Tissue Selenium Levels Research Articles

Effect of Supranutritional Dosage Selenium in Neonatal Goat Kids on Productive Performance, Physicochemical Profiles in Meat, Selenium Levels in Tissues, and Histopathological Findings.

Selenium (Se) is an essential element and antioxidant that catalyzes the destruction of hydrogen peroxide formed during cellular oxidative metabolism. Doses of Se as selenomethionine (SeMe) by oral route are 0.1-0.3 mgSe/kg DM, while the dose by parenteral route with sodium selenite (Na2SeO3) is 0.1 mgSe/BW. The effects of supranutritional Se supplementation on normal kids have rarely been studied. The objective of the study was to evaluate both Se sources on growth performance, Se in tissues, histopathological findings, and meat characteristics.Forty-five kids of the Pastoreña breed with 25-day age were distributed (4.7 ± 1.13kg) in three treatments: a) control group, C: consumption with goat milk (GM: containing 0.135mgSe/g); b) NaSe: GM plus Na2SeO3 injectable, 0.25 mgSe/kg BW; c) SeMe: GM plus oral dosage, 0.3mgSe as SeMe daily. Fifteen animals per treatment were slaughtered at 7, 14, and 21days.Feed conversion improved (P < 0.05) with Se supplement (P < 0.05) at 7 and 14days. SeMe had higher protein and fat meat content (P < 0.05). SeMe increased Se liver at 14 and 21days. NaSe and SeMe had higher (P < 0.05) levels of Se kidney. SeMe-21d showed 42% mononuclear and periportal cell infiltration lesions. In conclusion, Se administered through milk in goat kids was insufficient to prevent nutritional muscular dystrophy. The supranutritional dose of 0.25mg/kg as NaSe was sufficient to maintain the Se level in tissues. SeMe increased Se liver and kidney efficiently. Both Se sources improved the bioavailability of the mineral in kids.

Effects of Tauroursodeoxycholic Acid and 4-Phenylbutyric Acid on Selenium Distribution in Mice Model with Type 1 Diabetes

The effect of selenium on diabetes is significant. As pharmaceutical chaperones, tauroursodeoxycholic acid (TUDCA) and 4-phenylbutyric acid (4-PBA) can effectively improve the oxidative stress of the endoplasmic reticulum. This study established a mice model with type 1 diabetes (T1D) to evaluate the effects of pharmaceutical chaperones on selenium distribution. Streptozotocin was used to induce Friend virus B-type mice to establish a T1D mice model. Mice were administered with TUDCA or 4-PBA. Selenium levels in different tissues were measured by inductively coupled plasma-mass spectroscopy (ICP-MS). After treatment with TUDCA and 4-PBA, related laboratory findings such as glucose and glycated serum protein were significantly reduced and were closer to normal levels. At 2 weeks, 4-PBA normalized selenium levels in the heart, and 4-PBA and TUDCA maintained the selenium in the liver, kidney, and muscle at normal. At 2 months, 4-PBA and TUDCA maintained the selenium in the heart, liver, and kidney at normal levels. The serum selenium had a positive correlation with zinc and copper in the diabetes group and the control group, while the serum selenium had no significant association with magnesium and calcium at 2 weeks and 2 months. TUDCA and 4-PBA have crucial effects on selenium distribution in diabetic mice, and further research is needed to research their internal mechanisms.

Kidney tissue selenium levels of Toxocara canis infected mice given Nigella sativa

Nigella sativa (NS) has a protective effect on cellular damage caused by oxidative stress. Selenium has an antioxidative effect. Toxocara canis is one of the nematodes causing visceral larva migrans. Men infected with this parasite ingesting an embryonic egg. It is more common in children between 1-4 years than adults. From the ingested embryonic egg, the larvae released in the small intestine and they migrate to so many organs such as liver, spleen, kidney, lung, brain, retina of the eye, pancreas and causing lesions. In particular, it is known to cause intense damage to kidney tissue. In this study mice with Toxocara canis infection were administered Nigella sativa in prophylactic and treatment doses (100 and 200 mg/kg body weight) and selenium levels were determined in their kidney tissues. In the healthy control group, kidney selenium levels were 980,46±236,68 ng/g and in mice infected with Toxocara canis 1240,15±315,77 ng/g. Kidney tissue Se levels of mice given NS in two different doses for treatment (Treated N100, Treated N200) and prophylaxis (Prophylactic N100 and ProphylacticN200) respectively are 1297,95±354,37; 1361,29±410,46 ng/g; 1148,55±240,28 ng/g and 1465,81±450,25 ng/g. Kidney tissue selenium levels were high in both treatment and prophylaxis dose NS given mice. In conclusion, Nigella sativa can cause increases in kidney tissue selenium levels depends on given doses.

