The Effects of T-2 Toxin, Deoxynivalenol, and Fumonisin B1 on Oxidative Stress-Related Genes in the Kidneys of Laying Hens.

In the context of nephrotoxic risks associated with environmental contaminants, this study focused on the impact of mycotoxin exposure on the renal health of laying hens, with particular attention to oxidative stress pathways. Sixty laying hens were assigned to three groups-a control group (CON), a low-dose mycotoxin group (LOW), and a high-dose mycotoxin group (HIGH)-and monitored for 72 h. Mycotoxin contamination involved T-2/HT-2 toxin, DON/3-AcDON/15-AcDON, and FB1 at their EU-recommended levels (low mix) and at double doses (high mix). Clinical assessments revealed no signs of toxicity or notable weight changes. Analysis of the glutathione redox system parameters demonstrated that the reduced glutathione content was lower than that in the controls at 48 h and higher at 72 h. Glutathione peroxidase activity increased in response to mycotoxin exposure. In addition, the gene expression patterns of key redox-sensitive pathways, including Keap1-Nrf2-ARE and the AhR pathway, were examined. Notably, gene expression profiles revealed dynamic responses to mycotoxin exposure over time, underscoring the intricate interplay of redox-related mechanisms in the kidney. This study sheds light on the early effects of mycotoxin mixtures on laying hens' kidneys and their potential for oxidative stress.

Curcumin mitigates ochratoxin A-induced oxidative stress and alters gene expression in broiler chicken liver and kidney.

The study aimed to evaluate the effect of curcumin (CURC) supplementation on broiler chickens exposed to ochratoxin A (OTA), by examining biochemical parameters and the expression of glutathione redox system genes and their regulation. OTA reduced glutathione content in the liver while increasing glutathione peroxidase activity. CURC showed no significant effects. Kidney parameters remained mostly unaffected. Gene expression analysis revealed OTA-induced upregulation of KEAP1, NRF2, AHR, GPx4 and GSR genes in the liver. CURC supplementation led to the upregulation of GPx4 and AHR genes with OTA+CURC treatment, resulting in the downregulation of GPx4, KEAP1, NRF2 and AHR genes compared to OTA treatment alone. In the kidney, GPx4 was downregulated, and NRF2 and AHR were upregulated as an effect of OTA, while CURC upregulated the NRF2 gene only. OTA+CURC treatment led to the downregulation of GPx4, GSS and AHR genes compared to the control and downregulation of NRF2 and AHR genes compared to OTA. The results suggested that CURC is partly effective against OTA-induced oxidative stress and that the effect of OTA and CURC on the antioxidant response is regulated through the KEAP1-NRF2-ARE and AHR pathways.

Multi-Fusarium mycotoxin exposure activates Nrf2 and Ahr pathway in the liver of laying hens.

This study investigates gene expression changes in laying hens exposed to trichothecene mycotoxins, known to induce oxidative stress and affect xenobiotic transformation and antioxidants. A 3-day feeding trial tested low and high doses of T-2/HT-2 toxin, DON/3-AcDON/15-AcDON, and FB1 in hen feed. Results showed increased expression of AHR, AHRR, HSP90, and CYP1A2 genes on days 2 and 3, suggesting a response to mycotoxin exposure. High doses down-regulated CYP1A2, AHR, and AHRR on day 1. KEAP1 expression decreased on day 1 but increased dose-dependently on days 2 and 3. NRF2 was up-regulated by low and down-regulated by high doses on day 1, then increased on days 2 and 3. Antioxidant-related genes (GPX3, GPX4, GSS, GSR) showed dose-dependent responses. Low doses up-regulated GPX3 and GPX4 throughout, while high doses up-regulated GPX3 on days 2 and 3 and GPX4 on day 3. GSS was up-regulated on day 3. Results indicate that toxic metabolites formed by phase I biotransformation rapidly induce ROS formation at low doses through the AHR/Hsp90/CYP1A2 pathway at the gene expression level, but at high levels, ROS-induced oxidative stress manifests later. Study showed simultaneous activation of redox-sensitive pathways: aryl hydrocarbon receptor (Ahr) and nuclear factor erythroid-derived 2-like 2 (Nrf2) by multi-mycotoxin exposure.

Effects of Short- and Medium-Chain Fatty Acids on Production, Meat Quality, and Microbial Attributes-A Review.

