Contribution to the pathobiochemistry of furazolidone-induced oxidative toxicity in chickens.
Furazolidone (F) and its 5-nitrofuran derivatives, occasionally used in veterinary and human medicine, are active against some microorganisms. This drug is considered to be mutagenic in special bacterial test systems. For public health reasons, the presence of F and other 5-nitrofuran residues in edible mammalian and poultry tissues is strictly prohibited. One-month-old experimental chickens (n = 2 x 25) were fed 300 mg.kg-1 furazolidone for 3 days. A separate subgroup (n = 11) was used for monitoring the kinetics of F in the blood plasma. Liver, lung and blood plasma samples taken from the experimental and control chickens after treatment were tested for glutathione-peroxidase (GSH-Px), glutathione reductase (GSH-R), catalase (CAT), superoxide dismutase (SOD) activities, reduced and oxidized glutathione (GSH and GSSG), malondialdehyde (MDA), alpha-tocopherol (vE), selenium (Se) and F concentrations. On post-treatment day 2, SOD activity was significantly lowered in the liver only. GSH-Px did not show any characteristic change in any of the tissues. CAT and GSH-R activities were significantly reduced in both organs until post-treatment day 5. At the same time, a significant decrease of GSH accompanied by an increase in GSSG concentration, was found in both tissues. Oral F treatment produced a transient increase in lipid peroxidation levels measured by the formation of MDA. Alpha-tocopherol content significantly decreased in both organs by post-treatment day 2. Se concentrations showed an insignificant rate of decrease. F concentration in the blood plasma reached its peak already 30 min after treatment. In the liver and lungs, F decreased sharply, reaching the detection limit between days 2-5 after treatment. Furazolidone administered per os was found to alter the in vivo antioxidative enzymatic defense mechanisms. Increased lipid peroxidation and the concomitant oxidative stress may affect the functional integrity of the tissues.[1]References
- Contribution to the pathobiochemistry of furazolidone-induced oxidative toxicity in chickens. Sas, B. Acta Vet. Hung. (1993) [Pubmed]
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