Liver GPx Research Articles

Protective effect of Uncaria tomentosa extract against oxidative stress and genotoxicity induced by glyphosate-Roundup® using zebrafish (Danio rerio) as a model.

Oxidative stress and DNA damage are involved in the glyphosate-based herbicide toxicity. Uncaria tomentosa (UT; Rubiaceae) is a plant species from South America containing bioactive compounds with known beneficial properties. The objective of this work was to evaluate the antioxidant and antigenotoxic potential of UT extract in a model of acute exposure to glyphosate-Roundup® (GR) in zebrafish (Danio rerio). We showed that UT (1.0mg/mL) prevented the decrease of brain total thiols, the increase of lipid peroxidation in both brain and liver, and the decrease of liver GPx activity caused after 96h of GR (5.0mg/L) exposure. In addition, UT partially protected against the increase of micronucleus frequency induced by GR exposure in fish brain. Overall, our results indicate that UT protects against damage induced by a glyphosate-based herbicide by providing antioxidant and antigenotoxic effects, which may be related to the phenolic compounds identified in the extract.

Influence of feeding thermally peroxidized soybean oil on oxidative status in growing pigs.

The objectives of this study were to determine whether feeding thermally processed peroxidized soybean oil (SO) induces markers of oxidative stress and alters antioxidant status in pig tissue, blood, and urine. Fifty-six barrows (25.3 ± 3.3 kg initial BW) were randomly assigned to dietary treatments containing 10% fresh SO (22.5 °C) or thermally processed SO (45 °C for 288 h, 90 °C for 72 h, or 180 °C for 6 h), each with constant air infusion rate of 15 liters/minute. Multiple indices of lipid peroxidation were measured in the SO including peroxide value (2.0, 96, 145, and 4.0 mEq/kg for 22.5, 45, 90, and 180 °C processed SO, respectively) and p-anisidine value (1.2, 8.4, 261, and 174 for 22.5, 45, 90, and 180 °C processed SO, respectively); along with a multitude of aldehydes. Pigs were individually housed and fed ad libitum for 49 d which included a 5 d period in metabolism crates for the collection of urine and serum for measures of oxidative stress. On day 49, pigs were euthanized to determine liver weight and analyze liver-based oxidative stress markers. Oxidative stress markers included serum, urinary, and liver thiobarbituric acid reactive substances (TBARS), and urinary F2-isoprostanes (ISP) as markers of lipid damage; serum and liver protein carbonyls (PC) as a marker of protein damage; and urinary and liver 8-hydroxy-2'-deoxyguanosine (8-OH-2dG) as a marker of DNA damage. Superoxide dismutase (SOD), and catalase activity (CAT) were measured in liver, glutathione peroxidase activity (GPx) was measured in serum and liver, and ferric reducing antioxidant power (FRAP) was measured in serum and urine as determinants of antioxidant status. Pigs fed 90 °C SO had greater urinary ISP (P = 0.02), while pigs fed the 45 °C SO had elevated urinary TBARS (P = 0.02) in comparison to other treatment groups. Pigs fed 45 °C and 90 °C SO had increased serum PC concentrations (P = 0.01) and pigs fed 90 °C SO had greater (P = 0.01) liver concentration of 8-OH-2dG compared to pigs fed the other SO treatments. Furthermore, pigs fed 90 °C SO had reduced serum GPx activity in comparison to pigs fed fresh SO (P = 0.01). In addition, pigs fed 180 °C SO had increased liver CAT activity (P = 0.01). Liver GPx and SOD or serum and urinary FRAP were not affected by dietary treatment. These results indicate that dietary peroxidized soybean oil induced oxidative stress by increasing serum PC while diminishing serum GPx, increasing urinary ISP and TBARS, and increasing 8-OH-2dG and CAT in liver.

The protective effect of selenium nanoparticles and selenium against paracetamol

Objective(s): Nanotechnology has enabled researchers to synthesize nanosize particles that possess increased surface areas. Compared to conventional microparticles, it has resulted in increased interactions with biological targets.The objective of this study was to determine the protective ability of selenium nanoparticles compared to selenium against parasetamol hepatotoxicity and GPX concentration. Materials and Methods: Seventy-two male rats were used in the study, and arbitrarily assigned to six groups. There were 12 rats in each group that six rat were tested in each period. Blood samples were collected from rats for measuring liver enzymes and GPX activity. Results: The present study shows that parasetamol has a toxic effect on the liver as a result of inducing a marked oxidative damage and release of reactive oxygen species. This was shown by the significant increases in ALP, AST, ALT and LDH activity which was accom­panied by significant decrease in GPX activity in the parasetamol -treated group compared to the control, selenium and selenium nanoparticles groups. There was no significant difference between selenium and selenium nanoparticles groups and two period time (15 and 30 day). Conclusion: selenium nanoparticles and selenium have protective against paracetamol.

