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Influence of vitamins E and C on the toxic effects of ochratoxin A and T-2 toxin in chicks

Hoehler, D., Marquardt, R.R.
Poultry science 1996 v.75 no.12 pp. 1508-1515
chicks, ochratoxicosis, T-2 toxin, poisoning, vitamin E, ascorbic acid, lipid peroxidation, dosage, alpha-tocopherol, antioxidants, blood chemistry, feed intake, liveweight gain, feed conversion, liver, enzyme activity, uric acid, aspartate transaminase, malondialdehyde
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 x 3 factorial arrangement using three doses of vitamin E (dl-alpha-tocopheryl acetate) in the diet of Leghorn cockerels (required level according to NRC, 10x, and 100x 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 < 0.001) when OA was added to the diet, whereas the supplementation of the diet with vitamin E (100x the requirement) partially counteracted this effect (P = 0.07). The presence of T-2, and especially OA, in the diet decreased the concentration of alpha-tocopherol in the liver (P < 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 < 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.