Az antioxidánsok az egészségre számos kedvező hatással rendelkeznek, amelyek
közül napjainkig kevés figyelem irányult az élelmi rost antioxidáns
tulajdonságaira. Az élelmi rost antioxidáns hatása mögött az azt alkotó
poliszacharidkomplexhez kapcsolt polifenolvegyületek állnak, amelyek a
bélcsatornában felszabadulva fejtik ki hatásukat. Növényi sejtfalból izoláltak
egy, az előbbiektől eltérő molekulát, a kalcium-fruktoborátot, amelynek szintén
van antioxidáns kapacitása, annak aktív komponense azonban a bór. Számos olyan
élelmiszer és élelmiszeripari melléktermék ismert, amelynek jelentős antioxidáns
élelmirost-tartalma van, így ezek is hozzájárulhatnak a bélcsatorna, ennek révén
a szervezet antioxidáns védelméhez. Ilyenek például a gabonamagvak, a káposzta,
a kávébab és a guáva, vagy a melléktermékek közül a szőlőtörköly. Az antioxidáns
élelmi rost polifenolvegyületei az egyes növényekben eltérőek, így azok
antioxidáns kapacitása is változó, de grammonként hozzávetőlegesen 50–100 mg
DL-α-tokoferollal egyenértékűek. Ez olyan számottevő antioxidáns kapacitás,
amely alkalmassá teszi az antioxidáns élelmi rostot egyes, bizonyítottan
oxidatív stressz által kiváltott betegségek, így például az atherosclerosis,
egyéb cardiovascularis kórképek vagy a colorectalis carcinoma elleni
prevencióban. Orv. Hetil. 2018; 159(18): 709–712.
Glutathione peroxidase enzyme superfamily plays significant role in the elimination of reactive oxygen free radicals in the animals. Many characteristics of these proteins have been revealed already, but their regulation is still not known. Several data suggest that some environmental factors have certain regulatory effect, while others propose strict genetic regulation.In this report we present four different environmental induction models in which New Zealand white rabbits were used as experimental animals. In three models, free radical load of different origin, lipidperoxide load, application of a glutathione depletor or a prooxidant agent, was introduced. Beside these negative models a positive model was also constructed in which additive selenium was supplied.Glutathione peroxidase activity was measured in blood serum, erythrocyte haemolysate and liver. Reduced glutathione, and malondialdehyde concentration in the liver were also determined.According to the results, the established models are capable for analysing the enzyme activity´environmental interactions.
Selenium, as part of selenocysteine, is the active centre of selenoenzymes. Excess amount of selenium generates oxygen free radicals and reacts with thiol compounds such as reduced glutathione, composing seleno-diglutathione. These reactions impair the amount and/or activity of the biological antioxidant defence system. In the present experiment the effects of two inorganic selenium sources (Na2SeO3, Na2SeO4) on lipid peroxidation and on the content and activity of some components of the antioxidant defence mechanism were studied in Ross 308 hybrid cockerels. In the tissues examined, the glutathione redox system was altered in different ways as an effect of excess selenium. The amount of glutathione and, consequently, glutathione peroxidase activity declined in the blood plasma and in the red blood cell haemolysate, while in the liver malondialdehyde concentration increased only at the end of the experimental period as a result of the boosted enzyme activity. The authors suppose that the cause of increased lipid peroxidation was the potential toxic effect of selenium accumulation above the actual demand.
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.
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.
The purpose of the present study was to investigate the effect of experimental T-2 toxin load (2.35 mg/kg of feed) and vitamin E supply in the drinking water (10.5 mg/bird/day) on vitamin E levels of the blood plasma and liver in broiler chickens in a 14-day experiment. It was found that T-2 toxin load did not influence vitamin E content of the blood plasma except at day 3 after the toxin load when a moderate increase was detected in plasma vitamin E. No significant changes were found in vitamin E content of the liver. The simultaneous use of high-dose vitamin E supplementation and T-2 toxin load caused a significantly higher plasma vitamin E content but the changes were less expressed in the group subjected to T-2 toxin load. Vitamin E supply also resulted in a marked and significant increase in vitamin E concentrations of the liver on days 3 and 7 even in the T-2 loaded group, but this concentration significantly decreased thereafter. The results show that T-2 contamination of the diet has an adverse effect on the utilisation of vitamin E in broiler chickens.
The effect of feeding ochratoxin A (OTA) contaminated diet (379.6 and 338.1 μg/kg in starter and grower diets) on production traits, lipid peroxidation and some parameters of the glutathione redox system were investigated in weaned piglets over a seven-week period. Feed intake and feed conversion ratio (FCR) did not differ significantly, but in the first phase (0–28 days) the daily weight gain was significantly lower in the piglets fed the OTA-contaminated diet. Lipid peroxidation, as measured by the amount of malondialdehyde, glutathione content and glutathione peroxidase activity, did not change significantly in the blood plasma and red blood cell haemolysate in the OTA-loaded group, while malondialdehyde content increased significantly in the liver and markedly but not significantly in the kidney of piglets fed OTA-contaminated feed. Glutathione content did not differ significantly in the studied organs of the two groups while glutathione peroxidase activity of the OTA-loaded animals was significantly lower both in the liver and in the kidney. The results suggest that the use of feed-stuffs contaminated with low levels of OTA for seven weeks did not cause marked differences in the production traits or in lipid peroxidation and amount or activity of the glutathione redox system in the blood plasma, red blood cells and kidney, while significant changes occurred in the liver homogenate.
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.
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 B
, 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 B
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 + AFB
group than in the T-2 + HT-2 group. In this study, T-2 + HT-2 toxin and aflatoxin B
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.
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.
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.
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.