Effects of dietary methionine on productivity, reproductive performance, antioxidant capacity, ovalbumin and antioxidant-related gene expression in laying duck breeders.

The study investigated whether dietary methionine (Met) affects egg weight and antioxidant status through regulating gene expression of ovalbumin (OVAL), nuclear factor erythroid 2 like 2 (Nrf2) and haem oxygenase 1 (HO-1) in laying duck breeders. Longyan duck breeders (n 540, 19 weeks) were randomly assigned to six treatments with six replicates of fifteen birds each. Breeders were fed diets with six Met levels (2·00, 2·75, 3·50, 4·25, 5·00 and 5·75 g/kg) for 24 weeks. The egg weight (g), egg mass (g/d), feed conversion ratio, hatchability, 1-d duckling weight, albumen weight, albumen proportion and OVAL mRNA level improved with dietary Met levels, whereas yolk proportion decreased (P<0·05). The weight of total large yellow follicles increased linearly (P<0·001) and quadratically (P<0·05) with dietary Met concentration, and their weight relative to ovarian weight showed a linear (P<0·05) effect. Dietary Met level had a linear (P<0·05) and quadratic (P<0·001) effect on the gene expression of glutathione peroxidase (GPX1), HO-1 and Nrf2, and quadratically (P<0·05) increased contents of GPX and total antioxidant capacity (T-AOC) in liver of duck breeders. In addition, maternal dietary Met enhanced gene expression of GPX1, HO-1 and Nrf2, increased contents of GPX and T-AOC and reduced carbonylated protein in the brains of hatchlings. Overall, dietary Met concentration affected egg weight and albumen weight in laying duck breeders, which was partly due to gene expression of OVAL in oviduct magnum. A diet containing 4·0 g Met/kg would achieve optimal hepatic GPX1 and Nrf2 expression, maximise the activity of GPX and minimise lipid peroxidation.

Assessment of 8-hydroxy-2-deoxyguanosine activity, gene expression and antioxidant enzyme activity on rainbow trout (Oncorhynchus mykiss) tissues exposed to biopesticide

The goal of this study was to determinate toxicity mechanism of biopesticide with antioxidant enzymes parameters such as superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) and malondialdehyde (MDA) levels, oxidative DNA damage (8-hydroxy-2-deoxyguanosine (8-OHdG)), transcriptional changes of heat shock protein 70 (HSP70), and cytochromes P4501A (CYP1A), sod, cat, and gpx in liver and gill tissues of Oncorhynchus mykiss. For this aim, plant-based (natural pesticides, azadirachtin (AZA)) and synthetic pesticides (deltamethrin (DLM)) were exposed on the fish at different concentrations (0.0005 and 0.00025ppm of DLM; 0.24 and 0.12ppm of AZA) for 21 days.According to the results of the study, the activity of SOD, CAT and GPx decreased, but malondialdehyde (MDA) level and activity of 8-OHdG increased in the gill and liver of rainbow trout (p<0.05). Additionally sod, cat and gpx were down regulated; HSP70 and CYP1A were up regulated for transcriptional observation. The downwards regulation of antioxidant (sod, cat and gpx) and the upregulation of HSP70 and CYP1A was obvious with doses of AZA or DLM (p<0.05). The findings of this study suggest that biopesticide can cause biochemical and physiological effects in the fish gill and liver by causing enzyme inhibition, an increase in 8-OHdG levels and changes in both transcriptional parameters (sod, cat, gpx, HSP70 and CYP1A). We found that excessive doses of plant-based pesticide are nearly as toxic as chemical ones for aquatic organisms. Moreover, 8-OHdG, HSP70 and CYP1A used as a biomarker to determinate toxicity mechanism of biopesticide in aquatic environment.

Antioxidant enzymatic activities and lipid peroxidation in liver and ovary of zebrafish (Danio rerio) exposed to deltamethrin

ABSTRACTDeltamethrin (DM) is being used as a substitute for organochlorines and organophosphates in pest control because of its low environmental persistence and toxicity. But it has become an environmental contaminant as it has been used widely. In this study, we investigated the effect of DM (technical grade) on the antioxidant system of adult zebrafish. For this, six-month-old fish were exposed to 2, 4 and 6 μg/L of DM for 96 h. The tissues selected were liver and ovary. Our data showed that exposure to DM increases CAT (catalase), SOD (superoxide dismutase), GPx (glutathione peroxidase, antioxidant enzymes), LPO (lipid peroxidation, non-enzymatic antioxidant) and GST (glutathione S-transferase, detoxifying enzyme) in liver and ovary. Increased GST could detoxify the toxicant; still there could be enough DM to cause oxidative stress. It appears from our study that zebrafish used compensatory mechanisms in eliminating reactive oxygen species. These data will be useful as oxidative stress is being used as a biomarker for aquatic pollution.

