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PubMed1990

The effects of selenium depletion and repletion on the metabolism of thyroid hormones in the rat.

Rats were fed selenium-deficient (less than 0.005 mg selenium/kg) or selenium-supplemented diets (0.1 mg selenium/kg, as Na2SeO2) for up to five wks from weaning to assess the effects of developing selenium deficiency on the metabolism of thyroid hormones. Within two wks 3:5,3'-triiodothyronine (T3) production from thyroxine (T4) in liver homogenates from selenium-deficient rats was significantly lower compared with the activity in liver homogenates from selenium-supplemented rats. This decreased activity was probably responsible, in part, for the higher T4 and lower T3 concentrations in plasma from the selenium-deficient rats after 3, 4, and 5 weeks of experiment. Repletion of selenium-deficient rats with single intra-peritoneal injections of 200 micrograms selenium/kg body wt. (as Na2SeO3) 5 days before sampling reversed the effects of the deficiency on thyroid hormone metabolism and significantly increased liver and plasma glutathione peroxidase activities. However a dose of 10 micrograms selenium/kg body wt given to rats of similar low selenium status had no effect on thyroid hormone metabolism or glutathione peroxidase activity but did reverse the increase in hepatic glutathione S-transferase activity characteristic of severe selenium deficiency. Imbalances in thyroid hormone metabolism are an early consequence of selenium deficiency and are probably not related to changes in hepatic xenobiotic metabolizing enzymes associated with severe deficiency.

Animals↗
PubMed1984

Influence of dietary selenium on the mutagenic activity of perfusate and bile from rat liver, perfused with 1,1-dimethylhydrazine.

The mutagenic effect of 1,1-dimethylhydrazine (UDMH) was studied in the liver perfusion/cell culture system. Male Wistar rats, fed a selenium-deficient diet with or without selenium supplementation in the drinking water, were used as liver donors. UDMH caused an increased mutation frequency in Chinese hamster V79 cells exposed in the perfusate. The effect was statistically significant with both selenium-deficient and selenium-supplemented livers. With selenium-deficient livers, a significant mutagenic effect was also obtained when V79 cells were treated with bile collected after the administration of UDMH. Bile flow and bile acid excretion were not affected by UDMH treatment of selenium-deficient or selenium-supplemented livers. There was a tendency towards reduced C-oxygenation of N,N-dimethylaniline in microsomes from selenium-deficient livers perfused with UDMH. The lactate/pyruvate ratio in the perfusate was increased by UDMH, the effect being more pronounced with selenium-deficient than selenium-supplemented livers.

Aniline Compounds↗
PubMed2006

Enzymatic and non-enzymatic antioxidant status in stage (III) human oral squamous cell carcinoma and treated with radical radio therapy: influence of selenium supplementation.

BACKGROUND: Oxidative stress is implicated in oral carcinogenesis and has been found to be aggravated during radiotherapy. A great deal of attention has been focused on the possible therapeutic implications of selenium as a potent antioxidant. We determined whether selenium supplementation to radiation treated oral cancer patients render improvement in the antioxidant status against oxidative stress. METHOD: Blood samples were collected from stage (III) oral cancer patients before initiating radiotherapy (Group B) (n=63) and this group is bifurcated into Group C-patients given radiotherapy alone (n=27) and Group D-patients given radiotherapy and supplemented with selenium (400 mug/day for 6 months) (n=36). Both Group C and D were followed up for 6 months. We evaluated the plasma selenium concentration, non-enzymatic system including GSH, vitamins E, C, A and ceruloplasmin and enzymatic antioxidant system including superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase. RESULTS: The concentrations of selenium, all non-enzymatic antioxidants and the activities of enzymatic antioxidants were found to be lowered in oral cancer patients (Group B), compared to normal (Group A) (p<0.05). Similar decrease in the concentration of selenium and antioxidants status was observed in radiotherapy group (Group C) (p<0.05). On the contrary, selenium group (Group D) showed marked increase in the concentrations of selenium and antioxidant status at 6 months compared to radiation group (Group C) (p<0.05). CONCLUSION: The observed result represents the antioxidant property of selenium through the improvement of antioxidant defense system. Selenium supplementation could be of great interest in protecting cells against oxidative stress.

Adult↗
PubMed2005

Reduced growth and survival of larval razorback sucker fed selenium-laden zooplankton.