Variation in Blood and Colorectal Epithelia's Key Trace Elements Along with Expression of Mismatch Repair Proteins from Localized and Metastatic Colorectal Cancer Patients.

Colorectal cancer (CRC) is an increasingly common medical issue affecting millions worldwide, and contribution of the body's trace elements to CRC is arguable. The concentrations and buffered status of selenium, iron, copper, zinc, and phosphorus in blood and large intestinal tissues of CRC patients are, respectively, variable and vital for cell physiology. The aim of this study was to assess selenium, iron, copper, zinc, and phosphorus variations in blood and colorectal epithelia along with examining the expression of mismatch repair proteins in CRC patients with/without metastasis for potential diagnosis/therapy. Concentrations of selenium, iron, copper, zinc, and phosphorus in blood of healthy versus CRC patients and colorectal epithelia (adenocarcinomatous versus non-adenocarcinomatous/control) were measured in 40 CRC patients (55.87 ± 11.9years old) with/without metastasis before surgery using ICP-OES. Mismatch repair (MMR) protein expression was analyzed through histopathological/immunohistochemistry assays, which was sparse in 5 CRC patient's colorectal tissues (12%). Compared with healthy individuals, blood and colorectal tissue's levels of phosphorus, copper, and iron were significantly higher in the CRC patients, and more pronounced in metastatic CRC patients; conversely, blood and colorectal tissue's selenium levels were significantly lower in metastatic patients. Unlike blood zinc, cancerous colorectal tissue's zinc concentration was significantly lower in CRC patients compared to healthy control cohorts. There was no significant difference on the measured elements in samples from CRC patients with MMR- compared to CRC patients with MMR+. Receiver operating characteristic analysis revealed a correlation of blood iron, zinc, copper, and phosphorus to CRC, and inappropriately low levels of blood and colorectal selenium correlated with exacerbated metastasis. Altered levels of selenium, iron, copper, zinc, and phosphorus in vivo may impact the pathogenesis and detection of CRC, and their diagnostic/therapeutic potential in CRC would be revealing.

Brain Selenium in Alzheimer's Disease (BRAIN SEAD Study): a Systematic Review and Meta-Analysis.

Oxidative stress has been found to be implicated in the development of Alzheimer's disease (AD). In this meta-analytic review, we compared tissue levels between AD and non-AD brains of selenium, an important biological trace element well known for its vital role in the brain function. We included 14 studies with 40 observations on selenium concentrations in AD and control brains. The effect size as standardized mean difference (SMD) was generated using review manager 5.3. Random-effects meta-analysis indicated a decrease (SMD = - 0.42) in brain tissue selenium levels in AD as compared to non-AD controls. The subgroup meta-analysis demonstrated that the selenium levels were decreased in the temporal, hippocampal, and cortex regions in AD. The funnel plot with Egger's (p = 0.88) and Begg's tests (p = 0.24) detected no significant publication bias. The results of sensitivity analysis indicated that no single study/observation had significantly influenced the overall outcome. This meta-analysis provides consolidated evidence for a significant decrease of selenium status in AD brains compared to controls. In line with the evidence supporting selenium's antioxidant role and the involvement of oxidative stress in AD development, this meta-analysis supports new therapeutic strategies aimed at brain tissue selenium homeostasis in AD.

Toxicokinetics of selenium in the slider turtle, Trachemys scripta.

