Effects Of Selenium Deficiency Research Articles

Effect of Selenium Deficiency on the Development of Overt Hepatic Encephalopathy in Patients with Chronic Liver Disease.

Selenium is an essential trace element to maintain good health. This retrospective study investigated the prevalence of selenium deficiency and its effect on overt hepatic encephalopathy (OHE) in patients with chronic liver disease (CLD). Patients who underwent serum selenium level measurement between January 2021 and April 2022 were enrolled. The factors associated with selenium deficiency (≤10 µg/dL) and the association between selenium deficiency and OHE were analyzed. Among 98 eligible patients, 24% were observed to have selenium deficiency, with a median serum selenium level of 11.8 µg/dL. The serum selenium levels were significantly lower in patients with cirrhosis than in those with chronic hepatitis (10.9 µg/dL vs. 12.4 µg/dL; p = 0.03). The serum selenium levels were negatively correlated with mac-2 binding protein glycan isomer, the FIB-4 index, albumin-bilirubin (ALBI) score, and Child-Pugh score. The ALBI score remained significantly associated with selenium deficiency (odds ratio, 3.23; 95% confidence interval [CI], 1.56-6.67). During a median follow-up period of 2.9 months, nine patients experienced OHE. Selenium deficiency was associated with OHE (hazard ratio, 12.75; 95% CI, 2.54-70.22). Selenium deficiency is highly prevalent in patients with CLD and is associated with an increased risk of OHE development.

Effects of selenium deficiency on biological results of X-ray and carbon-ion beam irradiation in mice.

The impact of radiation-induced hydrogen peroxide (H2O2) on the biological effects of X-rays and carbon-ion beams was investigated using a selenium-deficient (SeD) mouse model. Selenium is the active center of glutathione peroxidase (GSH-Px), and SeD mice lack the ability to degrade H2O2. Male and female SeD mice were prepared by feeding a torula yeast-based SeD diet and ultrapure water. Thirty-day survival rates after whole-body irradiation, radiation-induced leg contracture, and MRI-based redox imaging of the brain were assessed and compared between SeD and normal mice. Thirty-day lethality after whole-body 5.6 Gy irradiation with X-rays or carbon-ion beams was higher in the SeD mice than in the normal mice, while SeD did not give the notable difference between X-rays and carbon-ion beams. SeD also did not affect the maximum leg contracture level after irradiation with carbon-ion beams, but delayed the leg contraction rate. In addition, no marked effects of SeD were observed on variations in the redox status of the brain after irradiation. Collectively, the present results indicate that SeD slightly altered the biological effects of X-rays and/or carbon-ion beams. GSH-Px processes endogenous H2O2 generated through mitochondrial respiration, but does not have the capacity to degrade H2O2 produced by irradiation.

Effects of selenium deficiency on testis development and autophagy in chicks

To investigate the effects of Selenium (Se) deficiency on testis development and autophagy in chicks. 20 1-day old cocks were randomly divided into two groups, named the control check (CK) group [a basic diet (containing 0.333 mg Se/kg) was fed] and the Se-deficiency (Low Se) group [a selenium deficiency diet (containing 0.033 mg Se/kg) was supplied]. After 30 days, the body and testicle weights of the chicks were measured, and the organ coefficient was calculated. While haematoxylin–eosin staining, enzyme-linked immunosorbent assay, colorimetric method was used to assess the histopathological changes of testis, the changes of sex hormone levels, and antioxidant enzyme activities in two groups of chicks, respectively, the mRNA and protein expression of autophagy-related factors in the testes was determined by using quantitative PCR and western blotting. We found that Se deficiency resulted in a significant decrease in body and testicle weights of the chicks, a reduction in organ coefficients, and damaged testis tissue. The levels of sex hormone testosterone, oestradiol, the activities of serum antioxidant enzymes T-AOC, GSH-ST and GSH-PX in the Low-Se group were significantly lower than those in the CK group. Furthermore, the level of autophagy was significantly increased in the Low-Se group compared with the CK counterpart. The mRNA levels of Beclin1, Dynein, ATG-4B, ATG5, LC3-A and LC3-B genes in the Low-Se group were significantly higher than those in the CK group, while the protein expression of ATG5 and LC3-B was significantly increased in the Low-Se group compared with the CK counterpart. These data indicates dietary selenium-deprived chicks exhibit poor testicular development, impaired sex hormone synthesis, reduced antioxidant enzyme activity, and increased mRNA and protein expression of autophagy-related factors. HIGHLIGHTS Se-deprived chicks display poor testicular development, impaired sex hormone synthesis, reduced activity of antioxidant enzymes, and increased mRNA and protein levels of autophagy-related factors.