Impact of generic antimalarial or Phyllanthus amarus and vitamin co-administration on antioxidant status of experimental mice infested with Plasmodium berghei

Oxidative stress is a key factor in malaria pathogenesis, particularly, malaria induced anaemia and pathological changes in some organs in the body. This research aimed at investigating the effect of Phyllanthus amarus seed extract (PASE), chloroquine (CLQ), and artesunate (ATS) used alone and co-administered with vitamin A, B, C, or E on oxidative stress in Plasmodium berghei-infected mice. A total of eighty (80) adult albino male mice infected with P. berghei (NK 65 strain) were randomly allotted to 16 treatment groups, mice in another group (17th group) were uninfected; n=5. Of the treatment groups, fifteen were administered sole generic antimalarials/PASE and combined vitamins A, B, C or E orally for 5days. Biochemical assay for glutathione peroxidase (GPx), and glutathione reductase (GR) were carried out on the serum. Assay for glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CA), and malondialdehyde (MDA) levels were carried out on homogenised liver and brain. Treatment with PASE, CLQ and ATS combined with vitamin A, B, or E respectively, demonstrated significant increase in the serum levels of GPx and GR concentration. Treatment with PASE/ATS alone and in combination with vitamin A, B, C, and E significantly increased the liver GPX, SOD, and CA levels with significant decrease in liver MDA levels. Treatment with PASE/CLQ alone and in combination with vitamin A, B, C, and E significantly increased the brain GPX, GR and SOD levels with significant decrease in brain MDA levels. PASE showed enhanced antioxidant capacity in plasmodiasis solely or combined with vitamins A, B and E. Furthermore the co-administration of generic agent like artesunate with vitamins A, B, and E enhanced the antimalarial activity and treatment outcome as shown by the antioxidant effects. However, co-administration with vitamin C may be counter-productive.

Effects of Initial Selenium Status on Apparent Dietary Selenium Requirements in Rodents

Robust biomarkers – that are specific for the nutrient, fall dramatically in deficiency, and reach well‐defined plateaus – are essential for the careful determination of dietary nutrient requirements (Adv Nutr 2016;7:1129). A second key component of dietary nutrient requirement studies is initial status at the start of an experiment. Se‐adequate male weanling rats fed Se‐deficient diets supplemented with graded levels of Se (as selenite) for 4 wk result in sigmoidal Se response curves with well‐defined plateaus for glutathione peroxidase (Gpx) activity, and with plateau breakpoints indicating minimum Se requirements of 0.06, 0.06, and 0.09 μg Se/g diet based on liver Gpx4, plasma Gpx3 and liver Gpx1 activity, respectively. Underlying these requirements, the Se requirement for liver Gpx1 mRNA is 0.06 μg Se/g diet. When second‐generation Se‐deficient weanling male rats were fed graded Se levels for 4 wk, apparent dietary Se requirements increased to 0.08, 0.1 and 0.14 μg Se/g for liver Gpx4, plasma Gpx3, and liver Gpx1 activities, respectively. The Se requirement for liver Gpx1 mRNA was 0.08 μg Se/g diet, which is 25% higher than when starting with Se‐adequate pups (Biol Trace Elem Res 2016, in press). Clearly, repleting Se‐deficient rats using an identical paradigm increased apparent dietary Se requirements by 33–67%, showing that limited dietary Se was being diverted to replete deeper body pools of Se. The higher dietary Se required to protect liver Gpx1 mRNA from nonsense mediated decay further substantiates this shift of Se from liver to other tissues. To explore in a preliminary study the role of Gpx1 mRNA and selenoprotein expression on restoration of Se status, Gpx1 wildtype (Gpx1+/+), heterozygote (Gpx1+/−), and knockout (Gpx1−/−) mice were fed Se‐deficient diets for 16 wk, then re‐supplemented with graded levels of dietary Se (0–0.3 μg Se/g) for 7 days to partially replete Gpx activities. Liver Gpx1 activity in Gpx1+/+ mice reached a plateau with 0.15 μg Se/g, whereas in Gpx1+/− mice, liver Gpx1 activity increased linearly over the full dietary range from 0 to 0.3 μg Se/g, showing the effect of limited Gpx1 mRNA as well as Se availability; there was no increase in Gpx1 activity in Gpx1−/− mice, as expected. In contrast, red blood cell (RBC) Gpx1 activity was little altered by 0 to 0.15 μg Se/g in both Gpx1+/+ and Gpx1+/− mice, but then reached a similar level for both genotypes at 0.3 μg Se/g, suggesting that Se availability but not mRNA was controlling level of RBC Gpx1. The plasma Gpx3 activity Se response curve for Gpx1+/+ mice was similar to the Se response curve for RBC Gpx1 activity for Gpx1+/+ mice, only reaching a maximum at 0.3 μg Se/g. Surprisingly, the Se response curve for plasma Gpx3 activity in Gpx1−/− mice overlay the response curve for Gpx1+/+ mice, indicating that similar quantities of Se were transported to kidney for Gpx3 synthesis, whereas Gpx1+/− mice fed 0.3 μg Se/g had considerable less Gpx3 activity than Gpx1+/+ or Gpx1−/− mice, again suggesting that Se was diverted to other tissues. Collectively, these studies illustrate that diversion of nutrient to depleted stores can result in higher apparent nutrient requirements when starting with initially depleted animals.Support or Funding InformationWisconsin Alumni Foundation Selenium Nutrition Research Fund (No. 2046295)

