Hepatic Se Research Articles

Selenomethionine alleviates environmental heat stress induced hepatic lipid accumulation and glycogen infiltration of broilers via maintaining mitochondrial and endoplasmic reticulum homeostasis

With the increasing of global mean surface air temperature, heat stress (HS) induced by extreme high temperature has become a key factor restricting the poultry industry. Liver is the main metabolic organ of broilers, HS induces liver damage and metabolic disorders, which impairs the health of broilers and affects food safety. As an essential trace element for animals, selenium (Se) involves in the formation of antioxidant system, and its biological functions are generally mediated by selenoproteins. However, the mechanism of Se against HS induced liver damage and metabolic disorders in broilers is inadequate. Therefore, we developed the chronic heat stress (CHS) broiler model and investigated the potential protection mechanism of organic Se (selenomethionine, SeMet) on CHS induced liver damage and metabolic disorders. In present study, CHS caused liver oxidative damage, and induced hepatic lipid accumulation and glycogen infiltration of broilers, which are accompanied by mitochondrial dysfunction, abnormal mitochondrial tricarboxylic acid (TCA) cycle and endoplasmic reticulum (ER) stress. Dietary SeMet supplementation increased the hepatic Se concentration and exhibited protective effects via promoting the expression of selenotranscriptome and several key selenoproteins (GPX4, TXNRD2, SELENOK, SELENOM, SELENOS, SELENOT, GPX1, DIO1, SELENOH, SELENOU and SELENOW). These key selenoproteins synergistically improved the antioxidant capacity, and mitigated the mitochondrial dysfunction, abnormal mitochondrial TCA cycle and ER stress, thus recovered the hepatic triglyceride and glycogen concentration. What's more, SeMet supplementation suppressed lipid and glycogen biosynthesis and promoted lipid and glycogen breakdown in liver of broilers exposed to CHS though regulating the AMPK signals. Overall, our present study reveals a potential mechanism that Se alleviates environment HS induced liver damage and glycogen and lipid metabolism disorders in broilers, which provides a preventive and/or treatment measure for environment HS-dependent hepatic metabolic disorders in poultry industry.

Environmental pollution and nutritional quality modulate immune response of the wood mouse (Apodemus sylvaticus) through hormonal disturbances

Cadmium (Cd) and lead (Pb) are known to enhance immune cell damages and to decrease cellular immunity, promoting higher susceptibility to infectious diseases. Selenium (Se) is an essential element involved in immunity and reactive oxygen species scavenging. This study aimed at evaluating how Cd and Pb and low nutritional (Se) quality modulate immune response to a bacterial lipopolysaccharide (LPS) challenge in wood mice (Apodemus sylvaticus). Mice were trapped near a former smelter in northern France in sites of High or Low contamination. Individuals were challenged immediately after capture or after five days of captivity, fed a standard or a Se-deficient diet. Immune response was measured with leukocyte count and plasma concentration of TNF-α, a pro-inflammatory cytokine. Faecal and plasma corticosterone (CORT), a stress-hormone involved in anti-inflammatory processes, was measured to assess potential endocrine mechanisms. Higher hepatic Se and lower faecal CORT were measured in free-ranging wood mice from High site. LPS-challenged individuals from High site showed steeper decrease of circulating leukocytes of all types, higher TNF-α concentrations, and a significant increase of CORT, compared to individuals from Low site. Challenged captive animals fed standard food exhibited similar patterns (decrease of leukocytes, increase of CORT, and detectable levels of TNF-α), with individuals from lowly contaminated site having higher immune responses than their counterparts from highly polluted site. Animals fed Se-deficient food exhibited lymphocytes decrease, no CORT variation, and average levels of TNF-α. These results suggest (i) a higher inflammatory response to immune challenge in free-ranging animals highly exposed to Cd and Pb, (ii) a faster recovery of inflammatory response in animals lowly exposed to pollution when fed standard food than more exposed individuals, and (iii) a functional role of Se in the inflammatory response. The role of Se and mechanisms underlying the relationship between glucocorticoid and cytokine remain to be elucidated.

