Evaluation of different vitamin E recommendations and bioactivity of α-tocopherol isomers in broiler nutrition by measuring oxidative stress in vivo and the oxidative stability of meat.

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 effect of vitamin E and plant extract mixture composed of carvacrol, cinnamaldehyde and capsaicin on oxidative stress induced by high PUFA load in young pigs.

The objective of our study was to determine the antioxidative potential of a plant extract (PE) mixture composed of carvacrol, capsicum oleoresin and cinnamaldehyde against high n-3 polyunsaturated fatty acid (PUFA)-induced oxidative stress in young pigs. Thirty-two weaned castrated male crossbred pigs (BW 10.9 kg; n = 32) were randomly assigned to four dietary treatments (n = 8). The negative control diet (Cont) contained 17.2% energy from fat. Oxidative stress was induced in three of the four experimental groups with the inclusion of n-3 PUFA rich linseed oil. Linseed oil substituted wheat starch in the diet to elevate the amount of energy from fat to 34.1%. One of these diets served as a positive control (Oil), one was additionally supplemented with 271.2 mg/kg of PE mixture and one with 90.4 mg/kg α-tocopheryl acetate (Vit E). After 14 days of treatment, blood and urine were collected for the determination of lipid peroxidation and DNA damage. Lipid peroxidation was studied by plasma malondialdehyde (MDA) concentrations, 24 h urinary MDA and F2-isoprostane (iPF2α-VI) excretion, total antioxidant status of plasma and glutathione peroxidase assays. Lymphocyte DNA fragmentation and 24 h urinary 8-hydroxy-2'-deoxyguanosine excretion were measured to determine DNA damage. Consumption of n-3 PUFA rich linseed oil increased the amount of MDA in plasma and urine, and induced DNA damage in lymphocytes, but did not elevate the amount of iPF2α-VI excreted in the urine. The supplementation with PE and with Vit E did not reduce MDA levels in plasma and urine, but it decreased the percentage of DNA damage in lymphocytes (P < 0.001). The PE reduced the urinary iPF2α-VI excretion in comparison to the Cont diet. The results show that PE and Vit E supplemented to pigs in concentrations of 271.2 mg/kg and 90.4 mg/kg, respectively, can effectively protect pig's blood lymphocytes against oxidative DNA damage, thus suggesting their potentially beneficial effects on the immune system under dietary-induced oxidative stress.

The comparison of in vivo antigenotoxic and antioxidative capacity of two propylene glycol extracts of Calendula officinalis (marigold) and vitamin E in young growing pigs.

The objective of the study was to evaluate the protective effect of Calendula officinalis propylene glycol extracts against oxidative DNA damage and lipid peroxidation induced by high polyunsaturated fatty acid (PUFA) intake in young growing pigs. Forty young growing pigs were assigned to five treatment groups: control; oil (linseed oil supplementation); C. officinalis 1 and 2 groups (linseed oil plus 3 ml/day of C. officinalis propylene glycol extracts); and vitamin E group (linseed oil plus 100 mg/kg of vitamin E). Lymphocyte DNA fragmentation and 24-h urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) excretion were measured to determine DNA damage. Lipid peroxidation was studied by analysing plasma and urine malondialdehyde (MDA), and urine isoprostane concentrations (iPF2α-VI), total antioxidant status of plasma and glutathione peroxidase (GPx) assays. C. officinalis 1 (extract from petals) effectively protected DNA from oxidative damage. It indicated a numerical trend towards the reduction of plasma MDA and urinary iPF2α-VI excretion. Its effect was comparable with that of vitamin E. C. officinalis 2 (extract from flower tops) showed less antioxidant potential than the extract from petals. We can conclude that the amount of C. officinalis extracts proposed for internal use by traditional medicine protects the organism against DNA damage induced by high PUFA intake.

Dose-dependent effects of T-2 toxin on performance, lipid peroxidation, and genotoxicity in broiler chickens.

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.

The role of dietary nucleotides in reduction of DNA damage induced by T-2 toxin and deoxynivalenol in chicken leukocytes.

The objective of present study was to determine the effect of T-2 toxin and deoxynivalenol (DON) on DNA fragmentation in spleen leukocytes and oxidative stress in chickens, and furthermore, to evaluate the potential of dietary nucleotides in reduction of toxin-induced DNA damage. Male broiler chickens were exposed to 10mg/kg feed of either T-2 toxin or DON with or without addition of dietary nucleotides. After 17 days of treatment DNA damage of spleen leukocytes was measured by Comet assay, lipid peroxidation was studied by malondialdehyde (MDA), total antioxidant status (TAS) of plasma and glutathione peroxidase (GPx) assays, and the hepatotoxicity was studied by measuring plasma liver enzyme levels (ALT, AST and GGT) levels. T-2 toxin and DON induced DNA fragmentation in chicken spleen leukocytes and supplementation with nucleotides reduced the amount of damage only when added to T-2 toxin. In comparison to control group, values of TAS and AST decreased significantly in the groups fed T-2 toxin with or without nucleotide supplementation. Plasma and liver MDA content in groups fed T-2 toxin and DON did not differ significantly from the control. Dietary nucleotides did not affect MDA formation when added to the diets with mycotoxins. The results obtained suggest that dietary nucleotides have the potency to reduce the extent of DNA damage induced by the action of T-2 toxin in immune cells. This underlines their possible beneficial effect on the immune system in mycotoxin intoxication.