P1494THE NEGATIVE EFFECT OF SELENIUM DEFICIENCY ON THYROID HORMONE IMPAIRMENT AND CARDIOVASCULAR DISEASE IN CHRONIC HEMODIALYSIS PATIENTS

Abstract Background and Aims Selenium is an essential trace element. It has been known to protect the cardiovascular disease(CVD) and thyroid disease by protecting the oxidative stress using selenium-dependent glutathione peroxidase. Chronic hemodialysis(HD) patients are more likely to have selenium deficiency compared to healthy subjects. Therefore, we investigated the degree of selenium deficiency in HD patients and try to analyze the effect of selenium deficiency on thyroid hormone impairment and its correlation with CVD. Method A total of 183-chronic HD patients were enrolled. Serum selenium level was assessed before HD using inductively coupled plasma-mass spectrometry. Based on tertile of selenium, the patients were divided into three groups: low-, intermediate-, and high- group. The presence of thyroid hormone impairment and cardiovascular disease were evaluated. Results The value of serum selenium in first and second tertile of subjects was 80.64 and 94.84 g/dL, respectively. Thyroid dysfunction and CVD with respect to serum selenium levels are summarized in Table 1. Although the prevalence of hypothyroidism was not different among the three groups, instances of subclinical hypothyroidism was higher in the lower selenium group than those in the other groups (34% vs. 15% vs. 8%; P=0.005). Moreover, total thyroid dysfunction was significantly higher in the lower selenium group (38% vs. 18% vs. 15%; P=0.005). The prevalence of ischemic heart disease was most prevalent in the lower selenium group among the three groups, (49% vs. 25% vs. 22%; P=0.002). The prevalence of total CVD was highest in the lower selenium groups. (57% vs. 33% vs. 26%; P=0.001). In the analysis of the relationship between thyroid dysfunction and CVD, The prevalence of IHD was highest in the lower selenium group with thyroid dysfunction(p=0.039) Conclusion This study showed that selenium deficiency is associated with thyroid hormone impairment and thyroid disease. And the thyroid hormone impairment showed the synergistic negative effect on CVD in HD with selenium deficiency patients.

PHYSIOLOGICAL AND REPARATIVE OSTEOGENESIS IN THE NORM AND UNDER CONDITIONS OF SELENIUM DEFICIENCY


 
 
 The study presents the results of investigation of selenium deficiency condition on the bone tissue and healing post-traumatic bone defects under conditions of selenium deficiency.The experimental part of the study was performed on 63 randomized brand albino male rats of 3-month age. Peculiarities of the reparative osteogenesis were studied on the model of a traumatic injury simulated one-type in the proximal meta-diaphysis of the femoral bone irrespective of the experimental conditions in the frontal plane in the form of perforated defect. The defect was made by means of a drill 1mm in diameter.The results of the study are indicative of a negative effect of selenium deficiency produced on physiological and reparative osteogenesis manifested by inhibition of the process and associated with disorders in the formation of osseous regeneration, deterioration of the structural-functional state of the osseous tissue, development of degenerative-necrotic changes in the osseous tissue and epiphyseal cartilage.
 