The non-therapeutic use of antimicrobials in poultry production contributes to the spread of drug-resistant pathogens in both birds and humans. Antibiotics are known to enhance feed efficiency and promote the growth and weight gain of poultry. New regulatory requirements and consumer preferences have led to a reduced use of antibiotics in poultry production and to the discovery of natural alternatives to antibiotic growth promoters. This interest is not only focused on the direct removal or inhibition of causative microorganisms but also on the prevention of diseases caused by enteric pathogens using a range of feed additives. A group of promising feed additives is composed of short- and medium-chain fatty acids (SCFAs and MCFAs) and their derivatives. MCFAs possess antibacterial, anticoccidial, and antiviral effects. In addition, it has been proven that these acids act in synergy if they are used together with organic acids, essential oils, or probiotics. These fatty acids also benefit intestinal health integrity and homeostasis in broilers. Other effects have been documented as well, such as an increase in intestinal angiogenesis and the gene expression of tight junctions. The aim of this review is to provide an overview of SCFAs and MCFAs as alternatives to antibiotic growth promoters and to summarize the current findings in the literature to show their possible benefits on production, meat quality, and gut health in poultry.

The Co-Occurrence of T-2 Toxin, Deoxynivalenol, and Fumonisin B1 Activated the Glutathione Redox System in the EU-Limiting Doses in Laying Hens.

Different mycotoxins in feed lead to combined exposure, increasing adverse effects on animal health. Trichothecene mycotoxins have been associated with inducing oxidative stress, which is neutralized by the glutathione system within the antioxidant defense, depending on the dose and duration of exposure. T-2 toxin, deoxynivalenol (DON), and fumonisin B1 (FB1) are commonly found in feed commodities simultaneously. In the present study, the intracellular biochemical and gene expression changes were investigated in the case of multi-mycotoxin exposure, focusing on certain elements of the glutathione redox system. In a short-term feeding trial, an in vivo study was performed with low (EU-proposed) doses: T-2/HT-2 toxin: 0.25 mg; DON/2-AcDON/15-AcDON.: 5 mg; FB1: 20 mg/kg feed, and high doses (twice the low dose) in laying hens. The multi-mycotoxin exposure affected the glutathione system; GSH concentration and GPx activity was higher in the liver in the low-dose group on day 1 compared to the control. Furthermore, the gene expression of antioxidant enzymes increased significantly on day 1 in both exposure levels compared to the control. The results suggest that when EU-limiting doses are applied, individual mycotoxins may have a synergistic effect in the induction of oxidative stress.

Role of the glutathione redox system in the susceptibility of pheasants (Phasianus colchicus) to ochratoxin A.

The purpose of the present study was to investigate the effects of different dietary concentrations of ochratoxin A (OTA) on the growth, feed intake, mortality, blood plasma protein content and some parameters of lipid peroxidation and the glutathione redox system of pheasant chicks in a three-week long trial. A total of 320 seven-day-old female pheasants were randomly assigned to four treatment groups (n = 40 in each), fed with a diet artificially contaminated with OTA [control (<0.02 mg/kg), 0.88 mg/kg, 1.14 mg/kg and 1.51 mg/kg] for 21 days (up to 28 days of age). The pheasant chicks were sacrificed at early (12, 24 and 72 h) and late (7, 14 and 21 days) stages of mycotoxin exposure to check the effect of OTA. Minimal feed refusal was found in the medium- and high-dose toxin groups (-9.8 and -7.9%, respectively), and body weight gain was nearly the same in all groups. The glutathione redox system was activated mainly in the liver, confirmed by significantly increased reduced glutathione content and glutathione peroxidase activity during the late phase of mycotoxin exposure and at a high-dose treatment. The results suggest that pheasants have low susceptibility to OTA, and activation of the glutathione redox system has importance in this tolerance.

Modification of the effects of aflatoxin B1 on the glutathione system and its regulatory genes by zeolite.

The purpose of the present study was to use oxidative stress markers for investigating the effect of zeolite (315 mg/kg of complete feed) in the case of aflatoxin B1 contamination (92 µg/kg complete feed). In a 21-day feeding trial with broiler chickens, oxidative stress parameters such as conjugated dienes, conjugated trienes, malondialdehyde, reduced glutathione content and glutathione peroxidase activity were not changed significantly by supplementation with this mycotoxin absorbent. The relative gene expression of transcription factors KEAP1 and NRF2 was not modified by the absorbent either. Still, the expression of GSS, GSR and GPX4 genes increased significantly due to the aluminosilicate supplementation. The results suggest that zeolite reduced lipid peroxidation in the blood plasma but not in the red blood cell haemolysate or the kidney. The relative expression of the genes encoding the glutathione redox system also changed as a result of zeolite supplementation, but these changes were not found at the protein level.