The effect of feeding different sources and levels of selenium on growth performance and antioxidant status of broilers raised at two different temperatures

ABSTRACT 1. This study examined the effects of different dietary sources and levels of selenium (Se) on growth performance, hepatic and breast meat Se content, glutathione peroxidase (GSH-Px) activity and total antioxidant status (TAS) in blood, when fed to broilers from 14 to 35 d of age and reared at two different temperatures (20°C and 35°C). 2. Five hundred and sixty male Ross 308 broilers were reared in a single floor pen and fed the same proprietary starter diet from 0 to 14 d age (229.9 g/kg CP and 12.67 MJ/kg ME, without Se supplementation). 3. The experiment started at 14 d age, and the birds randomly assigned to 112 raised-floor pens (0.36 m2 area, 5 birds/pen). Each of the seven experimental diets were offered to birds in 16 pens within four rooms. Two rooms were at 20°C and two rooms were maintained at 35°C. The experimental diets were fed from 14 to 35 d age and contained 214.9 g/kg CP and 13.11 MJ/kg ME. The experimental diets were as follows; control diet containing background Se only (0.189 mg/kg; C); low level sodium selenite (0.376 mg/kg; LSS): high level sodium selenite (0.558 mg/kg; HSS); low level commercial B Traxim® Se (0.244 mg/kg) (LBT); high level B Traxim® Se (0.448 mg/kg; HBT); low level selenised yeast (0.290 mg/kg; LSY); high level selenised yeast (0.487 mg/kg; HSY). 4. Birds consumed more when raised at 20°C compared to birds reared at 35°C (P ≤ 0.05). Birds fed lower Se level reared at 35°C had higher weight gain versus those fed higher Se level (P < 0.05). Birds fed SY had the lowest feed intake, weight gain and FCE (P < 0.05). The greatest GSH-Px activity was observed in birds fed SS diets (P < 0.001). There were interactions between diet x level for TAS, which were highest in birds fed LBT compared to birds fed HBT (P < 0.05). Breast Se content was higher in birds fed HSY compared to LSY (P < 0.001). The highest hepatic Se was seen in birds fed SY and lowest in C (P < 0.001). 5. Birds fed BT diets showed similar levels of Se to those birds fed inorganic Se, and similar levels of GSH-Px to birds fed SY. Further comparative work with broilers fed BT and other Se supplemented diets may elucidate the findings from this report.

The hepatic transcriptome of the turkey poult (Meleagris gallopavo) is minimally altered by high inorganic dietary selenium.

There is interest in supplementing animals and humans with selenium (Se) above Se-adequate levels, but the only good biomarker for toxicity is tissue Se. We targeted liver because turkeys fed 5 μg Se/g have hepatic Se concentrations 6-fold above Se-adequate (0.4 μg Se/g) levels without effects on growth or health. Our objectives were (i) to identify transcript biomarkers for high Se status, which in turn would (ii) suggest proteins and pathways used by animals to adapt to high Se. Turkey poults were fed 0, 0.025, 0.4, 0.75 and 1.0 μg Se/g diet in experiment 1, and fed 0.4, 2.0 and 5.0 μg Se/g in experiment 2, as selenite, and the full liver transcriptome determined by RNA-Seq. The major effect of Se-deficiency was to down-regulate expression of a subset of selenoprotein transcripts, with little significant effect on general transcript expression. In response to high Se intake (2 and 5 μg Se/g) relative to Se-adequate turkeys, there were only a limited number of significant differentially expressed transcripts, all with only relatively small fold-changes. No transcript showed a consistent pattern of altered expression in response to high Se intakes across the 1, 2 and 5 μg Se/g treatments, and there were no associated metabolic pathways and biological functions that were significant and consistently found with high Se supplementation. Gene set enrichment analysis also found no gene sets that were consistently altered by high-Se and supernutritional-Se. A comparison of differentially expressed transcript sets with high Se transcript sets identified in mice provided high Se (~3 μg Se/g) also failed to identify common differentially expressed transcript sets between these two species. Collectively, this study indicates that turkeys do not alter gene expression in the liver as a homeostatic mechanism to adapt to high Se.