Selenium (Se) is an essential element that can be harmful for wildlife. However, its toxicity in poikilothermic amniotes, including turtles, remains poorly investigated. The present study aims at identifying selenium toxicokinetics and toxicity in juvenile slider turtles (age: 7months), Trachemys scripta, dietary exposed to selenium, as selenomethionine SeMet, for eight weeks. Non-destructive tissues (i.e. carapace, scutes, skin and blood) were further tested for their suitability to predict selenium levels in target tissues (i.e. kidney, liver and muscle) for conservation perspective. 130 juvenile yellow-bellied slider turtles were assigned in three groups of 42 individuals each (i.e. control, SeMet1 and SeMet2). These groups were subjected to a feeding trial including an eight-week supplementation period SP 8 and a following 4-week elimination period EP 4 . During the SP8, turtles fed on diet containing 1.1±0.04, 22.1±1.0 and 45.0±2.0µgg(-1) of selenium (control, SeMet1 and SeMet2, respectively). During the EP4, turtles fed on non-supplemented diet. At different time during the trial, six individuals per group were sacrificed and tissues collected (i.e. carapace, scutes, skin, blood, liver, kidney, muscle) for analyses. During the SP8 (Fig.1), both SeMet1 and SeMet2 turtles efficiently accumulated selenium from a SeMet dietary source. The more selenium was concentrated in the food, the more it was in the turtle body but the less it was removed from their tissues. Moreover, SeMet was found to be the more abundant selenium species in turtles' tissues. Body condition (i.e. growth in mass and size, feeding behaviour and activity) and survival of the SeMet1 and SeMet2 turtles seemed to be unaffected by the selenium exposure. There were clear evidences that reptilian species are differently affected by and sensitive to selenium exposure but the lack of any adverse effects was quite unexpected. Fig.1 Design of the feeding trial. T, Time of tissues collection in weeks. The feeding trial included a supplementation period of 8weeks (i.e. SP8) followed by an elimination period of 4 weeks (i.e. EP4). Six turtles from each turtle group (i.e. control, SeMet1 and SeMet2) were sacrifice at each collection time, from T1 to T12. At T0, four turtles were sacrificed.

Selenide Targets to Reperfusing Tissue and Protects It From Injury*

Since blood selenium levels decrease after ischemia and reperfusion injury, and low blood selenium correlates with negative outcome, we designed and performed experiments to determine how selenium distribution is affected by ischemia reperfusion injury. Furthermore, we tested whether different chemical forms of selenium would affect outcome after ischemia and reperfusion injury. We also examined the metabolic effects of selenide administration. Laboratory investigation. Animal research laboratory. Adult male C57BL/6 mice. To determine selenium localization, we administered tracer doses of radioactive selenium 75 in the form of selenite or selenide and measured blood and tissue selenium levels after ischemia and reperfusion injury. Anesthetized mice were subjected to myocardial ischemia reperfusion injury (coronary artery occlusion for 60 min followed by 5 min of reperfusion after occlusion was removed) or hindlimb ischemia reperfusion injury (left leg tourniquet for 90 min followed by 5 min reperfusion after tourniquet removal). To determine whether exogenous selenium administration could reduce ischemia reperfusion injury, we synthesized and administered sodium hydroselenide and sodium selenite solutions (0.05-2.4 mg/kg). Solutions were administered at the end of coronary artery occlusion but before reperfusion. In order to determine the metabolic effects of selenide administration, we exposed mice to hydrogen selenide gas (0-5 ppm) mixed into air (20.95% oxygen) for up to 3 hours. In targeting assays, we measured blood and tissue selenium levels. We observed that blood selenium decreases after myocardial ischemia reperfusion and displays an inverse correlation with injury severity; selenium accumulation in heart correlates directly with injury severity. We also measured whether oxidized selenium, selenite, and reduced selenium, selenide, would target to injured heart tissue in myocardial ischemia reperfusion and injured leg muscle in a hindlimb model of ischemia reperfusion. Only selenide targets to injured tissue. We also measured damage after myocardial ischemia reperfusion injury using morphometry, neutrophil accumulation, blood cardiac troponin levels, and echocardiography and observed in all assays that selenide reduced damage to the heart; selenite was not effective. And finally, to assay metabolism, we measured oxygen consumption, carbon dioxide production, and body core temperature before, during, and after hydrogen selenide administration. All measurements indicate that selenide decreases metabolism. Selenide targets to reperfusing tissue and reduces reperfusion injury perhaps by affecting oxygen metabolism.