 

セレン欠乏によるマウス脳内の必須微量元素（Fe, Cu, Zn, Mn, Se）を含むタンパク質への影響

セレン通常食を食べさせて飼育したマウス（Se通常群マウス）とセレン欠乏食で飼育したマウス（Se欠乏群マウス）に，セレン-82安定同位体を濃縮した亜セレン酸｛82Se(IV)｝またはセレノメチオニン（82SeMet）を静脈注射したのち，必須微量元素（Fe, Cu, Zn, Mn, Se）の化学形態別分析を，高速液体クロマトグラフィー（HPLC）を結合させた誘導結合プラズマ質量分析法（ICPMS）で測定した．セレン欠乏群マウスでは，恒常性により内因性セレンは一定に保たれ，セレノプロテインP（Sel-P）の化学形態で保存されていたセレンは細胞内グルタチオンペルオキシダーゼ（cGPx）の合成に使われた．また，静脈注射したセレンはSel-Pの合成には使われずcGPxの合成に使われた．SeMetの方がSe(IV)よりもcGPxの合成に有効に使われた．Seが欠乏した脳内では，抗酸化作用を補うような反応が観測された．抗酸化作用を示すスーパーオキドジスムターゼ（SOD）やメタロチオネイン（MT）が，セレン通常群マウスと比べより多く合成されたのに対し，ヒドロキシルラジカルを合成するチトクロームc（Cyt c）は，通常群マウスと比べ合成が押さえられた．特に，Se(IV)注射した方が，SeMet注射した時と比較して，内因性のcGPx, SOD, 及びMTが大きく増加した．これは，Se(IV)を静脈注射した方がスーパーオキシドがより合成されるため，抗酸化作用を示すタンパク質がより多く必要とされたためである．これらの実験事実より，必須微量元素（Fe, Cu, Zn, Mn, Se）を含むタンパク質は，活性酸素種による脳細胞の損傷を少なくするために相補的に働いていると考えられた．

Effect of Selenium Deficiency on Nitric Oxide and Heat Shock Proteins in Chicken Erythrocytes.

Selenium (Se) deficiency induces various types of diseases, including hemolytic anemia, which is one of the basic pathologies of erythrocyte damage. To investigate the effect of Se deficiency on chicken erythrocytes, we detected the effects of Se deficiency on the nitric oxide (NO) content and the levels of heat shock proteins (Hsps) in chicken erythrocytes, including Hsp27, Hsp40, Hsp60, Hsp70, and Hsp90. One-day-old chickens (180) were randomly divided into two groups, a low-Se group (L group, fed with a 0.008 mg/kg Se diet) and a control group (C group, fed with a 0.2 mg/kg Se diet). Next, erythrocytes were collected at 35 days old, and the NO content, activity of inducible nitric oxide synthase (iNOS), and levels of Hsps (27, 40, 60, 70, and 90) were examined. Compared with the C group, the NO and iNOS levels were significantly higher (P < 0.05), and the Hsps in the mRNA and protein levels were generally higher (P < 0.05) in the L group. Meanwhile, the correlation analysis showed that there were positive correlations between Hsps and NO. Thus, as typical damage biomarkers, NO and Hsps may play special roles in chicken erythrocyte injury by Se deficiency.

Effect of Selenium Deficiency on Phosphorylation of the AMPK Pathway in Rats

Selenium is an important trace element for human health. Previous studies have raised concern that dietary selenium intake may change energy metabolism. AMP-activated protein kinase (AMPK) is a sensor of energy status that controls cellular energy homeostasis. We aimed to determine the effect of selenium on the phosphorylation of AMPK pathway between Se-deficient and normal Sprague-Dawley rats. Twenty-four weaning rats were fed either a Se-deficient diet (0.02mgSe/kg) or a standard diet (0.18mgSe/kg). After 109days, total serum levels of non-esterified fatty acid and total amino acids were significantly higher and the serum insulin concentration was significantly lower in Se-deficient rats than in healthy controls. Selenium concentration and the activity of glutathione peroxidase (GPx) in myocardial tissue were significantly lower in Se-deficient rats. Importantly, mRNA levels of acetyl-CoA carboxylase beta (ACACB), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and protein levels of p-AMPKα were increased in the Se-deficient group compared to normal controls (p<0.05). In conclusion, our results suggest that selenium deficiency induces changes in metabolic and molecular parameters involved in energy metabolism in the AMPK pathway.

Effects of selenium deficiency on principal indexes of chicken kidney function.