Zinc overload in weaned pigs: tissue accumulation, pathology, and growth impacts

Zinc oxide (ZnO) is commonly fed to pigs at pharmacologic concentrations (2,000-3,000 ppm) for the first 3 wk post-weaning to increase growth and reduce enteric bacterial disease. The safety of this high-dose treatment is assumed based upon lower bioavailability of ZnO compared to other common forms of Zn in feed; however, limited data are available regarding the specific serum and tissue concentrations of Zn expected in animals experiencing overload following feeding of excessive ZnO. Fifty-five 3-wk-old pigs were divided into 5 groups receiving various concentrations of ZnO (0-6,000 ppm) for 3 wk. Pigs receiving 6,000 ppm ZnO had higher mean pancreatic Zn concentrations (p < 0.001) compared to other treatments, and higher pancreatic Zn concentrations were associated with pancreatic acinar cell apoptosis (p < 0.0001). Hepatic Zn concentrations were highest for pigs receiving 6,000 ppm ZnO (mean ± SEM; 729 ± 264 ppm) and significantly higher than all other groups (p < 0.0001), with controls having concentrations <60 ppm. Similarly, serum Zn was highest in pigs receiving 6,000 ppm ZnO (4.81 ± 2.31 ppm) and significantly higher than all groups (controls, <1 ppm). Additionally, as pigs became overloaded with Zn, there were significant reductions in serum Cu and both serum and hepatic Se. Hepatic and serum Zn concentrations >500 ppm and >2 ppm, respectively, are indicative of Zn overload, and dietary trace mineral analysis is warranted if expected inclusion rates are ≤3,000 ppm ZnO.

Histology of Sculpin spp. in East Greenland. II. Histopathology and trace element concentrations

For many years, the sculpin has been utilized as a sentinel monitoring species for anthropogenic impacts on the marine environment. To further develop its potential as a screening model body burden of several trace elements, including cadmium (Cd), copper (Cu), mercury (Hg), lead (Pb) and selenium (Se), were investigated. In addition, histopathology in shorthorn sculpins (Myoxocephalus scorpius; n = 20) and fourhorn sculpins (Myoxocephalus quadricornis; n = 10) were examined at three sites around the Scoresby Sound settlement in Central East Greenland. Fourhorn sculpins caught at the most distant site from the settlement, contained significantly higher hepatic Cu and Cd concentrations as well as significantly elevated gill Pb levels compared to the shorthorn sculpins collected at two other sites closer to the settlement. Histological examinations showed that fish with significantly higher concentrations of hepatic Cd and Se exhibited greater nuclear alterations, interstitial hyperplasia/hypertrophy, interstitial mononuclear infiltrations and granulomas. Further, fish with higher Cd and Cu gill tissue levels displayed a significantly higher number of cytoplasmic alterations and lamellar epithelium lifting, hypertrophic and hyperplastic epithelium along with mucus cell hyperplasia. While the presence of liver lesions were not species or sex-specific, the presence of gill lesions decreased in the order female fourhorn sculpins > female shorthorn sculpins > male fourhorn sculpins > male shorthorn sculpins. Hepatic Hg concentrations exceeded known lowest observable effect doses (LOED) for fish (0.1–0.5 μg g−1 ww) in 27% of fish, while liver Cd residues in 80% exceeded LOED (0.42–1.8 μg g−1 ww). Based upon these results, data suggest that using the sculpin as a valuable sentinel fish species histopathology may serve as a reliable tool for assessing marine ecosystem exposure to trace metals. However, confounding physiological and ecological factors also need to be considered.

Relationship between selenoprotein P and selenocysteine lyase: Insights into selenium metabolism

Selenoprotein P (SelenoP) functions as a plasma transporter of selenium (Se) from liver to other tissues via incorporation into multiple selenocysteine (Sec) residues. Selenocysteine lyase (Scly) is an intracellular enzyme that decomposes Sec into selenide, providing Se for the synthesis of new selenoproteins. Both SelenoP and Scly are mostly produced by the liver. Previous studies demonstrated that male mice lacking SelenoP (SelenoP KO) or Scly (Scly KO) had increased or decreased total hepatic Se, respectively. While SelenoP regulation by Se is well-studied, Scly regulation by Se has not been reported. We hypothesize that Scly is negatively regulated by Se levels, and that absence of SelenoP jeopardizes Scly-dependent Se recycling. Using in vitro and in vivo models, we unveiled a tissue-specific Se regulation of Scly gene expression. We also determined that SelenoP, a considered source of intracellular Se, affects Scly expression and activity in vitro but not in vivo, as in the absence of SelenoP, Scly levels and activity remain normal. We also showed that absence of SelenoP does not increase levels of transsulfuration pathway enzymes, which would result in available selenocompounds being decomposed by the actions of cystathionine γ-lyase (CGL or CTH) and cystathionine β-synthase (CBS). Instead, it affects levels of thioredoxin reductase 1 (Txnrd1), an enzyme that can reduce selenite to selenide to be used in selenoprotein production. This study evaluates a potential interplay between SelenoP and Scly, providing further insights into the regulation of selenium metabolism.

