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   <subfield code="a">Influence of Vitamins E and C on the Toxic Effects of Ochratoxin A and T-2 Toxin in Chicks</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[DIRK HOEHLER, RONALD R. MARQUARDT]</subfield>
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   <subfield code="a">The objective of this study was to determine whether two antioxidant vitamins, vitamins E and C, were able to counteract the production of lipid peroxides and the corresponding toxic signs of two important but diverse mycotoxins, T-2 toxin and ochratoxin A (OA). Experiment 1 was designed in a 3 × 3 factorial arrangement using three doses of vitamin E (dl-α-tocopheryl acetate) in the diet of Leghorn cockerels (required level according to NRC, l0×, and l00× requirements) and three toxin treatments [no toxin (Diets 1, 2, and 3), 4 mg T-2/kg of diet (Diets 4, 5, and 6), and 2.5 mg OA/kg of diet (Diets 7, 8, and 9)]. The experimental design for Experiment 2 was the same as for Experiment 1 except that Vitamin C (0, 200, and 1,000 mg/kg of diet) was used in place of vitamin E and the concentration of T-2 in Diets 4, 5, and 6 was increased to 5 mg/kg of diet. Six replicates were used per treatment with four birds per replicate. In both experiments, OA and T-2 decreased the performance of the chicks significantly. The concentration of uric acid in the plasma increased (P &lt; 0.001) when OA was added to the diet, whereas the supplementation of the diet with vitamin E (l00× the requirement) partially counteracted this effect (P = 0.07). The presence of T-2, and especially OA, in the diet decreased the concentration of α-tocopherol in the liver (P &lt; 0.001). Consistent with these findings were increased values of malondialdehyde (MDA) in the liver due to OA. In Experiment 1, vitamin E supplementation partially ameliorated the prooxidative effects of OA by decreasing the concentrations of MDA (P &lt; 0.05). These data suggest that lipid peroxides are formed in vivo by T-2 and especially by OA and that these effects can be partially counteracted by an antioxidant such as vitamin E but not by vitamin C.</subfield>
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   <subfield code="a">© 1996 Poultry Science Association, Inc.</subfield>
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   <subfield code="a">Metabolism and Nutrition</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">ochratoxin A</subfield>
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   <subfield code="a">T-2 toxin</subfield>
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   <subfield code="a">lipid peroxidation</subfield>
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   <subfield code="a">antioxidants</subfield>
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   <subfield code="a">malondialdehyde</subfield>
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   <subfield code="a">MARQUARDT</subfield>
   <subfield code="D">RONALD R.</subfield>
   <subfield code="u">3To whom correspondence should be addressed.</subfield>
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   <subfield code="t">Poultry Science</subfield>
   <subfield code="d">Oxford University Press</subfield>
   <subfield code="g">75/12(1996-12), 1508-1515</subfield>
   <subfield code="x">0032-5791</subfield>
   <subfield code="q">75:12&lt;1508</subfield>
   <subfield code="1">1996</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
   <subfield code="b">CC BY-NC-4.0</subfield>
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