Selenium (Se) deficiency leads to many pathological changes in animals. However, there have been very few reports regarding chicken tissue injury in the kidney caused by Se deficiency. In this study, a chicken Se-deficient disease model has been constructed, and two renal function indexes [including creatinine (CREA) and uric acid (URIC)], seven renal antioxidative function indexes [including glutathione peroxidase (GPx), anti-hydroxyl radical (AHR), catalase (CAT), hydrogen peroxide (H2O2), nitrogen monoxide (NO), glutathione (GSH), and malonyldialdehyde (MDA)], and two organ/tissue injury-related indexes [including inducible nitric oxide synthase (iNOS) and inducible heme oxygenase (HO)-1] were detected and analyzed to investigate the effects of Se deficiency on chicken kidney tissue. The results showed that Se deficiency caused a significant increase in CREA and URIC levels and a decrease in renal antioxidative capacity. Meanwhile, Se deficiency upregulated the expression of organ/tissue injury-related genes, such as the messenger RNA (mRNA) of HO-1 and iNOS as well as their protein expression levels, in the chicken kidney tissue. These data suggest that Se deficiency in birds triggers renal function regression and oxidative stress in the kidney tissue.

Abstract PL01-05: Selenium, genes, and cancer prevention

Abstract Oxidative stress caused by reactive oxygen species (ROS) enhances tumor carcinogenesis whereas dietary antioxidants such as selenium may protect against this process. Numerous epidemiological studies have suggested an inverse association of selenium levels (measured in blood or toenails) with prostate cancer risk. In 1996, the Nutritional Prevention of Cancer (NPC) trial reported a significant 65% reduction in prostate cancer incidence in men receiving selenium supplementation of 200 mg daily. However, 12 years later, SELECT (the Selenium and Vitamin E Cancer Prevention Trial) found that neither selenium (200 mg daily) nor vitamin E supplementation, alone or in combination, had any effect on incidence of prostate cancer. The null results of SELECT and the concurrent Physicians’ Health Study II trial of vitamin E, together with other previous vitamin supplementation trials, raised concerns about the benefit of nutritional supplements for reducing cancer risk and all-cause mortality. How can we interpret these apparently inconsistent results for selenium and prostate cancer across different studies over the past two decades? Several questions arise. First, can selenium function as a chemopreventive agent? Selenium is an essential trace element and plays a pivotal role in normal physiology. Many experimental and population studies have demonstrated that low selenium status was associated with increased risk of prostate cancer whereas supplementation prevented the cancer, as shown by the NPC trial. One key question is “who is most likely to benefit from the intervention?” This group could include men with low baseline levels of selenium as well as men with a genetic predisposition for greater sensitivity to the ill effects of selenium deficiency. It is well known that there is a narrow range between selenium deficiency and toxicity, and a U-shape effect has been suggested by animal experiments. Indeed, even the first prospective study published in 1983 by Willett, Stampfer, and colleagues showed an apparent threshold in the association between selenium status and cancer; only individuals in the lowest quintile of serum selenium had a significantly increased risk of cancer. This observation was subsequently supported by several prospective studies of prostate cancer and selenium levels measured either in blood or toenails. The NCP trial further confirmed that Se supplementation was beneficial but only among those whose baseline selenium level was below 123 ng/ml. Interestingly, 75% of the subjects enrolled in SELECT had initial plasma levels of selenium higher than this level. Our recent research of genetic polymorphisms on antioxidant pathways such as manganese superoxide dismutase (MnSOD) and 15-kDa selenoprotein (Sep15) further demonstrated that common variants in certain antioxidant genes may influence both the development and progression of prostate cancer by modifying the effects of plasma selenium and other antioxidants, suggesting the possibility that some men may benefit more from antioxidants than others depending on their genotypes. These findings could explain why large randomized trials have failed to show any meaningful results in cancer prevention. Finally, when in the process of tumorigenesis might selenium chemoprevention be effective? It remains unclear at what stage of prostate cancer (initiation or progression) selenium can be most effective. Given our observation of selenium and advanced prostate cancer or cancers with high baseline PSA, it could be that selenium protects against tumor progression. This could largely explain the null effect of selenium on incident prostate cancer in the SELECT trial, in which 86% of men reported receiving PSA tests each year and 98.9% of prostate cancers were localized diseases. The fact that many PSA-detected prostate cancers are indolent and may never turn out to be life-threatening diseases, and that the short follow-up time of SELECT relative to the lead time provided by PSA testing, could also explain the null effect of selenium observed in the SELECT trial. In summary, a better understanding of selenium biology requires additional mechanistic, genetic and genomic approaches, a better characterization of high-risk prostate cancer in the era of PSA screening, which should be informative in designing future clinical studies that could target on a subset of the high-risk population with a certain disease state or selenium status, or even on individuals of a certain genotype, that can benefit most from this micronutrient. Citation Information: Cancer Prev Res 2010;3(12 Suppl):PL01-05.