Fructose exposure during gestation and lactation altered hepatic selenoprotein expression, oxidative balance and metabolic profile in female rat pups

Fructose-rich diets, an experimental model of induced metabolic syndrome (MS), affects pregnant and lactating rat dams, and moreover, it leads to an imbalance in their offspring’s metabolic profile. Selenium (Se) homeostasis and body distribution is also altered. Selenoproteins: Glutathione peroxidase (GPx) and selenoprotein P (SelP) appear to play a role in MS. To evaluate selenoproteins’ implication in the transmission of this pathology to the progeny, hepatic Se deposits, GPx activity, biomolecular oxidation and selenoproteins and AMPK expression were measured in the offspring of dams exposed to a fructose-rich diet (65%). Se intake and liver selenoproteins are affected by fructose exposition during early nutrition. Female fructose pups show a repletion of Se and oxidation in liver, higher GPx activity and expression of hepatic GPx1 and SelP, related to a lower activation of AMPK and serum insulin levels. Fructose exposure during early nutrition negatively alters selenoproteins, oxidation and metabolism in female pups.

Dietary levels and sources of selenium for post weaning piglets

ABSTRACT: An experiment was conducted to study the effects of two sources and dietary levels of selenium (Se) on performance, Se concentration and glutathione peroxidase activity in plasma and liver of piglets post weaning. A total of 126 weaned pigs male and female Large White × Landrace, at average body weight of 7.2±0.67kg were allotted to seven treatments in a randomized block design, with two Se sources (organic and inorganic), inclusion levels, two levels for the inorganic source (0.30 and 0.60ppm) and four for the organic source (0.15, 0.30, 0.45 and 0.60ppm) and one control diet without Se supplementation containing 0.095ppm, and six replicates of three animals per pen. The experimental period was 35 days post-weaning. The organic source contained 0.2067% (Se-yeast), and the inorganic 45.86% (sodium selenite) analyzed. Piglets that received supplemental Se had lower feed intake compared to those not supplemented. Furthermore, feed conversion was better with dietary supplementation of Se, and the organic source was better than the inorganic source at level of 0.30ppm. Plasma concentration of Se was higher (35.53%) in animals receiving dietary supplementation of this mineral, regardless of the sources studied. There was no effect of sources on plasma and hepatic Se, with the lowest values observed for the non-supplementation and organic Se at dietary level of 0.15ppm. There was a linear reduction of plasma GSH-Px activity with increased supplementation levels of organic Se, and the hepatic GSH-Px activity increased linearly with the increased supplementation, regardless of the source studied.

Selenium and vitamin E in sow diets: II. Effect on selenium status and antioxidant status of the progeny

This study was conducted to investigate the effects of 2 selenium (Se) sources and 2 vitamin E (VE) levels in gestating and lactating diets of sows on Se status and antioxidant status of their progenies at farrowing and 21-d postpartum. The study was conducted in a 2×2 factorial arrangement of Se sources (0.30mg/kg diet of sodium selenite or Se-enriched yeast) and VE levels (30 or 90IU/kg diet). A total of 234 multiparous sows were bred and started on 1 of 4 dietary treatment according to parity and body condition, and then maintained on feed until 21-d postpartum. At farrowing and at weaning, 8 piglets per treatment (1 piglet/litter) were selected on similar body weight and sampled to ensure 6 piglet samples per treatment. The Se content was determined in serum, whole blood, umbilical cord blood and tissues, whereas antioxidant status of liver and serum were determined by analyzing the total antioxidant capacity (T-AOC), activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and glutathione (GSH) and malondialdehyde (MDA) contents. The newly-born piglets from sows fed organic Se had higher Se contents in kidney (P<0.05) and loin (P<0.10), higher serum T-AOC (P<0.05) and SOD activity (P<0.05), lower serum MDA content (P<0.05), and higher hepatic T-AOC (P<0.05), and GSH content (P<0.05) than newborns from sows fed inorganic Se. The 21-d-old nursery piglets from sows fed organic Se have higher Se contents in heart (P<0.10), pancreas (P<0.05), thymus gland (P<0.05), thyroid and loin (P<0.05), higher serum GSH content (P<0.05), lower serum MDA content (P<0.05), and higher hepatic T-AOC (P<0.05) and GSH content (P<0.05), and greater SOD activity (P<0.10), than 21-d-old piglets from sows fed inorganic Se. No source×VE level interaction was evident for Se status and antioxidant status of the progeny (P>0.05) expect for hepatic Se content of newborns and serum Se content of 21-d-old piglets (P<0.05). The α-tocopherol level in serum of newborn and weaning piglets increased when sows fed elevated VE diet (P<0.05). In summary, Se status and antioxidant status of the progeny including newborns and 21-d-old nursery piglets were improved when Se was added as organic Se instead of inorganic Se in sow diet. However, the Se status and antioxidant status of the progeny were scarcely unaffected by maternal dietary Se source×VE level interaction. When sows were fed the treatment diets from breeding until weaning, sows fed organic Se had more weaned piglets with similar individual pig weight at weaning compared with sows fed inorganic Se.