Minimum Selenium Requirements Increase When Repleting Second-Generation Selenium-Deficient Rats but Are Not Further Altered by Vitamin E Deficiency.

Second-generation selenium-deficient weanling rats fed graded levels of dietary Se were used (a) to study the impact of initial Se deficiency on dietary Se requirements; (b) to determine if further decreases in selenoperoxidase expression, especially glutathione peroxidase 4 (Gpx4), affect growth or gross disease; and (c) to examine the impact of vitamin E deficiency on biochemical and molecular biomarkers of Se status. Rats were fed a vitamin E-deficient and Se-deficient crystalline amino acid diet (3ng Se/g diet) or that diet supplemented with 100μg/g all-rac-α-tocopheryl acetate and/or 0, 0.02, 0.05, 0.075, 0.1, or 0.2μg Se/g diet as Na2SeO3 for 28days. Se-supplemented rats grew 6.91g/day as compared to 2.17 and 3.87g/day for vitamin E-deficient/Se-deficient and vitamin E-supplemented/Se-deficient groups, respectively. In Se-deficient rats, liver Se, plasma Gpx3, red blood cell Gpx1, liver Gpx1 and Gpx4 activities, and liver Gpx1 mRNA levels decreased to <1, <1, 21, 1.6, 49, and 11%, respectively, of levels in rats fed 0.2μg Se/g diet. For all biomarkers, ANOVA indicated significant effects of dietary Se, but no significant effects of vitamin E or vitamin E × Se interaction, showing that vitamin E deficiency, even in severely Se-deficient rat pups, does not result in compensatory changes in these biochemical and molecular biomarkers of selenoprotein expression. Se requirements determined in this study, however, were >50% higher than in previous studies that started with Se-adequate rats, demonstrating that dietary Se requirements determined using initially Se-deficient animals can result in overestimation of Se requirements.

Differential modulation of cellular antioxidant status in zebrafish liver and kidney exposed to low dose arsenic trioxide

Zebrafish were exposed to a nonlethal dose (1/350LC50; 50µg/L) of As2O3 and sampled at 7, 15, 30, 60 and 90 days of treatment. The oxidative stress response was assessed in terms of time-dependent histopathological changes, lipid peroxidation, GSH status, activities of detoxification enzymes and expression of antioxidant genes in liver and kidney. As2O3 treatment enhanced lipid peroxidation except at day 90 in liver and day 30 in kidney. Glutathione depleted significantly in the liver except on day 30; whereas in kidney, it increased initially but thereafter depleted significantly. The liver GST activity was high until day 30, low on day 60 and high on day 90. On the other hand, activity of GST in kidney remained high throughout the exposure. GR activity in liver decreased initially but augmented from 30 days onwards whereas in kidney it remained high until 30 days of exposure. Significant increase in GPx and CAT activities in liver and kidney confirmed oxidative stress in zebrafish which correlated with mRNA expression of antioxidant genes. Upregulation in mRNA level of Cu-Zn Sod in liver and kidney was prominent. Gpx1 upregulation was more conspicuous in kidney as compared to liver while the pattern of Cat expression was almost similar in both the organs. Among the mitochondrial genes, expression of Cox1 was significantly high only after 90 days in liver, while in kidney it enhanced at 7, 30 and 60 days of arsenic exposure. Ucp2 was upregulated in liver after 15 days of exposure but significantly downregulated at day 90; in kidney it remained unchanged at other time points except at day 90. An overall increased expression of Bcl2 further confirmed As2O3 induced oxidative stress in zebrafish liver and kidney. The pattern of mRNA expression of Nrf2 was not uniform and was in accordance to its downstream antioxidant genes. Present findings elucidate that low dose of As2O3 exposure induces a time dependent differential modulation of antioxidant status in liver and kidney of zebrafish in a tissue-specific manner.

Antioxidant Enzyme Activity and Cognition in Obese Individuals with or without Metabolic Risk Factors.

