Monoamine Oxidase Inhibition and Furazolidone-Induced Cardiomyopathy in Turkey Poults

Abstract

Furazolidone (FZ), a potent inhibitor of monoamine oxidase (MAO), fed at concentrations of 700 ppm to turkey poults 2 through 5 weeks of age, produces cardiomyopathy and cardiomegaly. To determine the role of MAO inhibition in FZ-induced cardiomyopathy, the effects of FZ were compared with those of a chemically different MAO inhibitor, tranylcypromine (TCP), and a chemically similar non-MAO inhibitor, nitrofurazone (NFZ). At 14 days of age, poults were divided randomly into four groups. Control poults were fed a standard turkey starter ration, and poults in the experimental groups were fed the standard ration that included one of the following drugs at the given concentrations: 700 ppm FZ, 350 ppm NFZ, or 50 ppm TCP. Activity of MAO was assayed in liver and kidney homogenates from poults chosen at random at 14, 17, 21, 28, and 35 days of age in one trial and on heart homogenates at 14, 15, 17, 19, and 28 days of age in another trial. Development of cardiomyopathy was assessed using an electrocardiographic (ECG) technique and substantiated with necropsy examination. Inhibition of MAO was observed only in the heart in FZ-fed poults, only in the kidney in NFZ-fed poults, and in all three tissues studied in TCP-fed poults. Under the conditions of this study, an increase in the incidence of cardiomyopathy, based on ECG data and necropsy results, occurred only in the FZ-fed group. The inability of the potent MAO inhibitor, TCP, to produce cardiomyopathy in this study supports the conclusion that the primary mechanism of FZ-induced cardiomyopathy in turkey poults is probably not due to MAO inhibition.