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The aim of this study was to compare recommendations for vitamin E supplementation regarding high polyunsaturated fatty acid intake and to compare the bioactivity of RRR- and all-rac-α-tocopherol with respect to oxidative stress in vivo and the oxidative stability of broiler meat. Fifty male broilers were divided into 5 groups. All groups received diets with a high inclusion of fat (7.5%), one with palm fat and the others with linseed oil, which were either unsupplemented or supplemented with vitamin E to contain in total 85 or 200 IU of vitamin E as all-rac-α-tocopherol and 85 IU as RRR-α-tocopherol. Oxidative stress in vivo was studied by measuring the DNA damage; measuring malondialdehyde (MDA) in plasma, liver, and breast muscle; and analyzing the antioxidant capacity of the lipid-soluble compounds, total antioxidant status of plasma, and antioxidant enzyme assays. The tocopherols in plasma, liver, and breast muscle were also analyzed. In vitro oxidative stability was studied by measuring MDA in fresh, stored, and heat-treated breast meat. Linseed oil, as opposed to palm fat, induced DNA fragmentation and MDA formation. Both forms and concentrations of vitamin E reduced DNA damage and breast muscle MDA. The groups receiving 200 IU of all-rac-α-tocopherol and 85 IU of RRR-α-tocopherol had much higher values for antioxidant capacity of lipid-soluble compounds than did the controls. No differences were observed in the values of antioxidant enzymes. The α-tocopherol levels in tissues and plasma were significantly influenced by the level of α-tocopherol supplementation. Malondialdehyde formation in meat from the vitamin E-supplemented groups was decreased in comparison with that from the control linseed oil group. We conclude that both vitamin E concentrations were insufficient to prevent all harmful effects of lipid oxidation in vivo and that both were equally effective. On the contrary, to ensure good stability of meat lipids, higher vitamin E supplementation is needed, especially after heat treatment. The results of in vivo oxidative stress and meat lipid oxidation confirmed the currently accepted bioactivity of the RRR-α- to all-rac-α-tocopherol ratio of 1.39 in in vivo and in vitro systems.

The results from this study show that, besides being known as antihelmintic, antimicrobial and antiviral agent, Sweet chestnut wood extract could also be considered as a promising natural antioxidant in animal nutrition.

The objective of the present study was to evaluate the effects of different concentrations of T-2 toxin in feed on performance, lipid peroxidation, and genotoxicity in vivo. For a 17-d period, T-2 toxin was added to the diet of the chickens. Fifty 22-d-old male broiler chickens were divided into 5 groups that were supplemented with different concentrations of T-2 toxin: control (0.0 mg/kg of feed), T 0.5 (0.5 mg/kg of feed), T 1.5 (1.5 mg/kg of feed), T 4.5 (4.5 mg/kg of feed), and T 13.5 (13.5 mg/kg of feed). Deoxyribonucleic acid fragmentation in spleen leukocytes, malondialdehyde in plasma and liver, total plasma antioxidative status, glutathione peroxidase activity, and total serum Ig (IgA and IgG) were measured. Feed consumption and BW gain decreased when the concentration of T-2 toxin was 4.5 and 13.5 mg/kg of feed. Compared with the control group, the rate of DNA damage increased significantly in the group fed 13.5 mg of T-2 toxin/kg of feed. In contrast to DNA fragmentation, indicators of oxidative stress did not show differences between groups fed T-2 toxin and the control. More serum IgA was detected in the group T 13.5 compared with the control, whereas there were no differences in serum IgG levels. The results of the present study indicate that impaired performance, DNA fragmentation in spleen leukocytes, and elevated serum IgA levels induced by T-2 toxin are dose-dependent. Based on our results, we could not confirm the hypothesis that oxidative stress is among the mechanisms by which T-2 toxin induces DNA fragmentation.

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