Individual effects of different selenocompounds on the hepatic proteome and energy metabolism of mice

BackgroundSelenium (Se) exerts its biological activity largely via selenoproteins, which are key enzymes for maintaining the cellular redox homeostasis. However, besides these beneficial effects there is also evidence that an oversupply of Se might increase the risk towards developing metabolic disorders. To address this in more detail, we directly compared effects of feeding distinct Se compounds and concentrations on hepatic metabolism and expression profiles of mice. MethodsMale C57BL6/J mice received either a selenium-deficient diet or diets enriched with adequate or high doses of selenite, selenate or selenomethionine for 20weeks. Subsequently, metabolic parameters, enzymatic activities and expression levels of hepatic selenoproteins, Nrf2 targets, and additional redox-sensitive proteins were analyzed. Furthermore, 2D-DIGE-based proteomic profiling revealed Se compound-specific differentially expressed proteins. ResultsWhereas heterogeneous effects between high concentrations of the Se compounds were observed with regard to body weight and metabolic activities, selenoproteins were only marginally increased by high Se concentrations in comparison to the respective adequate feeding. In particular the high-SeMet group showed a unique response compromising higher hepatic Se levels in comparison to all other groups. Accordingly, hepatic glutathione (GSH) levels, glutathione S-transferase (GST) activity, and GSTpi1 expression were comparably high in the high-SeMet and Se-deficient group, indicating that compound-specific effects of high doses appear to be independent of selenoproteins. ConclusionsNot only the nature, but also the concentration of Se compounds differentially affect biological processes. General significanceThus, it is important to consider Se compound-specific effects when supplementing with selenium.

Dietary selenium requirement for on-growing gibel carp (Carassius auratus gibeliovar. CAS III)

A 12-week growth trial was conducted in a flow-through system to determine dietary selenium (Se) requirement for on-growing gibel carp (initial body weight: 76.2 +/- 0.05 g, mean +/- SEM). Selenomethionine was supplemented to the basal diet to formulate seven semi-purified diets containing 0.26, 0.58, 0.72, 1.14, 1.34, 1.73 and 2.09 mg Se kg(-1) diet. The results showed that plasma superoxide dismutase (SOD) activity significantly increased when fish were fed with 0.58 mg Se kg(-1) diet (P = 0.72 mg kg(-1) (P > 0.05). Whole-body and muscle Se concentrations were higher when fed with 1.34 mg Se kg(-1) diet (P = 1.34 mg kg(-1) (P > 0.05). In conclusion, based on broken-line regression of hepatic Se concentrations, hepatic SOD activity and hepatic T-AOC activity, dietary Se requirements for on-growing gibel carp was 0.73 mg kg(-1), 1.12 mg kg(-1) and 1.19 mg kg(-1) diet respectively.

Selenium status in neonates with connatal infection.

