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.
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.
Ring necked pheasant is the most significant game bird in Hungary. Around 300.000 pheasant harvested (hunted) annually and generally these birds are consumed by the hunters. As there are limited data on the quality of pheasant meat, in the present study we aimed to analyze some physical and chemical properties of it. At 20 weeks of age 63 pheasant hens were exterminated by cervical dislocation and meat, liver, spleen and heart samples were taken. The live weight of the birds was 1045±92g (870 to 1300g). The average weight of the liver, spleen and heart was 14.12±2.58, 0.47±0.13 and 4.30±0.49, respectively. The average drip loss was 5.90±2.38% (0.68±0.28g). As was expected the average protein content (26.2±0.7%) of the pheasant breasts was markedly higher than in broiler or turkey. The average fat content (0.4±0.2%) was similar to that in turkey. The unique chemical and physical properties of the pheasant meat make it suitable to fit in the human nutrition.
The effect of two different contamination levels of T-2 toxin (1.5 or 3.4 mg/kg feed) was investigated in a 28-days feeding trial on body weight, relative weight of liver and spleen, and some lipid peroxidation and glutathione redox parameters of 14-days old broiler chicken. The results showed that T-2 toxin decreased significantly the body weight at both contamination levels and showed a dose-dependent tendency. Relative weight of liver increased till the end of the trial, while relative weight of spleen was lower at both samplings at lower level of T-2 toxin exposure. Initial phase of lipid peroxidation (conjugated dienes and trienes) was not detected in the liver, but as product of later phase, thiobarbituric acid reactive substances increased significantly, except in the liver. Glutathione content on day 14 was higher in liver homogenate as compared to the control at the lower T-2 toxin contamination level. On day 28 it was higher in blood plasma at the higher and in liver homogenate at both levels of T-2 contamination. Glutathione peroxidase activity on day 14 was significantly higher in liver and spleen homogenates as compared to the control at the lower level of T-2 toxin contamination. On day 28, significantly higher activity was found at both T-2 toxin contamination levels in liver homogenate, and at the lower contamination level in spleen homogenate as compared to the control.The results revealed that T-2 toxin exposure initiates lipid peroxidation and activates the glutathione redox system as well, but the changes were irrespective of the dose-and partly duration of the exposure.
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