Individual and Combined Effects of Aflatoxin B1 and Sterigmatocystin on Lipid Peroxidation and Glutathione Redox System of Common Carp Liver.

The purpose of the study was to evaluate the short-term effects of aflatoxin B1 (AFB1 100 µg/kg feed) and sterigmatocystin (STC 1000 µg/kg feed) exposure individually and in combination (100 µg AFB1 + 1000 µg STC/kg feed) on the parameters of lipid peroxidation and glutathione redox system both in biochemical and gene expression levels in one-year-old common carp. Lipid peroxidation parameters were slightly affected, as significant differences were observed only in conjugated diene and triene concentrations. Reduced glutathione content decreased more markedly by STC than AFB1 or AFB1+STC, but glutathione peroxidase activity did not change. Expression of gpx4a, gpx4b, gss, and gsr genes was down-regulated due to STC compared to AFB1 or AFB1+STC, while an induction was found as effect of AFB1+STC in the case of gpx4a, but down-regulation for gpx4b as compared to AFB1. Expression of the glutathione biosynthesis regulatory gene, gss, was higher, but glutathione recycling enzyme encoding gene, gsr, was lower as an effect of AFB1+STC compared to AFB1. These results are supported by the changes in the expression of transcription factors encoding genes, nrf2, and keap1. The results revealed that individual effects of AFB1 and STC on different parameters are synergistic or antagonistic in multi-toxin treatment.

Role of glutathione redox system on the susceptibility to deoxynivalenol of pheasant (Phasianus colchicus).

There are only a few reports on the effects of mycotoxins on pheasant (Phasianus colchicus) and the susceptibility to deoxynivalenol of these birds have never been reported before. The present experiment focuses to investigate the effects of different dietary concentrations of deoxynivalenol on blood plasma protein content, some parameters of lipid peroxidation and glutathione redox system and on the performance of pheasant chicks. A total of 320 1-day-old female pheasants were randomly assigned to four treatment groups fed with a diet contaminated with deoxynivalenol (control, 5.11 mg/kg, 11.68 mg/kg and 16.89 mg/kg). Birds were sacrificed at early (12, 24 and 72 h) and late (1, 2 and 3 weeks) stages of the experiment to demonstrate the oxidative stress-inducing effect of deoxynivalenol. Feed refusal was dose dependent, especially in the last third of the trial, but only minor body weight gain decrease was found. Lipid-peroxidation parameters did not show dose-dependent effect, except in blood plasma during the early stage of the trial. The glutathione redox system, reduced glutathione content and glutathione peroxidase activity, was activated in the liver, but primarily in the blood plasma. Glutathione peroxidase activity has changed parallel with reduced glutathione concentration in all tissues. Comparing our results with literature data, pheasants seem to have the same or higher tolerance to deoxynivalenol than other avian species, and glutathione redox system might contribute in some extent to this tolerance, as effective antioxidant defence against oxidative stress.

Lack of Dose- and Time-Dependent Effects of Aflatoxin B1 on Gene Expression and Enzymes Associated with Lipid Peroxidation and the Glutathione Redox System in Chicken.

Effects of aflatoxin B1 (AFB1) on lipid peroxidation and glutathione system were investigated in chicken liver. In a three-week feeding trial, different doses (<1.0 µg/kg (control diet), 17.0 µg (diet A1), 92.0 µg (diet A2), and 182.0 µg (diet A3) AFB1 kg/feed) were used. Markers of lipid peroxidation, conjugated dienes and trienes showed higher values in A3, while amounts of thiobarbituric acid reactive substances were increased in the A1 group at day 21. Glutathione content was lower at day 14 in Group A2. Glutathione peroxidase 4 activity was increased at days 7 and 21 in the A3 group but reduced in the A2 and A3 groups at day 14. The GPX4 gene was downregulated at day 7 in the A2 group, but overregulated at days 14 and 21, and at day 14 in the A3 group. GSS was downregulated at day 14 in the A1 group but overregulated at day 21 in A1 and A2 groups. GSR was downregulated at days 7 and 21 in all treatment groups, but on day 14, induction was observed in the A3 group. The results indicated that AFB1 did not induce dose- or time-dependent effects on the glutathione redox system and its encoding genes at the dose range used, which means that oxidative stress is not the primary effect of AFB1 toxicity.