Four groups of larval razorback sucker, an endangered fish, were exposed to selenium-laden zooplankton and survival, growth, and whole-body residues were measured. Studies were conducted with 5, 10, 24, and 28-day-old larvae fed zooplankton collected from six sites adjacent to the Green River, Utah. Water where zooplankton were collected had selenium concentrations ranging from <0.4 to 78 microg/L, and concentrations in zooplankton ranged from 2.3 to 91 microg/g dry weight. Static renewal tests were conducted for 20 to 25 days using reference water with selenium concentrations of <1.1 microg/L. In all studies, 80-100% mortality occurred in 15-20 days. In the 28-day-old larvae, fish weight was significantly reduced 25% in larvae fed zooplankton containing 12 microg/g selenium. Whole-body concentrations of selenium ranged from 3.7 to 14.3 microg/g in fish fed zooplankton from the reference site (Sheppard Bottom pond 1) up to 94 microg/g in fish fed zooplankton from North Roadside Pond. Limited information prior to the studies suggested that the Sheppard pond 1 site was relatively clean and suitable as a reference treatment; however, the nearly complete mortality of larvae and elevated concentrations of selenium in larvae and selenium and other elements in zooplankton indicated that this site was contaminated with selenium and other elements. Selenium concentrations in whole-body larvae and in zooplankton from all sites were close to or greater than toxic thresholds where adverse effects occur in fish. Delayed mortality occurred in larvae fed the two highest selenium concentrations in zooplankton and was thought due to an interaction with other elements.

Animals↗
PubMed2006

Gestational exposure to methylmercury and selenium: effects on a spatial discrimination reversal in adulthood.

Selenium, a nutrient, and methylmercury, a developmental neurotoxicant, are both found in fish. There are reports that selenium sometimes ameliorates methylmercury's neurotoxicity, but little is known about the durability of this protection after low-level gestational exposure. Developmental methylmercury exposure disrupts behavioral plasticity, and these effects extend well into adulthood and aging. The present experiment was designed to examine interactions between developmental low-level methylmercury and nutritionally relevant dietary selenium on discrimination reversals in adulthood. Female rats were exposed, in utero, to 0, 0.5, or 5 ppm mercury as methylmercury via drinking water, approximating mercury exposures of 0, 40, and 400 microg/kg/day. They also received both prenatal and postnatal exposure to a diet containing selenium from casein only (0.06 ppm) or 0.6 ppm selenium, creating a 2 (chronic Se)x3 (gestational MeHg) full factorial design, with six to eight rats per cell. Behavior was evaluated with a spatial discrimination procedure using two levers and sucrose reinforcers. All groups acquired the original discrimination similarly. Rats exposed to low selenium (0.06 ppm), regardless of MeHg exposure, required more sessions to complete the first reversal and made more omissions during this reversal than high selenium (0.6 ppm) animals, but the two diet groups did not differ on subsequent reversals. Rats exposed to MeHg, regardless of selenium exposure, made more errors than controls on the first and third reversals, which was away from the original discrimination. MeHg-exposed animals also had shorter choice latencies than controls during the first session of a reversal. Low selenium increased the number of omissions during a reversal, whereas high MeHg exposure produced perseverative responding (errors) on the lever that was reinforced during the original discrimination. However, there was no interaction between selenium and MeHg exposure.

Age Factors↗
PubMed2006

Brain and blood mercury and selenium after chronic and developmental exposure to methylmercury.

Fish contain methylmercury and the potentially protective element, selenium. Blood and brain concentrations of these elements were determined in female rats after consuming AIN-93-based diets containing 0.06 or 0.6 ppm of selenium (Se) and drinking water containing 0, 0.5, or 5 ppm of mercury as methylmercury (MeHg) for 6 or 18 months. Brain and blood concentrations of mercury and selenium were also evaluated in neonates after gestational exposure. For adult rats in the high-Se, high-Hg condition, brain selenium content was 0.35 ppm and 1.8 ppm after 6 and 18 months, respectively, but for every other adult-onset condition, it was 0.1 ppm. Blood selenium varied less than two-fold despite a 10-fold difference in diet. After 6 months, mercury content in the brain showed a greater than 10-fold difference between the mercury groups, and interacted somewhat with dietary selenium. After 18 months, no mercury was detected in the brains of the 0.5 ppm groups, and their blood mercury also fell. For the 5.0 ppm groups, brain mercury increased slightly (low Se diet) or several-fold (high Se diet) over that seen at 6 months, and blood mercury also increased. Neonatal selenium concentrations were more labile than adults, and mercury in neonates was generally higher. All animals exposed to 5 ppm of mercury experienced a molar excess of mercury over selenium. Animals exposed to 0.5 ppm mercury showed a balance between mercury and selenium or a selenium excess, depending on the condition.