Comparation of Heavy Metals and Selenium Contents in The Digestive Gland and Gills of Mytilus galloprovincialis (Lamarck, 1819) Caught in Izmir Bay (Turkey)

Objective: The aim of this study was to evaluate heavy metals (Cr, Fe, Ni, Cu, Zn, As, Cd, Hg, Pb) and selenium levels in digestive gland and gill tissues of wild Mediterranean mussel Mytilus galloprovincialis (Lamarck, 1819) collected from four locations in Izmir Bay. Methods: A total of 180 samples of the wild Mediterranean mussel M. galloprovincialis with shell length of 50-60 mm were collected from four locations. Inductively coupled plasmamass spectroscopy was used to determine heavy metals and selenium concentrations in mussel samples after microwave digestion process. Results: The highest values (mg kg-1 dry weight) obtained for digestive gland and gills were 0.17 and 0.15 for Cr, 28.62 and 29.49 for Fe, 0.25 and 0.29 for Ni, 2.53 and 1.78 for Cu, 18.52 and 22.03 for Zn, 1.26 and 1.08 for As, 0.04 and 0.04 for Cd, 0.02 and 0.02 for Hg, 0.19 and 0.16 for Pb, 0.40 and 0.48 for Se, respectively. Statistically significant differences among digestive gland and gills (p<0.05) were found for Cr, Ni, Zn, As, Se and Cd. In general, the

Development of a Sol Particle Homogeneous Immunoassay for Measuring Full‐Length Selenoprotein P in Human Serum

Selenoprotein P (SeP), a selenium-rich extracellular glycoprotein, is the primary selenoprotein in the plasma. SeP plays an important role in the maintenance of selenium levels in the peripheral tissues. We developed a new sol particle homogeneous immunoassay (SPIA) for measuring full-length SeP (FL-SeP) levels in the human serum. We used colloidal gold particles coated with two types of anti-SeP monoclonal antibodies, one recognizing the N-terminal side domain of SeP and the other recognizing the C-terminal side domain. The assay range was 0.2-9 mg/l, and the linearity was excellent. The within-day and between-day coefficients of variation ranged from 0.73% to 2.24% and 0.45% to 1.11%, respectively. Serum samples (n = 200) were examined using the newly developed assay system (employing a Model 7070 Hitachi automatic clinical analyzer) and the conventional enzyme-linked immunosorbent assay. These two methods were compared using the Passing-Bablok regression analysis; the resulting regression equation and correlation coefficient were y = 0.940x + 0.165 and r = 0.954, respectively. Our new SPIA assay is a fully automated homogeneous immunoassay that can be used in conjunction with various commercial analyzers. The assay was sensitive, precise, and suitable for clinical measurement of the FL-SeP in the human serum.

Gene expression profiling reveals differential effects of sodium selenite, selenomethionine, and yeast-derived selenium in the mouse

The essential trace mineral selenium is an important determinant of oxidative stress susceptibility, with several studies showing an inverse relationship between selenium intake and cancer. Because different chemical forms of selenium have been reported to have varying bioactivity, there is a need for nutrigenomic studies that can comprehensively assess whether there are divergent effects at the molecular level. We examined the gene expression profiles associated with selenomethionine (SM), sodium selenite (SS), and yeast-derived selenium (YS) in the intestine, gastrocnemius, cerebral cortex, and liver of mice. Weanling mice were fed either a selenium-deficient (SD) diet (<0.01 mg/kg diet) or a diet supplemented with one of three selenium sources (1 mg/kg diet, as either SM, SS or YS) for 100 days. All forms of selenium were equally effective in activating standard measures of selenium status, including tissue selenium levels, expression of genes encoding selenoproteins (Gpx1 and Txnrd2), and increasing GPX1 enzyme activity. However, gene expression profiling revealed that SS and YS were similar (and distinct from SM) in both the expression pattern of individual genes and gene functional categories. Furthermore, only YS significantly reduced the expression of Gadd45b in all four tissues and also reduced GADD45B protein levels in liver. Taken together, these results show that gene expression profiling is a powerful technique capable of elucidating differences in the bioactivity of different forms of selenium.Electronic supplementary materialThe online version of this article (doi:10.1007/s12263-011-0243-9) contains supplementary material, which is available to authorized users.