Effect of selenium deficiency on the status of the antioxidant protection system of cows during pregnancy and obstetric pathology

The effect of blood selenium deficiency on the state of the enzymatic component of the antioxidant system and intensity of free-radical lipid oxidation processes in different periods of the reproduction of cows is studied. It is established that a selenium deficiency causes a decrease in the potential of the glutathione component of the antioxidant system.

Effect of selenium deficiency on the antioxidative status and muscle damage in growing turkeys

An experiment investigated the effect of different selenium supplementations on the antioxidant defence system and on the occurrence of muscle dystrophy in growing turkeys. Newly hatched male turkeys (B.U.T. Big 6) were divided into eight groups of 18 turkeys each and fed either a basal diet (selenium <0.010 mg/kg diet), or the basal diet supplemented with 0.10; 0.15; 0.20; 0.25; 0.30; 0.35 or 0.40 mg selenium/kg diet in the form of sodium selenate. Vitamin E was adequately supplemented in all diets. After 35 days, muscle damage parameters including aspartate aminotransferase, creatine kinase, creatine kinase M and B were significantly increased in the selenium deficient Group I. A significant reduction of weight gain, feed consumption and selenium dependent glutathione peroxidase activity was also observed in the liver of selenium deficient birds. The ratio of oxidised glutathione (GSSG) to total glutathione (tGSH) was substantially altered in the selenium deficient Group I as well as in Group II (0.10 mg selenium/kg feed). The activity of glutathione reductase (GR) and glutathione-S-transferase (GST) was not affected by selenium deficiency.

Testing the Hypothesis that Selenium Deficiency is a Risk Factor for Clozapine-Induced Agranulocytosis in Rats

Clozapine is an effective atypical antipsychotic associated with a relatively high incidence of drug-induced agranulocytosis. It forms a reactive nitrenium ion metabolite upon oxidation by peripheral neutrophils and their precursors in the bone marrow. Although the mechanism of this idiosyncratic drug reaction is still unknown, the observation that it does not occur rapidly on rechallenge of patients with a history of clozapine-induced agranulocytosis suggests that it is not immune-mediated. Previous studies by other research groups had found that patients on clozapine had lower plasma and red blood cell levels of selenium. The reactive metabolite of clozapine reacts with glutathione, and therefore, it is likely that it also binds to selenocysteine-containing proteins, such as glutathione peroxidase, thioredoxin reductase, and protein disulfide isomerase. We set out to test the hypothesis that clozapine-induced agranulocytosis is associated with selenium deficiency with rats on a selenium-deficient diet. We studied the effects of clozapine on selenium levels and the effect of selenium deficiency on leukocyte and neutrophil counts and clozapine covalent binding. We did not observe any significant difference between clozapine-treated rats given a selenium-adequate or deficient diet. Therefore, it is unlikely that selenium deficiency is a major risk factor for clozapine-induced agranulocytosis.

Effects of selenium deficiency on fatty acid metabolism in rats fed fish oil-enriched diets