Animals↗
PubMed2002

Selenium and its redox speciation in rainwater from sites of Valparaiso region in Chile, impacted by mining activities of copper ores.

The determination of the total concentration of selenium does not provide sufficient information about its toxicity and its bioavailability. The determination of its chemical forms is the basis for understanding the biogeochemical cycle in terrestrial and aquatic ecosystems and for detecting the species which might be toxic to biota. In this work we describe an analytical procedure to carry out the redox speciation of selenium present at ultratrace levels in rainwater from sites of Valparaiso region in Chile, impacted by mining activities of copper ores. A simple preconcentration step of the rainwater sample on a rotavapor system, in vacuum at low temperature permits the concentration of the different redox selenium species until levels quantifiable by sensitive techniques such as differential pulse cathodic stripping voltammetry or by spectrometric techniques, based on the hydride generation and detection by atomic absorption or atomic fluorescence spectrometry. These techniques coupled to redox chemical reactions allow the redox speciation of selenium. The results show that the open evaporation system can be used to concentrate water samples when the aim of the analysis is the determination of the total selenium concentration. On the contrary, to carry out its redox speciation only the preconcentration performed on rotavapor system, in vacuum can be used. When synthetic solutions containing different redox species of selenium, at ultratrace levels, were slowly evaporated on open system, Se(II) and Se(IV) were oxidized. The optimized procedure was then applied to the selenium determination and its redox speciation in rainwater samples collected in sites impacted by mining activities of copper ores. It was found that the amounts of total selenium in rainwater, as copper, from Puchuncavi valley decrease exponentially with the distance from the source, indicating that these elements in this region arise from the industrial complex Las Ventanas. In the redox speciation of selenium, Se(IV) and Se(VI) were the species found in all rainwater samples analyzed, providing selenium in species which are most favorable for their uptake by the vegetation grown in these soils.

Biological Availability↗
PubMed2003

Pharmacokinetic model of daily selenium intake from contaminated seafood in Taiwan.

Contaminated seafood has been reported as an important source of human exposure to metals in Taiwan. Seafood represents a non-negligible source of selenium in the human diet. This study was designed to determine the concentration of selenium in different types of seafood and predict the concentration of selenium in the blood of Taiwanese using a one-compartment steady-state pharmacokinetic (PK) model. Samples involved three subgroups, including fish, crustaceans and bivalve molluscs. Quantitative analysis for selenium was performed using an ICP-AES (Perkin Elmer) instrument. Selenium concentrations in seafood ranged from 0.63 to 2.01 microg/g wet wt. The highest selenium concentration found in fish was 2.01+/-0.36 microg/g wet wt in Salmo salar Linnaeus. In general, selenium concentration increased in the order of bivalve molluscs<crustacean<fish. The daily selenium intakes resulting from a high-seafood diet and an average diet were 145.2 and 60.2 microg/day, respectively. Daily selenium intake from seafood alone is higher than the US recommended daily allowance (RDA) of 55 microg/day and the World Health Organization (WHO) normative requirement of 40 microg/day. From PK model estimates, the concentrations of selenium in the blood of a typical seafood consumer and a high-seafood consumer were approximately 93 and 224 microg/l based on daily seafood intake of 60.2 and 145.2 microg/day, respectively.

Diet↗
PubMed2001

A randomized, controlled chemoprevention trial of selenium in familial prostate cancer: Rationale, recruitment, and design issues.

Deficiencies of selenium have been associated with an increased cancer risk, and several clinical and animal trials have suggested that improved selenium nutrition may reduce the incidence of several kinds of cancer, including lung, colorectal, and breast. Results from recent trials also show an anticarcinogenic effect of selenium in the prostate. There is converging evidence from epidemiologic, experimental animal, and molecular biology studies for an antitumor effect of selenium. Evidence suggests there are two modes of action of selenium affecting cancer risk: first, by functioning as an essential nutrient that provides the catalytic centers of a number of selenoenzymes, including some with antioxidant and redox functions; second, by serving as a source of selenium metabolytes that affect carcinogenesis in other ways. The first mechanism appears most relevant to protection against cancer initiation, the second against cancer progression. There is conclusive evidence of the increased risk of prostate cancer for a male with a family history of the disease. As a result of this evidence, and the evidence supporting the chemopreventive properties of selenium, this study proposed that a trial to test the effect of selenium on men at high risk for development of prostate cancer is appropriate. This article describes the Australian Prostate Cancer Prevention Trial Using Selenium (APPOSE) trial to test the hypothesis that daily dietary supplementation with selenium will reduce prostate cancer incidence in a population of men who are at increased risk because of a first-degree relative with prostate cancer.