Background: The metabolic syndrome may be associated with cognitive impairment and increased oxidative stress. Aim: To document the association between metabolic syndrome, cognitive impairment and oxidative stress activity in metabolically healthy obese and in metabolically unhealthy obese individuals. Methods: 60 obese individuals aged (49±10 years, 52% male) were enrolled. Obesity was defined as BMI>30. Metabolic syndrome was defined according to ATP III guidelines. Obese individuals were divided into 2 groups: Group 1, metabolically healthy obese (≤2 components of metabolic syndrome), and Group 2, metabolically unhealthy obese (>2 components of metabolic syndrome). Cognitive dysfunction was determined by Montreal cognitive assessment score. Liver Fibro scan (Elastography), Inflammation (CRP), pro oxidants (MDA), antioxidant activity (SOD, PON, GSH, GPx) and insulin resistance (HOMA-IR) were measured. Results: Of the 30 metabolically unhealthy obese individuals, 13% developed dementia, 51% had mild cognitive impairment, and 36% had a normal cognitive score. In the metabolically healthy obese group, 3% developed dementia, 7% had mild cognitive impairment, and 90% had a normal cognitive score. There was a significant difference in liver stiffness (7±3 vs. 5.2±2.7 kpa, p<0.001), liver fat measurement (337±51 vs. 280±20 db/m, p<0.001), MDA (4.7±0.9 vs. 5.47±1.12 mM, P<0.003), Glutathione GSH (27.2±2.4 vs. 28.4±2.3, P<0.03), CRP (9±6 vs. 7±6 P<0.001) and insulin resistance (2.5±1 vs. 6±5.5 p<0.02) between the 2 groups. Correlations were significant between GPx activity and liver stiffness (r=0.37), GPx activity and abdominal girth (r=-0.22) and glucose concentration and SOD activity (r=0.4). Multivariate analysis showed that HOMA-IR, MDA and GSH were the most powerful predictors of metabolically unhealthy obesity. Conclusion: There is a significant mild cognitive impairment and increased oxidative stress activity in the metabolically unhealthy obese. Whether treatment with anti-oxidants improves cognitive dysfunction remains to be determined.

Dietary carbohydrates improve oxidative status of common dentex (Dentex dentex) juveniles, a carnivorous fish species

Common dentex (Dentex dentex) is an appreciated carnivorous fish with high growth rate and life cycle adaptable to existing farming techniques. Since the use of carbohydrates is an economic and sustainable alternative for a protein-sparing effect, the study of how this macronutrient affects the welfare of carnivorous species must be studied. The aim of the present study was to evaluate the effects of different types and levels of carbohydrates on common dentex oxidative status. Nine isonitrogenous (43%) and isoenergetic (22MJkg−1) diets were formulated combining three types (pregelatinized starch-PS, dextrin-Dx and maltodextrin-Mx) and three levels (12, 18 and 24%) of carbohydrates. The activities of catalase-CAT, superoxide dismutase-SOD, glutathione peroxidase-GPX, glutathione reductase-GR and glucose 6-phosphate dehydrogenase-G6PDH, SOD isoenzymatic profile, lipid peroxidation-LPO and protein oxidation-PO were determined in liver and white muscle. SOD and CAT were not affected. GPX in liver and white muscle and GR in liver increased at higher inclusion carbohydrates levels. The lowest levels of GR and G6PDH in both tissues and LPO in liver were observed in maltodextrin groups. No significant effects by carbohydrate source were observed in liver PO and white muscle LPO. Regarding carbohydrate level effect, 18% and 24% dietary inclusion level decreased LPO in white muscle and PO in liver. LPO in liver was also decreased at 24% inclusion level. Altogether, results indicate the use of carbohydrates as an alternative energy source does not produce negative effects on oxidative status of common dentex, on the contrary, even contribute to their oxidative protection.

Effects of oregano essential oil or quercetin supplementation on body weight loss, carcass characteristics, meat quality and antioxidant status in finishing pigs under transport stress

This study compared the effects of dietary oregano essential oil (OEO), quercetin or vitamin E (vit E), on the live body weight loss, carcass characteristics, meat quality and antioxidant status of pigs after transportation. A total of 340 finishing pigs (Large White×Landrace) with an initial body weight of 74kg (±4.0kg) were randomly assigned to one of four treatment groups (five replicate pens per treatment, 17 pigs per pen). Pigs consumed the basal diet (control) or the basal diet supplemented with 200mg vit E/kg (positive control), 25mg OEO/kg or 25mg quercetin/kg for 4 weeks. After this period, 144 pigs (36 pigs per treatment) were transported for 5h before slaughter. Compared with the control group, the OEO or quercetin groups had a higher average daily gain (P<0.05), and the OEO group also had a lower feed intake/gain (P<0.05). The live body weight loss was less in the OEO group after 5h transportation (P<0.05) than in the control group. The hot carcass weight and dressing percentage were higher in the OEO group after 5h of transportation (P<0.05) than in the control group. After slaughter, the pH value at 45-min postmortem and Opto-star value (meat color) at 24-h postmortem increased in the vit E, OEO or quercetin groups (P<0.05) compared with the control group. The vit E or quercetin groups also exhibited higher 24-h postmortem pH values (P<0.05) than the control group. The Longissimus thoracis et lumborum muscle of pigs from the OEO or quercetin groups produced lower 24-h drip loss values (P<0.05) than that of pigs from the control group. Compared with the control group, the OEO or quercetin groups had reduced levels of TBARS (thiobarbituric acid reactive substances) and ROS (reactive oxygen species) in serum, muscle and liver (P<0.05), while the vit E group had reduced levels in serum only (P<0.05). The OEO or quercetin groups also had increased levels of Gpx (glutathione peroxidase) and T-SOD (total superoxide dismutase) activity in serum and liver compared with the control group (P<0.05). Conversely, there were no differences between the vit E and control groups in Gpx or T-SOD activities. In conclusion, supplementation with dietary OEO or quercetin may be superior to supplementation with dietary vit E in alleviating the negative effects of transportation on pigs by improving the pigs’ antioxidant status.