The hepatic fatty acid metabolism was investigated in rats stressed by selenium deficiency and enhanced fish oil intake. Changes in the composition of lipids, peroxides, and fatty acids were studied in the liver of rats fed either a Se-deficient (8 μg Se/kg) or a Se-adequate (300 μg Se/kg) diet, both rich in n-3 fatty acid-containing fish oil (100 g/kg diet) and vitamin E (146 mg alpha-tocopherol/kg diet). The two diets were identical except for their Se content. Se deficiency led to a decrease in hair coat density and quality as well as to changes in liver lipids, individual lipid fractions and phospholipid fatty acid composition of the liver. The low Se status did reduce total and reduced glutathione in the liver but did not affect the hepatic malondialdehyde level. In liver phospholipids (PL), Se deficiency significantly reduced levels of palmitic acid [16:0], fatty acids of the n-3 series such as DHA [22:6 n-3], and other long-chain polyunsaturates C-20–C-22, but increased n-6 fatty acids such as linoleic acid (LA) [18:2 n-6]. Thus, the conversion of LA to arachidonic acid was reduced and the ratio of n-6/n-3 fatty acids was increased. As in liver PL, an increase in the n-6/n-3 ratio was also observed in the mucosal total fatty acids of the small intestine. These results suggest that in rats with adequate vitamin E and enhanced fish oil intake, Se deficiency affects the lipid concentration and fatty acid composition in the liver. The changes may be related to the decreased levels of selenoenzymes with antioxidative functions. Possible effects of Se on absorption, storage and desaturation of fatty acids were also discussed.

Effect of selenium deficiency on ovine immune status, free radicals production and its correlation to disease occurrence

Effect of selenium deficiency on ovine immune status, free radicals production and its correlation to disease occurrence

Selenium and thyroid function in infants, children and adolescents.

Selenium is an integral component of the enzymes glutathione peroxidase (GPx) and iodothyronine deiodinases. Although selenium nutrition could conceivably affect thyroid function in infants, children and adolescents, available data suggest that the effect of selenium deficiency on thyroid function is relatively modest. In patients with isolated selenium deficiency (such as patients with phenylketonuria receiving a low-protein diet), peripheral thyroid hormone metabolism is impaired but there are no changes in thyrotropin (TSH) or clinical signs of hypothyroidism, suggesting that these patients are euthyroid. Selenium supplementation may be advisable to optimize tissue GPx activity and prevent potential oxidative stress damage. In areas where combined selenium and iodine deficiencies are present (such as endemic goiter areas in Central Africa), selenium deficiency may be responsible for the destruction of the thyroid gland in myxoedematous cretins but may also play a protective role by mitigating fetal hypothyroidism. In these areas, selenium supplementation should only be advocated at the same time or after iodine supplementation. In patients with absent or decreased production of thyroid hormones and who rely solely on deiodination of exogenous L-thyroxine for generation of the active triiodothyronine (such as patients with congenital hypothyroidism), selenium supplementation may optimize thyroid hormone feedback at the pituitary level and decrease stimulation of the residual thyroid tissue.

Selenite and Selenomethionine Promote HL-60 Cell Cycle Progression

The essential role of selenium (Se) in nutrition is well established. The elucidation of the mechanisms by which selenium regulates the cell cycle can lead to a better understanding of the nature of selenium's essentiality and its role in disease prevention. In this study, the effects of selenium deficiency or adequacy (0.25 micromol/L selenite or selenomethionine) on HL-60 cell cycle progression were examined in serum-free media. Selenium was critical for promotion of HL-60 cell growth. Cell-cycle analysis revealed that selenium deficiency caused a decrease in G1 phase cells that corresponded to an increase in G2 and sub-G1 phase cells. Gene array analysis suggested that c-Myc, cyclin C, proliferating cell nuclear antigen, cyclin-dependent kinase (cdk)1, cdk2, cdk4, cyclin B and cyclin D2 mRNA levels were lower in selenium-deficient cells than in the cells supplemented with 0.25 micromol/L selenomethionine. The decrease in the c-Myc mRNA level in selenium-deficient cells was confirmed by reverse transcription-polymerase chain reaction analysis. Furthermore, the phosphorylation state of total cellular protein was higher (57%) in selenium-supplemented cells than in selenium-deficient cells. Collectively, these results suggest a novel role for selenium at 0.25 micromol/L in up-regulation of the expression of numerous cell cycle-related genes and total cellular phosphorylated proteins in HL-60 cells in serum-free culture media. This leads to the promotion of cell cycle progression, particularly G2/M transition and/or the reduction of apoptosis, primarily in G1 cells. These observations may have additional implications for understanding the nature of selenium's essentiality.

