Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/19/1997
Publication Date: N/A
Citation: N/A Interpretive Summary: Poultry are often given chemicals called feed additives in their diets to control certain diseases or to help improve their rate of growth or help them use their feed more efficiently. Two of these feed additive chemicals are called roxarsone and monensin. There have been some reports that feeding these chemicals to poultry might cause leg problems including weakness. We conducted research to see if roxarsone or monensin had any affect on the leg tendons of growing chickens. We fed the chemicals in the diet and then studied several enzymes and other factors to see if there were any toxic or disabling effects. Our studies showed that neither roxarsone nor monensin caused any significant leg problems in chickens. These studies are important because they add to our knowledge of how various feed additives affect poultry.
Technical Abstract: Roxarsone and monensin are common poultry feed additives that are used alone or in combination with other drugs to improve growth and feed utilization. The effects of monensin and roxarsone on the physiology of flexoral tendons of broiler chickens was examined to understand their relations to leg weakness which has been occasionally reported with these drugs. Day-old chickens were fed either roxarsone or monensin for a period of 6 wk (roxarsone, 45.4 or 90.8 g/ ton feed; monensin, 100 or 150 g/ ton feed). None of the treatments caused any significant leg problem. Roxarsone at 45.4 g/ ton caused a significant gain in body weight. The biomechanical strength of flexoral tendons were compared measuring load at break, the modulus of elasticity, and stress parameters which showed no differences between groups. There were no differences in collagen, proteoglycan, and pyridinoline content of tendons. Sequential extraction of tendons with different solvents revealed a significant increase in the percentage of guanidine HCl soluble collagens in monensin fed birds, and a decrease in the acid extractible collagen in both roxarsone and monensin treated groups. Approximately 84-90% of collagen was extractible with pepsin and 8-11% with collagenase. These were not different between different treatment groups. Roxarsone treatment had no effect on the guanidine soluble collagen pool. The effects of monensin on guanidine soluble pool of collagen may relate to its disruptive effects on cellular secretory processes. However, in the current study, neither roxarsone nor monensin alone produced any significant changes in tendon to cause any leg problem.