Infectious diseases impair Se metabolism, and low Se status is associated with mortality risk in adults with critical disease. The Se status of neonates is poorly characterised, and a potential impact of connatal infection is unknown. We hypothesised that an infection negatively affects the Se status of neonates. We conducted an observational case-control study at three intensive care units at the Charité-Universitätsmedizin Berlin, Germany. Plasma samples were collected from forty-four neonates. On the basis of clinical signs for bacterial infection and concentrations of IL-6 or C-reactive protein, neonates were classified into control (n 23) and infected (n 21) groups. Plasma Se and selenoprotein P (SePP) concentrations were determined by X-ray fluorescence and ELISA, respectively, at day of birth (day 1) and 48 h later (day 3). Se and SePP showed a positive correlation in both groups of neonates. Se concentrations indicative of Se deficit in adults (500 ng/l). During antibiotic therapy, SePP increased significantly from day 1 (1·03 (sd 0·10) mg/l) to day 3 (1·34 (sd 0·10) mg/l), indicative of improved hepatic Se metabolism. We conclude that both Se and SePP are suitable biomarkers for assessing Se status in neonates and for identifying subjects at risk of deficiency.

Selenium Content in the Liver of Wistar Rats Fed Diets of Different Fatty Acid Quality.

The purpose of this work was to measure the amounts of selected mineral elements (sodium, calcium, iron, selenium, magnesium, zinc, copper, and manganese) in the liver of Wistar rats and evaluate possible correlations between the levels of these minerals and the lipid metabolism in the studied animals. Three experimental groups each containing six Wistar rats were designed. Each group was fed a different diet. The control group was fed a diet prepared with fresh soybean oil and named control group--CG. The second group (named experimental group B--EGB) and third group (named experimental group C--EGC) were fed a diet containing soybean oil that had been used to fry different foods for four or ten cycles, respectively. The mineral elements in Wistar rat livers were measured by inductively coupled plasma optical emission spectrometry (ICP OES). Only the elements calcium and selenium differed significantly between the control and experimental groups. There was a significant reduction of 33% for Ca and 41% for Se in the EGB in comparison to the control group. The reduction in mineral concentration, especially Se, is the result of interactions with fatty acid metabolism. The animals in the EGC exhibited more intracytoplasmic accumulation of fat and more intense vasodilatation, in relation to the other groups. Collectively, evidence hereby collected suggests that impaired dietary lipid quality in otherwise balanced diets can reduce hepatic Se levels and potentially harm liver function.

Trace-elements, methylmercury and metallothionein levels in Magellanic penguin (Spheniscus magellanicus) found stranded on the Southern Brazilian coast

Magellanic penguins have been reported as good biomonitors for several types of pollutants, including trace-elements. In this context, selenium (Se), total mercury, methylmercury, inorganic mercury (Hginorg), cadmium (Cd) and lead (Pb), as well as metallothionein (MT) levels, were evaluated in the feathers, liver and kidney of juvenile Magellanic penguins found stranded along the coast of Southern Brazil. The highest concentrations of all trace-elements and methylmercury were found in internal organs. Concentrations of Cd and Se in feathers were extremely low in comparison with their concentrations in soft tissues. The results showed that both Se and MT are involved in the detoxification of trace-elements (Cd, Pb and Hginorg) since statistically significant relationships were found in liver. Conversely, hepatic Se was shown to be the only detoxifying agent for methylmercury.