Aged↗
PubMed1985

Selenium deficiency.

Selenium is undoubtedly an essential trace element: its involvement in GPx structure, the presence of deleterious effects of selenium deficiency in animals, and the recognition of deficiency states in man attest to its importance. However, if the consequences of selenium deficiency in man are now widely recognized, the mechanisms underlying these conditions are poorly understood. The definition of the exact role of selenium in human homeostasis has been hampered by the lack of a sensitive parameter, usable in routine investigation, to assess selenium status. Measurements of plasma and urinary levels, although useful in clinical practice, are inadequate indicators. The only true evidence of selenium deficiency lies in a positive response to selenium therapy. Deficiency states have been demonstrated for inhabitants of regions where selenium supply is limited, in protein-energy malnutrition, and in patients maintained on total parenteral nutrition without selenium supplementation. The benefit of selenium supplementation, together with other antioxidant drugs, in non-deficient subjects is still a matter of debate; its protective effect in neoplastic, cardiovascular and neurological degenerative diseases is not yet proven.

Animals↗
PubMed1999

The trace element selenium and the thyroid gland.

Apart from the essential trace element iodine, which is the central constituent of thyroid hormones, a second essential trace element, selenium, is required for appropriate thyroid hormone synthesis, activation and metabolism. The human thyroid gland has the highest selenium content per gram of tissue among all organs. Several selenocysteine-containing proteins respectively enzymes are functionally expressed in the thyroid, mainly in thyrocytes themselves: three forms of glutathione peroxidases (cGPx, pGPx, and PH-GPx), the type I 5-deiodinase, thioredoxin reductase and selenoprotein P. The thyroidal expression of type II 5-deiodinase still is controversial. As thyrocytes produce H2O2 continuously throughout life an effective cell defense system against H2O2 and reactive oxygen intermediates derived thereof is essential for maintenance of normal thyroid function and protection of the gland. In experimental animal models long-term and strong selenium deficiency leads to necrosis and fibrosis after high iodide loads. Combined iodide and selenium deficiency such as in central Zaire is thought to cause the myxedematous form of endemic cretinism. Inadequate selenium supply and prediagnostically low serum selenium levels are significantly correlated with the development of thyroid carcinoma and other tumors. Though selenium supply controls expression and translation of selenocysteine-containing proteins no direct correlation is found between selenium tissue content and expression of various thyroidal selenoproteins, indicating that other regulatory factors contribute to or override selenium-dependent expression control, e.g., in thyroid adenoma, carcinoma or autoimmune disease. As both trace elements, iodine and selenium, were washed out from the upper layers of the soil during and after the ice ages in many regions of the world adequate supply with these essential compounds needs to be provided either by a balanced diet or supplementation.

Animals↗
PubMed2000

Selenium stimulates estradiol production in bovine granulosa cells: possible involvement of nitric oxide.

Reduction in fertility is well known to be possibly related to selenium deficiencies, even if target organ for selenium action is, at present, unclear. The present study was aimed to examine whether selenium directly influences granulosa cells. Bovine granulosa cells from different size follicles were used to investigate the effect of selenium (5 ng/ml), with or without bovine follicle-stimulating hormone (bFSH) (100 ng/ml), on proliferation and steroidogenesis. In addition, we sought to determine if selenium modulates the production of nitric oxide, which is known to play an important role in ovarian activity. Our data demonstrate that selenium significantly (P < 0.001) stimulates the proliferation of the cells from small follicles; moreover, it further potentiates the stimulatory effect of the gonadotropin in the same cells. Furthermore, selenium significantly (P < 0.01) augments E2 output by cells from both kinds of follicles. bFSH increases E2 production (P < 0.01) by cells from large follicles, whereas it exerts a stimulatory (P < 0.01) effect only in the presence of selenium in the cells from the small ones. The production of nitric oxide is significantly increased (P < 0.001) by bFSH, but only in cells from small follicles. Selenium inhibits (P < 0.001) nitric oxide production in cells from both kinds of follicles and significantly decreases (P < 0.001) bFSH-induced nitric oxide production in cells from the small ones. We conclude that selenium acts on granulosa cells by modulating their proliferation and E2 synthesis; moreover, its effect could be mediated, at least in part, through an inhibition of nitric oxide.

