INHIBITION OF MONOAMINE OXIDASE IN CHICKENS AND DUCKLINGS BY A MICROBIAL METABOLITE OF FURAZOLIDONE

In the chicken, monoamine oxidase (MAO) activity in the brain, heart and alimentary tract was inhibited when furazolidone was given at the therapeutic dose (0·04%, w/w, in the feed for 10 days). The inhibition of MAO activity was most marked in the rectal caeca and least in the liver, where no inhibition was found. Furazolidone treatment, probably in consequence of MAO inhibition, increased the amount of 5‐hydroxytryptamine (5‐HT) in the brain and potentiated the vasopressor action of tyramine. The amounts of adrenaline and noradrenaline in the brain were unaffected by the treatment, as was the vasopressor action of noradrenaline. Furazolidone (0·04%, w/w, in the feed, 10 days) inhibited MAO activity in the liver of ducklings but not chickens, indicating that hepatic clearance of the inhibitor was less efficient in the former species than in the latter. In other organs from the treated birds no species difference was apparent in the degree of MAO inhibition, and the effect of the treatment on the amounts of 5‐HT, adrenaline and noradrenaline in the brain was similar in chickens and ducklings. Neomycin antagonized the furazolidone acting as a MAO inhibitor in chickens and ducklings, following administration of the drugs by crop tube. This observation suggests that in these birds the alimentary microflora transformed furazolidone to an active metabolite which subsequently inhibited MAO activity in other organs. Although furazolidone is considered highly toxic in the duck, in the present experiments ducklings survived when it was given in the feed at a concentration of 0·04% (w/w) for 10 days or by crop tube at a dose of 200 mg/kg. It is suggested that the husbandry of the duck affects its susceptibility to furazolidone.