Determination of selenium status using the nail biologic monitor in a canine model

Toenails and fingernails are routinely used to estimate selenium status in epidemiological studies; however, literature validating nail selenium concentration as a surrogate for critical organs is limited. In this study diets of intact male dogs were selenium supplemented at two physiological levels (3 and 6 μg/kg/day) in two different forms, selenomethionine and selenium-enriched bioformed yeast. The selenium-adequate basal diet consumed by the treatment and control groups during the 4-week run-in period and throughout the trial contained 0.3 ppm selenium. After 7 months the dogs in the two treatment groups and the control group were euthanized. Representative tissue samples from prostate, brain, liver, heart and skeletal muscle were collected, rinsed and frozen. Toenail clippings from multiple toes were also collected. Selenium was determined by neutron activation analysis using Se77m (half life = 17.4 s) at the University of Missouri Research Reactor Center. NIST SRM 1577, Bovine Liver was analyzed as a quality control. The analysts were blinded to control and treatment group assignments. As expected, tissue selenium levels increased proportionally with supplementation. A slightly greater increase in tissue selenium was observed for the purified selenomethionine compared to the bioformed yeast; however this trend was significant only for brain tissue. Toenail selenium concentrations and tissue selenium were highly correlated (p < 0.003) with Pearson coefficients of 0.759 (skeletal muscle), 0.745 (heart), 0.729 (brain), 0.723 (prostate), and 0.632 (liver). The toenail biologic monitor accurately assesses selenium status in skeletal muscle, heart, brain, prostate, and liver in the canine model.

Whole blood selenium levels (WBSL) in patients with prostate cancer (PC), benign prostatic hyperplasia (BPH) and healthy male inhabitants (HMI) and prostatic tissue selenium levels (PTSL) in patients with PC and BPH

Background. The aim of this exploratory study was to evaluate whether significant differences exist between whole blood selenium levels (WBSL) in patients with prostate cancer (PC), benign prostatic hyperplasia (BPH), healthy male inhabitants (HMI) in northern Bavaria and the normal value. Furthermore, we investigated whether differences exist between prostatic tissue selenium levels (PTSL) in patients with PC, BPH and the benign tissue surrounding the PC. Material and methods. We prospectively evaluated WBSL in 24 patients with PC, 21 patients with BPH, and 21 HMI. Measurements of PTSL were performed in 17 patients with PC and 22 patients with BPH. In 9 cases with PC, measurements were also done in the benign tissue surrounding the carcinoma. Measurements were performed using automated graphite furnace atomic absorption spectrophotometry. Results. In patients with PC, there is a significantly lower WBSL in comparison to HMI (p=0.04). There is no significant difference in WBSL between BPH-patients and HMI (p=0.13) and between PC- and BPH-patients (p=0.67). In all patients and the HMI, there is a significantly lower WBSL in comparison to the recommended normal value of 85 – 162 µg/l (p<0.01). There is no significant difference in PTSL between PC and BPH (p=0.49), and between PC and the tissue compartment surrounding the PC (p=0.56). PTSL seemed to be reduced in the compartment surrounding the PC in comparison to BPH (p=0.03). In PC-patients, there is no significant correlation between WBSL and prostate specific antigen (PSA) (?=−0.20; p=0.36), Gleason score (?=0.32, p=0.13), and T-stage (?=0.22; p=0.23). Conclusion. Since the WBSL measured in all men with PC and BPH, and in HMI participating in our study were significantly lower than the recommended normal range, our findings may support the recommendation of selenium supplementation.

Postmitotic tissue selenium and manganese levels in alpha-lipoic acid-supplemented aged rats

Redistribution of selenium and manganese in postmitotic tissues of alpha-lipoic acid-supplemented aged rats has been proposed to contribute to metal-catalyzed protein oxidation. dl-Alpha-lipoic acid (LA) (100 mg/[kg body wt. day]) was administered intraperitoneally to the Sprague–Dawley rats for 14 days. Serum selenium levels were lowered in the aged rats with LA supplementation compared with those of the rats without LA supplementation. Similarly, the selenium levels of the heart, brain and muscle were found to be significantly lower in LA-supplemented rats when compared to control rats. On the other hand, serum manganese levels were not changed in the aged rats with LA supplementation compared with those of the rats without LA supplementation. The heart manganese levels detected in LA-supplemented rats were significantly lower than controls. Manganese levels of the brain and muscle tissues were increased in the aged rats with LA supplementation compared with those of the rats without LA supplementation. Based on the findings of our study, we conclude that LA may exhibit pro-oxidant effect depending on the altered selenium and manganese homeostasis. Thus, our results stress the importance of monitoring the dose of LA supplementation and serum selenium levels, duration of treatment and its potential harmful pro-oxidant effects in the postmitotic tissues of aged rats.