Animals↗
PubMed2000

Selenium causes growth inhibition and apoptosis in human brain tumor cell lines.

We examined the effect of the trace element selenium on human glioma cell lines: T98G, U373MG, and U87MG, in addition to dermal fibroblast cells. Cultures were incubated with sodium selenite, and the following parameters were studied: cell growth, mitochondrial function, and ultrastructure. Cell growth was assayed by counting the number of viable cells after treatment with selenium. Mitochondrial function was analyzed using the MTT (tetrazolium salt reduction) assay. Apoptosis was determined by evaluating nuclear chromatin condensation by electron microscopy. The results indicated that selenium had a significant inhibitory effect on the growth of the tumor cells but had little effect upon dermal fibroblasts which had been passaged numerous times. Selenium also induced mitochondrial damage as shown by MTT assay in two brain tumor cell lines and in minimally passaged fibroblasts, but it had little effect upon the high-passage fibroblasts. Ultrastructurally, mitochondria had electron-dense inclusions resulting from selenium treatment. High rates of apoptosis were induced by selenium in the tumor cell lines and in the minimally passaged fibroblasts, whereas the fibroblasts with a high number of passages had some resistance to selenium treatment. This study correlates the adverse effects of selenium on mitochondrial function, inhibition of cell growth, and apoptosis and shows that selenium similarly affects three different brain tumor cell lines and minimally passaged fibroblasts. Further, the results with fibroblasts show that some types of cells after repeated passages can develop resistance to selenium damage.

Apoptosis↗
PubMed2002

Selenoprotein W gene regulation by selenium in L8 cells.

The effects of selenium on selenoprotein W gene expression were examined in cultured L8 rat skeletal muscle cells. Selenoprotein W contains selenium as selenocysteine in the primary protein structure and levels of this selenoprotein are affected by selenium. Northern blots indicated that there were no significant changes (P < 0.05) in selenoprotein W mRNA levels during cell proliferation and differentiation. Reduction of selenium concentration in the medium decreased the selenoprotein W mRNA levels. Nuclear run-on experiments with isolated L8 nuclei showed the same rate of selenoprotein W mRNA synthesis in cells cultured in either low selenium or selenium supplemented medium, suggesting that the transcription rate of the selenoprotein W gene is independent of selenium. Measurement of the selenoprotein W mRNA half-life in myoblasts treated with the transcription inhibitor, alpha-amanitin, showed that selenoprotein W mRNA levels decreased over time with an estimated half-life of 57 h for cells grown in low selenium medium. Selenium treatment increased the selenoprotein W mRNA half-life 2-fold. These data suggest that selenium stabilizes selenoprotein W mRNA but has no effect on transcription.

Animals↗
PubMed1995

Low selenium status in the elderly influences thyroid hormones.

1. Iodothyronine 5'-deiodinase, which is mainly responsible for peripheral triiodothyronine (T3) production, has recently been demonstrated to be a selenium-containing enzyme. In the elderly, reduced peripheral conversion of thyroxine (T4) to T3 and overt hypothyroidism are frequently observed. 2. We measured serum selenium and erythrocyte glutathione peroxidase (as indices of selenium status), thyroid hormones and thyroid-stimulating hormone in 109 healthy euthyroid subjects (52 women, 57 men), carefully selected to exclude abnormally low thyroid hormone levels induced by acute or chronic diseases or calorie restriction. The subjects were subdivided into three age groups. To avoid conditions of under-nutrition or malnutrition, dietary records were obtained for a sample of 24 subjects, randomly selected and representative of the whole population for age and sex. 3. In order to properly assess the influence of selenium status on iodothyronine 5'-deiodinase type I activity, a double-blind placebo-controlled trial was also carried out on 36 elderly subjects, resident at a privately owned nursing home. 4. In the free-living population, a progressive reduction of the T3/T4 ratio (due to increased T4 levels) and of selenium and erythrocyte glutathione peroxidase activity was observed with advancing age. A highly significant linear correlation between T4, T3/T4 and selenium was observed in the population as a whole (for T4, R = -0.312, P < 0.002; for T3/T4 ratio, R = 0.32, P < 0.01) and in older subjects (for T4, R = -0.40, P < 0.05; for T3/T4 ratio, R = 0.54, P < 0.002). 5. The main result of the double-blind placebo-controlled trial was a significant improvement of selenium indices and a decrease in the T4 level in selenium-treated subjects; serum selenium, erythrocyte glutathione peroxidase activity and thyroid hormones did not change in placebo-treated subjects. 6. We concluded that selenium status influences thyroid hormones in the elderly, mainly modulating T4 levels.

