Short-term effects of T-2 toxin exposure on some lipid peroxide and glutathione redox parameters of broiler chickens

Summary The purpose of this study was to investigate the short‐term effects of T‐2 toxin exposure (3.09 mg/kg feed) on lipid peroxidation and glutathione redox system of broiler chicken. A total of 54 Cobb 500 cockerels were randomly distributed to two experimental groups at 21 days of age. Samples...

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Veröffentlicht in:Journal of animal physiology and animal nutrition 2016-06, Vol.100 (3), p.520-525
Hauptverfasser: Bócsai, A., Pelyhe, Cs, Zándoki, E., Ancsin, Zs, Szabó-Fodor, J., Erdélyi, M., Mézes, M., Balogh, K.
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container_issue 3
container_start_page 520
container_title Journal of animal physiology and animal nutrition
container_volume 100
creator Bócsai, A.
Pelyhe, Cs
Zándoki, E.
Ancsin, Zs
Szabó-Fodor, J.
Erdélyi, M.
Mézes, M.
Balogh, K.
description Summary The purpose of this study was to investigate the short‐term effects of T‐2 toxin exposure (3.09 mg/kg feed) on lipid peroxidation and glutathione redox system of broiler chicken. A total of 54 Cobb 500 cockerels were randomly distributed to two experimental groups at 21 days of age. Samples (blood plasma, red blood cell, liver, kidney and spleen) were collected every 12 h during a 48‐h period. The results showed that the initial phase of lipid peroxidation, as measured by conjugated dienes and trienes in the liver, was continuously, but not significantly higher in T‐2 toxin‐dosed birds than in control birds. The termination phase of lipid peroxidation, as measured by malondialdehyde, was significantly higher in liver and kidney as a result of T‐2 toxin exposure at the end of the experimental period (48th hour). The glutathione redox system activated shortly after starting the T‐2 toxin exposure, which is supported by the significantly higher concentration of reduced glutathione and glutathione peroxidase activity in blood plasma at 24 and 48 h, in liver at 12, 24 and 36 h, and in kidney and spleen at 24 h. These results suggest that T‐2 toxin, or its metabolites, may be involved in the generation of reactive oxygen substances which causes an increase in lipid peroxidation, and consequently activates the glutathione redox system, namely synthesis of reduced glutathione and glutathione peroxidase.
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A total of 54 Cobb 500 cockerels were randomly distributed to two experimental groups at 21 days of age. Samples (blood plasma, red blood cell, liver, kidney and spleen) were collected every 12 h during a 48‐h period. The results showed that the initial phase of lipid peroxidation, as measured by conjugated dienes and trienes in the liver, was continuously, but not significantly higher in T‐2 toxin‐dosed birds than in control birds. The termination phase of lipid peroxidation, as measured by malondialdehyde, was significantly higher in liver and kidney as a result of T‐2 toxin exposure at the end of the experimental period (48th hour). The glutathione redox system activated shortly after starting the T‐2 toxin exposure, which is supported by the significantly higher concentration of reduced glutathione and glutathione peroxidase activity in blood plasma at 24 and 48 h, in liver at 12, 24 and 36 h, and in kidney and spleen at 24 h. 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A total of 54 Cobb 500 cockerels were randomly distributed to two experimental groups at 21 days of age. Samples (blood plasma, red blood cell, liver, kidney and spleen) were collected every 12 h during a 48‐h period. The results showed that the initial phase of lipid peroxidation, as measured by conjugated dienes and trienes in the liver, was continuously, but not significantly higher in T‐2 toxin‐dosed birds than in control birds. The termination phase of lipid peroxidation, as measured by malondialdehyde, was significantly higher in liver and kidney as a result of T‐2 toxin exposure at the end of the experimental period (48th hour). The glutathione redox system activated shortly after starting the T‐2 toxin exposure, which is supported by the significantly higher concentration of reduced glutathione and glutathione peroxidase activity in blood plasma at 24 and 48 h, in liver at 12, 24 and 36 h, and in kidney and spleen at 24 h. 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subjects Animal Feed - analysis
Animals
chicken
Chickens - blood
Chickens - metabolism
Drug Administration Schedule
glutathione
Glutathione - metabolism
glutathione peroxidase
Kidney - drug effects
Lipid Peroxidation - drug effects
Liver - drug effects
malondialdehyde
Malondialdehyde - blood
Oxidation-Reduction
Spleen - drug effects
T-2 toxin
T-2 Toxin - administration & dosage
T-2 Toxin - toxicity
Triglycerides
title Short-term effects of T-2 toxin exposure on some lipid peroxide and glutathione redox parameters of broiler chickens
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