Effect of Sterigmatocystin or Aflatoxin Contaminated Feed on Lipid Peroxidation and Glutathione Redox System and Expression of Glutathione Redox System Regulatory Genes in Broiler Chicken.

Authors studied the effect of sterigmatocystin from infected corn (STC), purified sterigmatocystin (PSTC), and aflatoxin B1 from infected corn (AFB1) on lipid peroxidation and glutathione redox parameters, including the expression of their encoding genes in a sub-chronic (14 days) trial. A total of 144 three-week-old cockerels was divided into four experimental groups (n = 36 in each). Control feed was contaminated with STC or PSTC (1590 µg STC/kg or 1570.5 µg STC/kg feed), or with AFB1 (149.1 µg AFB1/kg feed). Six birds from each group were sampled at day 1, 2, 3, 7 and 14 of mycotoxin exposure. As parameters of lipid peroxidation, conjugated dienes (CD) and trienes (CT) were measured in the liver, while malondialdehyde (MDA) concentration was determined in blood plasma, red blood cell hemolysate and liver. Reduced glutathione (GSH) concentration and glutathione peroxidase (GPx) activity were determined in the same samples, and expression of glutathione peroxidase 4 (GPX4), glutathione synthetase (GSS) and glutathione reductase (GSR) genes was measured by RT-PCR in the liver. STC, PSTC or AFB1 caused a slight, but not significant, increase in CD and CT levels; however, in the case of MDA, no increase was found in the liver. Glutathione redox system was activated in the liver by AFB1, but less markedly by STC/PSTC. PSTC and AFB1 resulted in a higher expression of GPX4, while GSS expression was down-regulated by AFB1 on day 1, but up-regulated by STC on day 2 and by both mycotoxins on day 7. However, on day 14, GSS expression was down-regulated by PSTC. Expression of GSR was low on day 1 in AFB1 and PSTC groups, but later it was up-regulated by AFB1. The observed changes regarding gene expression strengthen the hypothesis that the mild oxidative stress, caused by the applied STC doses, activates the glutathione redox system of broiler chickens.

Long-Term Effects of Ochratoxin A on the Glutathione Redox System and Its Regulation in Chicken.

The purpose of this study was to evaluate the effect of three-weeks ochratoxin A (OTA) exposure on some lipid peroxidation parameters, reduced glutathione concentration and glutathione-peroxidase activity, as well as expression of oxidative stress response-related (KEAP1, NRF2) and glutathione system (GPX3, GPX4, GSS, GSR) genes in chickens. Three levels of exposure (106, 654 and 1126 µg/kg feed) were applied. The results showed that OTA initiated free radical formation, which was suggested by the increase in the malondialdehyde content in the liver and kidney, which was more marked in the liver, depending on the length of exposure and dose. Reduced glutathione concentration increased as an effect of the highest OTA dose in blood plasma and in liver, but not in red blood cell hemolysates and the kidney. Glutathione peroxidase activity did not change in the blood and showed increasing tendency in the liver, and significant increase in the kidney. Expression of KEAP1 gene showed up-regulation in the liver, and down-regulation in the kidney, but overexpression of NRF2 gene was found in the liver and kidney at the highest dose. However, down-regulation of Nrf2 dependent genes, GPX3, GPX4, GSS and GSR, suggested an improper antioxidant response at the protein level, thus oxidative stress occurred, even at the dose of the EU regulatory limit for poultry diets.

Comet assay study of the genotoxic effect of T-2 and HT-2 toxins in chicken hepatocytes.

BACKGROUND AND AIMS: The aim of this study was to verify that the comet assay can be used to investigate the DNA damaging effects of T-2 and HT-2 toxins in the liver of broiler chickens. The comet assay is a favorable genotoxic analysis because it is cheap, simple, and can be used in many organisms and different tissues. MATERIALS AND METHODS: Male broiler chickens were fed with T-2/HT-2 toxins-contaminated diet for 14 days. The comet assay was successfully adapted to chicken liver cells, and the DNA damage was determined by a decrease in the comet parameter (DNA % in the tail) in the experimental groups. RESULTS: The method of evaluation was found to be critical because DNA damage could not be detected exactly using the CometScore software, due to inaccurate separation of head and comet. However, this problem can be solved by visual evaluation. CONCLUSION: In the case of the visual evaluation, each toxin-treated group differed significantly from the control group, indicating that the assay can be useful for the assessment of primary DNA damage caused by T-2/HT-2 toxins.