Mercury and selenium relationship in a tropical estuarine fish

Event Abstract Back to Event Mercury and selenium relationship in a tropical estuarine fish André Pinheiro Almeida1, Ana Carolina Pizzochero1 and Paulo Renato Dorneles1* 1 Federal University of Rio de Janeiro, Carlos Chagas Filho Biophysics Institute, Brazil Aquatic systems have been considered as final sinks for persistent and bioaccumulative toxicants (PBTs), such as metals and organohalogen compounds. Among the trace elements, non-essential metals deserve special attention due to their toxicity. In this context, mercury (Hg) should be highlighted due to its toxic effects, which comprise neurotoxicity, nephrotoxicity, hepatotoxicity, genotoxicity, among others. Several studies have highlighted the selenium-mediated methylmercury detoxification process, via mercury selenide formation in tissues of marine vertebrates. Despite being an essential element, selenium may also be toxic in high concentrations. This study focused on Guanabara Bay (GB), a heavily polluted urban estuary in Rio de Janeiro state (Brazil), where the whitemouth croaker (Micropogonias furnieri) provides a valuable fishery resource. Therefore, hepatic (Hg and Se) and muscular (Hg) concentrations of these elements were determined in GB whitemouth croakers. Mercury and selenium measurements were performed by cold vapor atomic absorption spectrometry (CV-AAS) and electrothermal AAS (ET-AAS), respectively. Total mercury (THg) concentrations in muscle (n=19) ranged from 184.9 to 858.6 (ng/g), while in liver they varied from 11.05 to 1188 (ng/g). Hepatic selenium concentrations ranged from 7820 to 40085 (ng/g). The hepatic Se:THg molar ratio ranged from 40,8 to 3102,5. The results showed a significant correlation between hepatic mercury and selenium levels, but the molar ratio suggests the absence of mercury selenide formation. Some of the Se concentrations found were above the threshold level for freshwater fish (12000 ng/g); however, it is not yet clear if these concentrations are toxic for marine fish as well. More studies are necessary for evaluating the impact of such exposure in fish from Guanabara Bay. Acknowledgements This study was supported by CNPq (National Research Council, Brazilian Ministry of Science and Technology) and FAPERJ (Rio de Janeiro state Research Support Foundation). Keywords: Whitemouth croaker, Micropogonias furnieri, Guanabara Bay, Tropical estuary, mercury selenide. Conference: XV European Congress of Ichthyology, Porto, Portugal, 7 Sep - 11 Sep, 2015. Presentation Type: Poster Presentation Topic: Physiology, Behavior and Toxicology Citation: Almeida A, Pizzochero A and Dorneles P (2015). Mercury and selenium relationship in a tropical estuarine fish. Front. Mar. Sci. Conference Abstract: XV European Congress of Ichthyology. doi: 10.3389/conf.FMARS.2015.03.00146 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 24 Nov 2015; Published Online: 27 Nov 2015. * Correspondence: PhD. Paulo Renato Dorneles, Federal University of Rio de Janeiro, Carlos Chagas Filho Biophysics Institute, Rio de Janeiro, Rio de Janeiro, 21941-902, Brazil, dornelespr@biof.ufrj.br Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers André Pinheiro Almeida Ana Carolina Pizzochero Paulo Renato Dorneles Google André Pinheiro Almeida Ana Carolina Pizzochero Paulo Renato Dorneles Google Scholar André Pinheiro Almeida Ana Carolina Pizzochero Paulo Renato Dorneles PubMed André Pinheiro Almeida Ana Carolina Pizzochero Paulo Renato Dorneles Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Effects of selenium and vitamin E supplementation on selenium distribution and meat quality of pigs

The study was conducted on 60 pigs kept in individual pens. The animals were allocated to four groups. The growing-finishing pigs from the control group were fed with basic feed containing 0.3 mg selenium (Se) derived from Na2SeO3 kg−1 and 60 mg of dl-α-tocopheryl acetate kg−1. The remaining three groups were differentiated by adding 0.2 mg kg−1 Se-enriched yeast (Saccharomyces cerevisiae) and/or 60 mg vitamin E to feed (grower and finisher). Our results show that the addition of organic Se to inorganic Se commonly used in pig feed caused a significant increase in hepatic Se and muscle. This indicates the possibility of using these products as functional foods to improve Se status in humans residing within regions which are deficient in this trace element. We found no beneficial effect of supplementation with vitamin E and Se on the quality of the meat.

Selenium dietary supplementation as a mechanism to restore hepatic selenoprotein regulation in rat pups exposed to alcohol

Ethanol exposure during gestation and lactation decreases selenium (Se) intake, disrupting body Se balance and inducing oxidative stress in rat offspring. Selenium-supplemented diet (0.5 ppm) was administered to ethanol-exposed (20% v/v) dams during gestation and lactation. When the dams' pups were 21 days old, the pups' levels of the main hepatic selenoproteins glutathione peroxidase (GPx1 and GPx4) and selenoprotein P (SelP) were measured. The pups were divided into control (C), alcohol (A), control-selenium (CS), and alcohol-selenium (AS) groups. The purpose was to evaluate the effect of the selenium-supplemented diet on the levels of Se deposits present in the livers of their pups. Alcohol decreases hepatic Se deposits, GPx activity, and GPx1 expression; alcohol increases GPx4 and SelP expression. Se was measured by furnace graphite atomic absorption spectrometry, the antioxidant activity of GPx and concentration of hepatic phospholipids (PL) were determined by spectrophotometry, and the selenoprotein expressions were detected by Western blotting. Selenite treatment prevented alcohol's effects of diminishing the Se deposits, GPx activity, and GPx1 expression, while maintaining the high levels of the expression of GPx4 and SelP. These results suggest that depletion of hepatic Se levels in rat pups, caused by ethanol exposure to their dams, affects the synthesis of the 3 main hepatic selenoproteins in different ways, which is related to a decrease in GPx activity and PL concentration, and an increase in serum Se levels. Selenium supplementation to the dams increased the expression of GPx1, GPx4, and SelP in their pups.