Adult↗
PubMed2006

[Selenium and cataract--risk factor or useful dietary supplement?].

BACKGROUND: The exact role of selenium in cataract development is still unclear. Both protective and toxic effects and mechanisms have been postulated in the past. Accordingly, the selenium contents in human lenses and blood sera in different forms of cataract were investigated. METHODS: 123 patients (76 female and 37 male) with a mean age of 69.8 years (range: 17 to 91 years) were enrolled in this study. Overall, 84 lenses (after ECCE) and 110 blood serum samples were investigated by atomic absorption spectroscopy. Interpretation of data was accompanied by exact preoperative investigations including Scheimpflug techniques. RESULTS: A significant increase of selenium content of the lenses was found with increasing lens opacification and colouration. Lenses with a mature cataract showed the highest selenium contents in the lens compared to other cataract forms. Opposite results were detected in blood serum. Lenses of diabetics showed already at a younger age changes in selenium content. Smokers showed both decreased selenium contents in the lens and decreased selenium concentration in blood serum. CONCLUSIONS: An obvious correlation between the type of cataract and selenium content of the lens seems to exist. The question by which mechanism selenium acts directly or by selenium-dependent enzymes acts lens opacification remains speculative up to now.

Adolescent↗
PubMed1998

Selenium depletion in patients with gastrointestinal diseases: are there any predictive factors?

BACKGROUND: Patients with intestinal disease are at risk of developing selenium deficiency due to impaired intestinal absorption. The aim of the present study was to evaluate selenium status and to identify predictive factors of selenium depletion in patients with gastrointestinal disease. METHODS: The concentration of selenium and the activity of glutathione peroxidase in plasma and erythrocytes were measured by fluorometry and by spectrophotometry. Eighty-six patients with Crohn's disease, 40 patients with ulcerative colitis, and 39 patients with various other gastrointestinal diseases were studied. Twenty-seven patients (16%) received home parenteral nutrition. Stool mass, faecal fat, and vitamin B12 absorption were analysed in 100 patients. RESULTS: The plasma selenium concentration was decreased in 85% of the patients receiving supplementary parenteral nutrition and in 20% of the patients receiving oral nutrition, among them in 26% of the patients with Crohn's disease. Almost all patients with ulcerative colitis had normal selenium levels. A statistically significant correlation was found between plasma selenium and vitamin B12 absorption, stool mass, faecal fat excretion, body mass index, P-albumin, P-zinc, and the length of the remaining small bowel. Stepwise regression analyses showed that the strongest predictors of selenium deficiency were stool mass, vitamin B12 absorption, and the length of the small-bowel resection. CONCLUSION: Selenium deficiency is common in patients with severe gastrointestinal disorders. The deficiency is mainly related to malabsorption, and a low selenium level was almost invariably present in patients who needed parenteral supplementation due to gut failure.

Adult↗
PubMed1983

Red blood cell and serum selenium concentrations as influenced by age and selected diseases.

Red blood cell and serum selenium concentrations were investigated to determine normal concentrations for our geographic area and if potential differences existed in patients with selected diagnoses (hepatic, renal, malignant, and chronic diseases). Selenium was quantified in samples of red blood cells, serum and urine by neutron activation analysis. The results were analyzed by comparing 1) pooled data from all ages for each disease with normal values, and 2) normal values with age-matched patients in each disease category. Decreases in red blood cell selenium concentrations (P less than 0.05) occurred in normal subjects over 60 years of age without concurrent significant decreases in serum selenium. Although differential results were noted in age-matched groups, overall results showed that decreased concentrations of selenium in both red cells and in serum occurred with alcoholic cirrhosis, malignancies, and chronic renal failure (P less than 0.025). Red blood cell selenium concentrations also were decreased in patients with stable chronic disease. Decreased serum selenium concentrations were positively correlated with albumin concentrations in patients with cirrhosis. There was no correlation between serum selenium and bilirubin concentrations in patients with liver disease or between serum selenium and creatinine concentrations in patients with chronic renal failure whose urinary excretion of selenium was far below control levels.

Adult↗