Effect of a Selenium-Deficient Diet on Blood Values of T3 and T4 in Cows

Pastures in the south of Chile have been shown to be selenium deficient, and as selenium is a component of deiodinase type 1, which is necessary for the synthesis of triiodothyronine (T3) at peripheral levels, the effect of selenium deficiency on the blood concentration of theses hormones in cows was studied. Twelve pregnant Friesian cows were randomly allocated into two homogeneous groups of six animals each - selenium supplemented and selenium deficient. The selenium deficient diet consisted of 11.5 kg of hay, 500 g of soya bran, 150 g of mineral mix (without selenium), 500 g of fat for animal feeding, and was given from day 15 of lactation until the end of the study. A commercial concentrate (Cosetan) and urea was also given according to lactation requirements (up to 5 kg and up to 120 g, respectively). The selenium content was 0.05 ppm of dry matter (equivalent to 18% of the daily requirements). The supplemented group was injected subcutaneously with 1 mg Se/kg, using the commercial product Deposel (1 ml/50kg). Blood samples were obtained by coccygeous vein venepuncture before supplementation (prepartum basal values) and thereafter every 15 days. GSH-Px activity in plasma was measured using a HITACHI 4020 spectrophotometer. Serum T3 and thyroxine (T4) concentrations were measured by electrochemiluminiscence. ANOVA, Tuckey test and Student’s t-test were used to establish the significance of the intra group differences, with p=<0.05 being considered significant. There were no significant differences in blood values of T4 in either the supplemented or non-supplemented groups during pregnancy and lactation. However the blood values of T4 decreased significantly (p=<0.05) during days 30–60 of lactation to values below the reference range. The T3 serum concentrations in the supplemented group of cows were significantly lower (p=<0.05) at 60, 90 and 150 days of lactation than cows that had been supplemented with selenium.

Selenium and thyroid hormone metabolism

Selenium is an essential trace element for both men and animals at lower concentrations and has toxic effects at higher concentrations. The element’s essentiality was first recognised in 1957. Low bioavailability could be contributing to cancers, cardiovascular disease, and subfertility. Selenium and its compounds are widely used in stainless steel production, as a pigment in ceramics, vulcanizing agent of rubber, lubricants, fungicides, medicines used in dermatology and in radionulide imaging of the pancreas. Selenium’s annual world production is estimated at 1,350 tonnes. In the last decade selenium was shown to be an essential component of type I oidothyronine 5’ deiodinase which converts tyroxin to the more biologically active hormone 3,5,3’‐triiodothyronine. The function of selenium in thyroid hormone metabolism has important implications for the interpretation of the effects of selenium deficiency, especially in an elderly population. The population of the elderly has grown in numbers during recent years, throughout the world. The thyroid gland function in a great measure defines the quality of life in elderly people. The purpose of this review is to show the role of selenium in thyroid hormone metabolism.

Effects of selenium deficiency on expression of selenoproteins in bovine arterial endothelial cells.

Damage to the vascular endothelium by reactive oxygen species causes many cardiovascular diseases including atherosclerosis. Such damage can be prevented by selenium (Se), which is thought to exert its actions mainly through the expression of selenoproteins. Se deficiency increased the susceptibility to tert-butylhydroperoxide (t-BuOOH) and enhanced lipid peroxidation in bovine arterial endothelial cells (BAEC). We investigated the effects of Se deficiency on the expression of the selenoproteins in BAEC. 75Se metabolic labeling analysis and RT-PCR analysis revealed that BAEC expressed two glutathione peroxidase (GPx) isozymes, cytosolic GPx (cGPx) and phospholipid hydroperoxide GPx (PHGPx), three thioredoxin reductase (TrxR) isozymes, TrxR1, TrxR2 and TrxR3, and selenoprotein P (SelP). Se deficiency reduced both enzyme activity and mRNA level of cGPx, but did not affect those of PHGPx. SelP mRNA level was also reduced by Se deficiency, although the extent of reduction was much smaller than that of cGPx mRNA. We further found that TrxR activity was also decreased by Se deficiency but none of the mRNA levels of TrxR isozymes were reduced. These results indicate that vascular endothelial cells express several selenoproteins including cGPx, PHGPx, TrxR isozymes and SelP which might play important roles in the defense system against oxidative stresses and that the expressions of these selenoproteins are differently regulated by Se status.