Multi-trichothecene mycotoxin exposure activates glutathione-redox system in broiler chicken.

Co-occurrence of mycotoxin contamination of feeds is a frequent problem, therefore the purpose of this study was to evaluate the combined effect of T-2 toxin and deoxynivalenol (DON) on lipid peroxidation, parameters and regulation of the glutathione redox system in broiler chickens in a sub-chronic (7 day) study. The applied doses were: low mix: 0.23 mg T-2 toxin and 4.96 mg DON/kg feed; medium mix: 1.21 mg T-2 toxin and 12.38 mg DON/kg feed; and high mix: 2.42 T-2 toxin and 24.86 mg DON/kg feed. Liver samples were taken on days 0, 1, 2, 3, and 7 of the feeding trial. Lipid peroxidation decreased significantly as compared to the control on days 3 and 7 as effect of low and high doses, which can be related to the activation of the antioxidant system, which is supported by the elevated glutathione peroxidase activity and reduced glutathione concentration as compared to the control on day 3 in the medium and high dose groups. Gene expression of glutathione peroxidase 4 (GPX4) elevated on day 1 in a dose dependent manner, and showed continuous elevation in the highest dose group thereafter. The results suggested that common exposure of T-2 toxin and DON induced oxidative stress in the liver of broiler chickens, which activated the enzymatic antioxidant system, and consequently decreased lipid peroxidation.

Role of Glutathione Redox System on the T-2 Toxin Tolerance of Pheasant (Phasianus colchicus).

The purpose of the present study was to evaluate the effects of different dietary concentrations of T-2 toxin on blood plasma protein content, lipid peroxidation and glutathione redox system of pheasant (Phasianus colchicus). A total of 320 one-day-old female pheasants were randomly assigned to four treatment groups fed with a diet contaminated with different concentrations of T-2 toxin (control, 4 mg/kg, 8 mg/kg and 16 mg/kg). Birds were sacrificed at early (12, 24 and 72 hr) and late (1, 2 and 3 weeks) stages of the experiment to demonstrate the effect of T-2 toxin on lipid peroxidation and glutathione redox status in different tissues. Feed refusal and impaired growth were observed with dose dependent manner. Lipid-peroxidation was not induced in the liver, while the glutathione redox system was activated partly in the liver, but primarily in the blood plasma. Glutathione peroxidase activity has changed parallel with reduced glutathione concentration in all tissues. Based on our results, pheasants seem to have higher tolerance to T-2 toxin than other avian species, and glutathione redox system might contribute in some extent to this higher tolerance, in particular against free-radical mediated oxidative damage of tissues, such as liver.

[Antioxidant effect of the fibre content of foods]. / Az élelmiszerek rosttartalmának antioxidáns hatása.

Antioxidants have some health benefit, but up to now there was less attention paid to the antioxidant properties of dietary fibre. The antioxidant effect of dietary fibre is based on the polyphenol compounds bound to polysaccharide complexes, which are released in the gut and functioning as antioxidants. Another type of antioxidant, calcium fructoborate was also isolated from plant cell wall. It has a marked antioxidant capacity, however, its active component is not a polyphenol, but the boron. There are lots of food plants which have relatively high antioxidant dietary fibre content, thus they support the antioxidant defence of the gastrointestinal tract, and consequently the whole body. The important ones in human nutrition are for instance cereal grains, cabbage, grape pomace, coffee bean or guava. There are different polyphenol compounds in the antioxidant dietary fibres in the plants, therefore their antioxidant capacity varies, but it is approximately equivalent to 50-100 mg DL-α-tocopherol per gram. This antioxidant capacity is considerable, and would be suitable for the prevention of some, oxidative stress-related diseases, such as atherosclerosis or other cardiovascular diseases, and colorectal carcinoma. Orv Hetil. 2018; 159(18): 709-712.

Short-term effects of T-2 toxin or deoxynivalenol on glutathione status and expression of its regulatory genes in chicken.