Liver and intestine oxidative status of gilthead sea bream fed vegetable oil and carbohydrate rich diets

This study investigated the effects of dietary lipid source and carbohydrate content on liver and intestine oxidative status of gilthead sea bream juveniles, by assessing antioxidant defences enzymes (superoxide dismutase, SOD; catalase, CAT; glutathione peroxidase, GPX; glutathione reductase, GR; and glucose-6-phosphate dehydrogenase, G6PD); total, reduced, and oxidized glutathione (GSH); and lipid peroxidation (LPO). Fish were fed for 13weeks with four diets (2×2 factorial design) differing in lipid source (Fish oil- FO or a blend of vegetable oil-VO) and carbohydrate level (0 or 20% of digestible starch). Dietary VO reduced liver and intestine LPO, and enhanced liver GSH redox status (total and reduced GSH), GPX, GR, and G6PD activities, while in the intestine a decrease of G6PD activity and an increase of catalase activity and of reduced GSH (only in the carbohydrate diet) were recorded. Dietary carbohydrate promoted an increase of hepatic SOD and G6PD activities, and a decrease of CAT activity, total, oxidized, and reduced GSH, LPO, and oxidative stress index (OSI) (only in the FO diet). In the intestine, dietary carbohydrate did not induce alterations in LPO or enzymatic antioxidant defences but negatively affected GSH redox status (OSI, reduced and oxidized GSH). Overall, few interactions between dietary lipid source and carbohydrates were recorded. Dietary VO appeared to have a protective role against LPO in both tissues. Dissimilarities in liver and intestine susceptibility to LPO by dietary carbohydrate may reflect differences in glucose and GSH metabolism in the two tissues. Statement of relevancePlant related macronutrients improve fish oxidative status.

Ellagic and ferulic acids alleviate gamma radiation and aluminium chloride-induced oxidative damage

AimIonizing radiation interacts with biological systems through the generation of free radicals, which induce oxidative stress. Aluminium (Al) can negatively impact human health by direct interaction with antioxidant enzymes. Ellagic acid (EA) and Ferulic acid (FA) are plant polyphenolic compounds, have gained attention due to their multiple biological activities. To date, no studies investigating the antioxidant effect of EA/FA in a model involving both γ radiation and aluminium chloride (AlCl3) have been reported. Herein, we investigated the protective effect of EA and FA against oxidative stress induced by γ radiation and AlCl3 in rats. MethodsRats were divided into thirteen groups: a negative control group, 3 positive control groups (γ-irradiated, AlCl3−treated and γ-irradiated+AlCl3−treated) and 9 groups (3 γ-irradiated, 3 AlCl3−treated and 3 γ-irradiated+AlCl3−treated) treated with EA and/or FA. Liver function and lipid profile were assessed. Levels of lipid peroxidation, protein oxidation and endogenous antioxidants as well as the concentrations of copper, iron and zinc were estimated in liver tissue homogenate. Furthermore, liver tissue sections were histologically examined. ResultsOral administration of EA and/or FA resulted in 1) amelioration of AlCl3 and/or γ-radiation-induced hepatic function impairment, dyslipidemia and hepatic histological alterations; 2) reduction in liver MDA and PCC levels; 3) elevation of liver CAT, GPx and SOD activity as well as GSH level; 4) elevation in liver Cu concentrations which was accompanied by a reduction in Fe and Zn concentrations. ConclusionsOral administration of EA and/or FA may be useful for ameliorating γ radiation and/or AlCl3-induced oxidative damage.

Selenoprotein Transcript Level and Enzyme Activity as Biomarkers for Selenium Status and Selenium Requirements of Chickens (Gallus gallus).