Larval Deformities Associated with Selenium Accumulation in Northern Pike (Esox lucius) Exposed to Metal Mining Effluent

The objective of this study was to investigate selenium toxicosis in larval northern pike (Esox lucius) originating from reproductively mature pike collected downstream of a uranium milling operation in northern Saskatchewan, Canada. Eggs were obtained from female pike collected from a reference site and three sites representing an exposure gradient (approximately 2, 10, and 15 km downstream of effluent discharge). Embryos were incubated following a two-way (crossover) analysis of variance experimental design that allowed discrimination between effects due to maternal transfer to eggs and effects due to site water exposure in the developing embryos. The major finding of this study was a significant increase in the frequencies of individual deformities (skeletal curvatures, craniofacial deformities, and fin deformities) and edema in fry originating from high and medium exposure site females (mean selenium concentrations of 48.23 and 31.28 microg/g egg dry weight and 38.27 and 16.58 microg/g muscle dry weight, respectively) compared to reference site females. Selenium concentrations resulting in a 20% increase in total deformities above background levels (EC20S) were 33.55 and 21.54 micro/g dry weight in eggs and muscle, respectively. Mathematical conversion of the egg- and muscle-derived relationships to whole body selenium levels resulted in similar EC20S of 15.56 and 17.72 microg/g dry weight, respectively. These relationships between tissue selenium levels and larval deformities suggest that northern pike are within the same range of sensitivity to selenium as the majority of warm water (e.g., centrarchids and cyprinids) and cold water (e.g., salmonids) fish species studied to date.

Hepatic and renal tissue selenium levels in a mouse model of candidiasis

Hepatic and renal tissue selenium levels in a mouse model of candidiasis

Characteristics of selenazolidine prodrugs of selenocysteine: toxicity, selenium levels, and glutathione peroxidase induction in A/J mice

We have previously reported the synthesis and characterization of two new classes of selenazolidine-4(R)-carboxylic acids (2-oxo and 2-methyl-SCAs) (OSCA and MSCA, respectively), as well as the “parent” compound, selenazolidine-4(R)-carboxylic acid (SCA, selenaproline). These compounds were designed as prodrugs of L-selenocysteine with potential application in cancer chemoprevention or other clinical uses. We will be exploring the chemopreventive activity of the new compounds in the well-established A/J mouse model of tobacco-induced lung carcinogenesis. The objectives of the present study were to investigate several fundamental biochemical endpoints after selenazolidine administration compared with other selenium-containing agents. Groups of mice were fed either AIN-76A diet alone or the diet supplemented with the following selenium compounds (ppm Se): sodium selenite (5), L-selenomethionine (3.75), L-selenocystine (15), Se-methyl-L-selenocysteine (3), MSCA (5, 10, or 15), OSCA (5, 10, or 15), or SCA (5, 10, or 15). After 28 days of supplementation, toxicity of the selenazolidines was not evident, as measured by outward appearance and behavior, body and organ weight changes, and histological evaluation of liver and lung tissue. Select treatment groups showed significant increases in selenium levels in blood and tissues. Increased activity of selenium-dependent glutathione peroxidase (GPx) in blood and liver illustrated that the selenazolidines provided a source of biologically-available selenium.

Characteristics of selenazolidine prodrugs of selenocysteine: toxicity, selenium levels, and glutathione peroxidase induction in A/J mice