Short-term (48-hour) effects of 3.74/1.26 mg kg-1 T-2/HT-2 toxin or 16.12 mg kg-1 DON in feed were investigated in the liver of three-week-old cockerels (body weight: 749.60 ± 90.98 g). Markers of lipid peroxidation showed no significant changes. At hour 24, glutathione content in the T-2/HT-2 toxin group was significantly higher than in the control. Glutathione peroxidase activity was significantly higher than the control at hour 24 in the T-2/H-2 toxin group and at hour 48 in the DON group. In the DON group, expression of the glutathione peroxidase 4 gene (GPX4) was significantly lower than in the control at hours 12 and 14, and higher at hour 48. Expression of the glutathione reductase gene (GSR) was significantly lower than in the control at hour 12 in the T-2/HT-2 toxin group, and at hours 12, 24 and 48 in the DON group. However, at hour 36 higher GSR expression was measured in the DON group. Due to the effect of both trichothecenes, expression of the glutathione synthetase gene (GSS) was significantly lower than in the control at hours 24 and 48. In conclusion, T-2/HT-2 toxin and DON had a moderate short-term effect on free radical formation. T-2/HT-2 toxin induced more pronounced activation of the glutathione redox system than did DON.

Effect of diets with different inclusion levels of distillers dried grain with solubles combined with lysine and methionine supplementation on the lipid peroxidation and glutathione status of chickens.

To study the possible effects of different inclusion levels of distillers dried grain with solubles (DDGS) on the lipid peroxidation and glutathione redox status of chickens, 200 three-week-old Ross 308 cockerels were assigned to four treatment groups of 50 birds each. The groups were fed a control and three experimental, isocaloric and isonitrogenous grower diets containing 15, 20 and 25% DDGS, respectively, combined with lysine (Lys) and methionine (Met) supplementation until 6 weeks of age. It was found that DDGS inclusion increased the ether extract content of the diets which resulted in higher reduced glutathione (GSH) content and elevated glutathione peroxidase activity (GSHPx) in the liver. However, DDGS addition with Lys and Met supplementation did not influence the malondialdehyde content of the blood and the liver. The oleic acid proportion of the diet showed a close positive correlation with GSH content of the liver. A smaller ratio of methionine and cysteine in the diet with DDGS resulted in significantly higher liver GSH content. GSHPx activity increased parallel with the elevated GSH content of the liver homogenate, suggesting that the enzyme is activated by the actual supply of its co-substrate. In conclusion, the results show that DDGS, even at a high inclusion level combined with Lys and Met supplementation, has no initiative effect on lipid peroxidation in the blood and liver of broiler chickens.

Effect of combined treatment with aflatoxin B1 and T-2 toxin and metabolites on some production traits and lipid peroxide status parameters of broiler chickens.

Three groups of cockerels were fed with a control diet, with a diet contaminated with T-2 and HT-2 toxin (0.31 and 0.26 mg/kg) or with that containing a combination of T-2 and HT-2 toxin (0.32 and 0.25 mg/kg) and aflatoxin B1 (AFB1, 0.38 mg/kg) for 21 days. Body weight gain and feed conversion ratio did not differ significantly among the groups. Malondialdehyde concentration of the liver was lower in the group fed the diet contaminated with the combination of T-2 + HT-2 toxin and aflatoxin B1 as compared to the control group or the group fed T-2 + HT-2 toxins. Reduced glutathione (GSH) content of the liver was lower in the T-2 + HT-2 group than in the group fed a combination of T-2, HT-2 and aflatoxin. Reduced glutathione content of the heart was higher in the T-2 + HT-2 group than in the control group. Mycotoxin contamination had no effect on glutathione peroxidase (GSH-Px) activity in comparison to the control, but significantly lower GSH-Px activity was found in the heart of chickens in the T-2 + HT-2 + AFB1 group than in the T-2 + HT-2 group. In this study, T-2 + HT-2 toxin and aflatoxin B1 contamination of the diets did not affect the production traits adversely and did not exert additive effects on lipid peroxidation and on the glutathione redox system.

Investigation of lipid peroxide and glutathione redox status of chicken concerning on high dietary selenium intake.

This study was designed to investigate the effects of excess (24.5 mg Se/kg feed) inorganic and organic dietary selenium supplementation on 3-week-old broilers. The experiments lasted 4 days. Intensity of lipid peroxidation processes (malondialdehyde, MDA) and the amount (reduced glutathione, GSH) and activity (glutathione peroxidase activity, GSHPx) of gluathione redox system were measured in blood plasma, red blood cell hemolysate and liver. Voluntary feed intake in the selenium-treated groups reduced remarkably. Elevated GSH concentration and GSHPx activity were measured in plasma and liver of both selenium-treated groups compared to the untreated control and the 'pair-fed' controls. The lipid peroxidation processes in the liver showed higher intensity than the control due to both selenium treatment. The applied dose of selenite and selenomethionine does not inhibit, but even improves the activity of glutathione redox system in the liver during the early period of selenium exposure.