The NRC selenium (Se) requirement for broiler chicks is 0.15 μg Se/g diet, based primarily on weight gain and feed intake studies reported in 1986. To determine Se requirements in today’s rapidly growing broiler chick, day-old male chicks were fed Se-deficient basal diets supplemented with graded levels of Se (0, 0.025, 0.05, 0.075, 0.1, 0.2, 0.3, 0.5, 0.75, and 1.0 μg Se/g) as Na2SeO3 (5/treatment). Diets contained 15X the vitamin E requirement, and there were no gross signs of Se-deficiency. At 29 d, Se-deficient chicks weighed 62% of Se-supplemented chicks; 0.025 μg Se/g reversed this effect, indicating a minimum Se requirement of 0.025 μg Se/g diet for growth for male broiler chicks. Enzyme activities in Se-deficient chicks for plasma GPX3, liver and gizzard GPX1, and liver and gizzard GPX4 decreased dramatically to 3, 2, 5, 10 and 5%, respectively, of Se-adequate levels, with minimum Se requirements of 0.10–0.13 μg Se/g, and with defined plateaus above these levels. Pancreas GPX1 and GPX4 activities, however, lacked defined plateaus, with breakpoints at 0.3 μg Se/g. qPCR measurement of all 24 chicken selenoprotein transcripts, plus SEPHS1, found that SEPP1 in liver, GPX3 in gizzard, and SEPP1, GPX3 and SELK in pancreas were expressed at levels comparable to housekeeping transcripts. Only 33%, 25% and 50% of selenoprotein transcripts were down-regulated significantly by Se deficiency in liver, gizzard and pancreas, respectively. No transcripts could be used as biomarkers for supernutritional Se status. For export selenoproteins SEPP1 and GPX3, tissue distribution, high expression and Se-regulation clearly indicate unique Se metabolism, which may underlie tissues targeted by Se deficiency. Based on enzyme activities in liver, gizzard, and plasma, the minimum Se requirement in today’s broiler chick is 0.15 μg Se/g diet; pancreas data indicate that the Se requirement should be raised to 0.2 μg Se/g diet to provide a margin of safety.

Selenium Requirements in Rats, Mice, Lambs, Chicks and Turkeys Based on Selenoprotein Enzyme Activity and Transcript Level

Over the past several years, my lab has conducted a series of studies to evaluate selenium (Se) status and requirements in rats, mice and lambs, all using virtually the same diets. These studies progressed from using glutathione peroxidase (GPX) activity as the primary biomarker, to use of GPX protein and GPX mRNA levels as biomarkers, and recently we expanded to include additional selenoenzyme activities as well as transcript levels for the full selenoproteome. Literature reports of Se requirements of turkeys have consistently indicated that turkeys have a markedly higher Se requirement than mammals (NRC: 0.2 μg Se/g). Thus we evaluated the Se requirements of turkey poults, and in parallel, of chicks. The objective here is to compare resulting requirements and to identify clues to better understand the underlying differences in Se requirements and in Se‐deficiency target tissues. For all studies, animals were fed a basal torula yeast diet (0.005–0.007 μg Se/g) with graded levels of Se supplemented as selenite for 4 weeks (lambs 8 wk). Se response curves result in well‐defined Se‐adequate plateaus for all biomarkers except RBC GPX1 activity. Based on plasma GPX3, liver GPX1, and RBC GPX1 activities, the mammalian minimal dietary Se requirement is uniformly 0.1 μg Se/g, whereas the turkey requirement is clearly 3‐times higher at 0.3 μg Se/g; the chick minimum Se requirement is 0.15 μg Se/g based on plasma GPX3 and GPX1 activities. Liver GPX4 activity is only modestly affected by Se deficiency in rats, but falls to ~10% of plateau levels in mice, chicks and poults. In contrast to selenoenzyme activity biomarkers, requirements based on liver GPX1 mRNA are uniformly 0.04–0.11 μg Se/g for rodents and avians, with GPX1 mRNA in Se deficiency falling more dramatically in rodents vs. avians. GPX4 mRNA is little affected by Se deficiency in rodents but falls to 30% in avians. Other unique species differences include high expression of GPX3 mRNA in avian liver; plasma GPX3 activity in Se deficiency falls to 1–3% of plateau levels in rats, chicks, poults and lambs and but only to 35% in mice. Sigmoidal Se response curves are observed for liver GPX1 activity in rats, chicks, turkeys and lambs, and for plasma GPX3 activity in mice, indicating that Se is preferentially directed to other selenoenzymes and/or tissues under Se‐deficient conditions. No mRNA response curves are markedly sigmoidal. Notably, there are no selenoprotein mRNAs that can be used as biomarkers for supernutritional Se status. These studies demonstrate that the minimum dietary Se requirement of young mammals falls over a narrow range, while the requirement of chicks is slightly higher, and turkey requirements are 3‐times that of mammals. Differences in these biomarker Se response curves may help to understand Se metabolism and targeting of tissues in Se deficiency, and thus help to better characterize Se requirements.Support or Funding InformationUSDA Hatch 233618 and 1004389, Northeast Agricultural Univ NECT‐1207‐02 and 1252‐ NCET‐009, and UW Selenium Nutrition Research Fund

Selenoprotein Transcript Level and Enzyme Activity as Biomarkers for Selenium Status and Selenium Requirements in the Turkey (Meleagris gallopavo).