Role of selenium and glutathione peroxidase on development, growth, and oxidative balance in rat offspring

Selenium (Se), an essential trace metal, is important in both growth and reproduction and is the constituent of different selenoproteins. The glutathione peroxidase (GPx) family is the most studied as it prevents oxidative stress. Liver oxidation is considered as another mechanism involved in low birth weight. Therefore, in order to ascertain whether GPx is related to the effects of Se on growth during gestation and lactation, three groups of rat pups were used: control, Se deficient (SD), and Se supplemented (SS). Morphological parameters and reproductive indices were evaluated. Hepatic Se levels were measured by graphite furnace atomic absorption while spectrophotometry was used for activity of antioxidant enzymes and oxidative stress markers in liver and western blotting for expression of hepatic GPx1 and GPx4. The SD diet increased mortality at birth; decreased viability and survival indices; and stunted growth, length, and liver development in offspring, thus decreasing hepatic Se levels, GPx, glutathione reductase, and catalase activities, while increasing superoxide dismutase activity and protein oxidation. The SS diet counteracted all the above results. GPx1 expression was heavily regulated by Se dietary intake; however, although Se dietary deficiency reduced GPx4 expression, this decrease was not as pronounced. Therefore, it can be concluded that Se dietary intake is intimately related to growth, length, and directly regulating GPx activity primarily via GPx1 and secondly to GPx4, thus affecting liver oxidation and development. These results suggest that if risk of uterine growth retardation is suspected, or if a neonate with low birth weight presents with signs of liver oxidation, it may be beneficial to know about Se status.

Comparing functional metabolic effects of marginal and sufficient selenium supply in sheep

This study was performed to characterise key data of long-term ovine Se metabolism and to work out the best biomarker of Se status. An upgrade from marginal (<0.05mg Se/kg diet, ‘Se−’) to sufficient (0.2mg Se/kg diet, ‘Se+’) nutritional Se supply using sodium selenite was monitered biweekly by analysing Se concentration, glutathione peroxidase (Gpx) activity and routine biochemistry in blood/serum over 2 years. Se, Cu, Zn, cytosolic Gpx and thioredoxin reductase (TrxR) activity were measured in the liver (biopsies/post-mortem). Se, Gpx, TrxR, glutathione-S-transferase-alpha (aGST) and iodothyronine deiodinase (Dio1) were analysed in the kidney, heart muscle and thyroid. Relative mRNA expression of hepatic aGST1 and Gpx1 was determined.Improvement of Se supply strongly increased serum and liver Se concentration within 10 and 20 days, respectively followed by a plateau. Whereas the achievement of a maximum whole blood Gpx activity was reached after 3 months, serum Gpx3 activity increased with high variations. Hepatic Gpx activity reached a maximum during days 100–200, decreasing thereafter. Distinct group differences in Se and cytosolic Gpx activity were evident in all organs (except Se in kidney). TrxR and Dio1 activity was affected only in the liver. The Se− sheep showed an ongoing decrease in serum Se concentration within 2 years, whereas liver Se remained almost unaffected. High relative Gpx1 mRNA expression in the Se+ group was consensual to high hepatic Gpx activity. Relative mRNA expression of hepatic aGST1 was higher in the Se− sheep. Clinical signs and abnormalities in routine biochemistry were absent.In summary, the best biomarker of Se deprivation and nutritional Se upgrade, respectively was Se in serum. Moreover, hepatic Se concentrations reliably reflected the upgrade of Se supply within days. Whole blood Gpx reacts slowly depending on newly formed erythrocytes restricting its diagnostic use. Vital organs are affected by Se deficiency due to a decrease of cytosolic Gpx activity attenuating the antioxidative system. Cellular up-regulation of aGST1 mRNA expression in the Se− group is assumed to partially compensate for the decreased antioxidant defence due to a loss in Gpx activity. This sheep model appears advantageous for long-term studies on sub-clinical metabolic effects in experimental modifiable nutritional Se supply.