We have previously reported the synthesis and characterization of two new classes of selenazolidine-4(R)-carboxylic acids (2-oxo and 2-methyl-SCAs) (OSCA and MSCA, respectively), as well as the “parent” compound, selenazolidine-4(R)-carboxylic acid (SCA, selenaproline). These compounds were designed as prodrugs of L-selenocysteine with potential application in cancer chemoprevention or other clinical uses. We will be exploring the chemopreventive activity of the new compounds in the well-established A/J mouse model of tobacco-induced lung carcinogenesis. The objectives of the present study were to investigate several fundamental biochemical endpoints after selenazolidine administration compared with other selenium-containing agents. Groups of mice were fed either AIN-76A diet alone or the diet supplemented with the following selenium compounds (ppm Se): sodium selenite (5), L-selenomethionine (3.75), L-selenocystine (15), Se-methyl-L-selenocysteine (3), MSCA (5, 10, or 15), OSCA (5, 10, or 15), or SCA (5, 10, or 15). After 28 days of supplementation, toxicity of the selenazolidines was not evident, as measured by outward appearance and behavior, body and organ weight changes, and histological evaluation of liver and lung tissue. Select treatment groups showed significant increases in selenium levels in blood and tissues. Increased activity of selenium-dependent glutathione peroxidase (GPx) in blood and liver illustrated that the selenazolidines provided a source of biologically-available selenium.

Increasing human intake of selenium by supplementing food animals with organic selenium

The concentration of global crop and food animal production in regions where plant selenium content is low has led to a decline in the amount of selenium in the human food supply. The central reason is that where soil pH is acidic, selenium cannot be absorbed by plants, thereby preventing transfer of selenoamino acids up the food chain through cereal grains and food animal products. Direct addition of inorganic selenium salts prevents acute deficiency symptoms, however selenium salts added to food animal diets do not provide meaningful amounts of selenium in edible animal tissues. Because human selenium status is a public health concern, researchers have examined nutritional means of increasing the selenium content of meat, milk and eggs using selenium produced by yeast, which like higher plants are able to form selenoamino acids. While part of the focus is on producing ‘designer’ foods, a more general question pertains to both existing selenium levels in food animal products and to those when commercial food animals are given selenium in naturally-occurring organic vs inorganic form. The following summarizes selenium levels in edible tissues in commercial and controlled research settings where inorganic and organic (Sel-PlexTM selenium yeast, Alltech Inc.) were compared.

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

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

Plasma and gastric tissue selenium levels in patients with Helicobacter pylori infection.

We investigated plasma and gastric mucosal selenium levels in patients with Helicobacter pylori (HP)-associated histopathologic findings in their gastric antral mucosa. Before and after a successful HP eradication therapy, we quantitated the plasma and antral selenium levels in patients with HP-associated chronic antral gastritis using atomic absorption flame emission spectrometry. The same measurements were done in patients with dyspeptic complaints who had normal antral histology and negative urease test. Thirty-four patients were studied, of whom 24 had HP-associated chronic antral gastritis confirmed by histology and positive urease test; the control group included 10 healthy patients. There was no difference between the groups with regard to age, gender, and number of smokers. All patients with HP infection were diagnosed with diffuse antral gastritis. Histopathology showed that 11 (49%) had some degree of atrophy. Of the 11 patients, 7 were classified as having chronic atrophic gastritis (CAG) without intestinal metaplasia (IM), 4 had IM, and none had dysplasia. The plasma concentrations of selenium were found to be very similar in controls and HP-infected subjects (68.0 +/- 25.97 microg/L and 71 +/- 32.9 microg/L, respectively; p > 0.05). The antral biopsy samples of the patients with HP-associated gastritis contained significantly higher levels of tissue selenium than the controls (20.17 +/- 19.74 microg/g and 2.83 +/- 1.42 microg/g, respectively; p < 0.05). Also, it was shown that antral tissue selenium levels decrease after successful HP eradication therapy (20.17 +/- 19.4 microg/g and 7.4 +/- 4.56 microg/g, respectively; t < 0.05). The patients with HP gastritis were assigned to mild, moderate, and severe gastritis groups, according to the histopathologic degree of inflammation present. The antral gastric selenium levels were significantly higher in patients with moderate and severe HP gastritis (21.13 +/- 22.5 microg/g and 22.81 +/- 17.35 microg/g, respectively) than in patients with mild gastric inflammation (9.53 +/- 10.3 microg/g; p < 0.05). The selenium concentrations in the biopsies of patients with CAG were significantly lower than in those with HP gastritis who did not have CAG (9.45 +/- 6.44 microg/g vs. 19.13 +/- 22.48 microg/g, respectively; p < 0.05). Selenium accumulates in gastric tissue when it is needed, as is the case in HP-related antral inflammation. This reactive increase in gastric mucosal selenium seems to disappear in the presence of precancerous gastric lesions in the setting of HP-associated gastritis.