium toxicosis in the dam and to assess the effects of subclinical selenium toxicosis on the bovine immune system. Fifteen pregnant cows were fed diets containing 0.25 (control), 6.0, and 12.0 ppm selenium beginning at 80-110 days gestation. Although selenium toxicosis has been reported to cause abortion, this study failed to reproduce abortions. A single cow in the 12-ppm selenium treatment group gave birth to a weak calf, which subsequently died. This calf had myocardial lesions consistent with those described for selenium toxicosis and had hepatic selenium levels of 9.68 ppm (wet weight). Elevated dietary selenium resulted in the depression of several leukocyte function parameters in pregnant cows. A statistically significant depression in forced antibody response was identified in both selenium-supplemented groups. A significantly diminished mitogenic response to concanavalin A and pokeweed mitogen was also observed in the 12-ppm selenium group. Although a similar pattern of depression was also observed with phytohemagglutinin, differences were not significant. These findings indicate that even in the absence of clinical alkali disease, elevated selenium levels may adversely affect both pregnancy outcome and the bovine immune system.

Analysis of Variance↗
PubMed1992

Selenium deficiency and type II 5'-deiodinase regulation in the euthyroid and hypothyroid rat: evidence of a direct effect of thyroxine.

Selenium deficiency in rats is characterized by elevated serum T4 and decreased serum T3 concentrations, and low liver type I (5'D-I) and brain type II (5'D-II) iodothyronine 5'-deiodinase activities. These findings are partially explained by the demonstration that type I 5'D is a selenoprotein; however, 5'D-II does not contain selenium. Since 5'D-II varies inversely with serum T4 concentrations, and serum T4 is elevated in selenium deficiency, the decreased cerebrocortical 5'D-II activity may be secondary to the increased serum T4 levels. To determine the mechanism(s) by which selenium influences 5'D-II activity, we examined the effects of altered selenium intake on brain 5'D-II levels and enzyme turnover in euthyroid and thyroidectomized rats. Rats were fed a selenium-supplemented or selenium-deficient diet for 5 weeks from weaning; half of the animals were also thyroidectomized 3 weeks before death. Selenium deficiency was confirmed by decreased liver and brain glutathione peroxidase activities. In euthyroid rats, selenium deficiency caused a 38% increase in serum T4, and 91% and 39% decreases in 5'D-I and 5'D-II, respectively, compared to those in selenium-supplemented rats. In the thyroidectomized hypothyroid rats, selenium deficiency caused a 60% decrease in 5'D-I, but had no effect on 5'D-II activity, fractional turnover of the enzyme, or the calculated enzyme synthesis rate. The lack of effect of selenium deficiency on 5'D-II levels in hypothyroid rats is consistent with the finding that 5'D-II is not a seleno-enzyme. Thus, the decrease in brain and pituitary 5'D-II activity in selenium-deficient euthyroid rats is due to the T4-dependent increase in the turnover of the enzyme polypeptide.

Animals↗
PubMed1992

Effects of selenium deficiency on thyroid hormone economy in rats.

In selenium-deficient rats, peripheral T4 to T3 conversion is markedly decreased due to the loss of the selenoprotein, type I iodothyronine 5'-deiodinase (5'D-I). Despite the marked increase in circulating T4 that results from this loss of 5'D-I, serum T3 concentrations in selenium-deficient rats remain in the normal range. To determine the physiological mechanism(s) that maintains circulating T3 when peripheral T4 to T3 conversion is impaired, we examined the interrelationships between selenium intake and the metabolism of T3 and T4 in the rat. In euthyroid rats, selenium deficiency caused the expected loss of 5'D-I, with a 52% increase in serum T4, which paralleled an increase in the T4 biological half-life. Consistent with the prolonged t1/2 of T4, short term thyroidectomy (48 h) in selenium-deficient rats failed to decrease serum T4 concentrations to the levels observed in short term thyroidectomized, selenium-supplemented rats. Short term thyroidectomy also caused an expected 33% decrease in liver 5'D-I and a 44% increase in brain type II iodothyronine 5'-deiodinase (5'D-II) activities in selenium-supplemented rats. However, in selenium-deficient rats, short term thyroidectomy did not affect 5'D-I or 5'D-II activities. In contrast to the selenium-dependent changes in circulating T4 levels, little or no change in circulating T3 concentrations occurred. There was a 20% increase in the T3 half-life in selenium-deficient rats. The serum T3 sulfate concentration was increased, and T3 deiodination was reciprocally decreased in the selenium-deficient rats. These data suggest that increased T3 sulfate generation in selenium-deficient rats may lead to greater T3 availability through enterohepatic recycling of the iodothyronine and may explain why there are only minor changes in serum T3 concentrations in selenium-deficient rats.

Animals↗