The current National Research Council (NRC) selenium (Se) requirement for the turkey is 0.2 μg Se/g diet. The sequencing of the turkey selenoproteome offers additional molecular biomarkers for assessment of Se status. To determine dietary Se requirements using selenoprotein transcript levels and enzyme activities, day-old male turkey poults were fed a Se-deficient diet supplemented with graded levels of Se (0, 0.025, 0.05, 0.1, 0.2, 0.3, 0.4, 0.5, 0.75, 1.0 μg Se/g diet) as selenite, and 12.5X the vitamin E requirement. Poults fed less than 0.05 μg Se/g diet had a significantly reduced rate of growth, indicating the Se requirement for growth in young male poults is 0.05 μg Se/g diet. Se deficiency decreased plasma GPX3 (glutathione peroxidase), liver GPX1, and liver GPX4 activities to 2, 3, and 7%, respectively, of Se-adequate levels. Increasing Se supplementation resulted in well-defined plateaus for all blood, liver and gizzard enzyme activities and mRNA levels, showing that these selenoprotein biomarkers could not be used as biomarkers for supernutritional-Se status. Using selenoenzyme activity, minimum Se requirements based on red blood cell GPX1, plasma GPX3, and pancreas and liver GPX1 activities were 0.29–0.33 μg Se/g diet. qPCR analyses using all 10 dietary Se treatments for all 24 selenoprotein transcripts (plus SEPHS1) in liver, gizzard, and pancreas found that only 4, 4, and 3 transcripts, respectively, were significantly down-regulated by Se deficiency and could be used as Se biomarkers. Only GPX3 and SELH mRNA were down regulated in all 3 tissues. For these transcripts, minimum Se requirements were 0.07–0.09 μg Se/g for liver, 0.06–0.15 μg Se/g for gizzard, and 0.13–0.18 μg Se/g for pancreas, all less than enzyme-based requirements. Panels based on multiple Se-regulated transcripts were effective in identifying Se deficiency. These results show that the NRC turkey dietary Se requirement should be raised to 0.3 μg Se/g diet.

DOES ROSEMARY EXTRACT HAS ANY PROTECTIVE EFFECT AGAINST ACETAMENOPHEN INTOXICATION OF LIVER AND KINDNEY? AN EXPERIMENTAL STUDY

Introduction :The first case was reported in 1966 and today acetaminophen liver toxicity due to the widespread use of these drugs, liver damage caused by the most common cause of acute liver failure in the world., in this study, the effect of rosemary extract on liver function and examined all the toxicity of acetaminophen Method: This research is an experimental study in 2015 in Yasuj Medicinal Plant Research Center to investigate liver and kidney protective effects of alcoholic extract of rosemary in acetaminophen induced liver toxicity in male Westar rats were used. In this study, 48 male Westar rats weighing 200 to 250 g are randomly divided into 6 groups of 8 animals and for two days and interference were studied. Findings: H epatic and renal protective effect of rosemary extracts on liver and kidney damage caused by acetaminophen overdose by changes in biochemical markers of liver and all such as SGOT and SGPT and BUN and serum Cr and MDA liver and kidney and liver GPX treated groups (receiving acetaminophen + rosemary) as mentioned Methods in the methods section 48 hours after the mice were examined. Result: Microscopic examination slices prepared from rats with acetaminophen liver toxicity were slightly apoptosis; focal inflammation and sinusoidal dilation compared with healthy control group were observed. Also in this group are cutting all low cell loss, and a significant increase in mitosis were observed in tubular epithelial cells.

Effects of dietary supplementation with sage (Salvia officinalis L.) essential oil on antioxidant status and duodenal wall integrity of laying strain growers.

The objective of this study was to compare the influence of four different concentrations of Salvia officinalis essential oil (EO) on animal health. A total of 50 laying strain chicks were randomly divided at the day of hatching into five dietary-treatment groups. Control group was given the basal diet (BD), the other four experimental groups contained BD supplemented with 0.1, 0.25, 0.5, 1.0 g S. officinalis EO/kg diet, respectively. 0.1 g/kg EO increased glutathion peroxidase activity (GPx) in duodenal mucosa, liver and kidney, phagocytic activity in blood (PA), transepithelial electrical resistance (TEER) in duodenal tissue and decreased malondialdehyde (MDA) concentration in plasma and liver. 0.25 g/kg EO increased GPx in liver, total antioxidant status (TAS) in plasma, PA in blood and TEER in duodenal tissue. Our results demonstrate that lower concentrations of EO improve animals' health status, and that it is necessary keep in mind the selection of sufficient concentration of EO used as animal feed additive.