Effects of roxarsone and monensin on digital flexoral tendons of broiler chickens

Roxarsone and monensin are common poultry feed additives that are used alone or in combination with other drugs to improve growth and feed utilization in young birds. The effects of monensin and roxarsone on the physiology of flexoral tendons of broiler chickens were examined to understand their relationships to leg weakness that have been occasionally associated with these drugs. Day-old chickens were fed either roxarsone or monensin for a period of 6 wk with two regimens of each of the drugs (roxarsone, 45.4 or 90.8 g/ton feed; monensin, 100 or 150 g/ton feed). None of the treatments had any adverse effect on the growth of the birds or caused any significant leg problem. Roxarsone at 45.4 g/ton caused a significant gain in body weight. The biomechanical strength of digital flexoral tendons was measured in several ways. There were no statistical differences in load at break, the modulus of elasticity, or stress or strain levels between different treatment groups and birds that received no medication. 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 extractible collagens in monensin-treated birds, and a decrease in the acid extractible collagen in both roxarsone- and monensin-treated groups. The relative content of collagen in acid extractible collagens were significantly small relative to total collagen content. Majority of collagen (84 to 90%) was extractible with pepsin. About 8 to 11% of total collagen was resistant to pepsin that was extractible with collagenase; this did not differ between treatment groups. Roxarsone treatment had no effect on the guanidine soluble collagen pool. The effect of monensin on the increase in guanidine soluble pool of collagen may relate to its disruptive effects on cellular secretory processes, which may be of significance in modulating connective tissue function in conjunction with other factors. However, in the present study, neither roxarsone nor monensin alone produced any significant leg problems nor caused any significant differences in the physiology of flexoral tendons or altered their biomechanical properties.