Differential sensitivity to monensin-induced myopathy in fast and slow growing lines of broiler chicken?

Artificial genetic selection in broiler chickens has been extremely successful in improving desirable production characteristics such as growth rate and meat yield. However, intensive selection may also be associated with a number of detrimental musculoskeletal metabolic disorders, such as growth associated myopathy. Recent unpublished studies suggest that such selection strategies for improved performance may also have increased tissue-specific susceptibility to stressful challenges, such as infection, toxins and high temperatures. Monensin is a sodium (Na+) selective ionophore antibiotic widely used in the poultry industry to prevent coccidiosis. The safety margin for this type of drug is relatively low and toxicosis because of overdose and differential host sensitivity has been frequently reported. A common feature of the toxic syndrome is skeletal muscle damage and the mechanism of induction of this myopathy has been characterised. These previous studies have shown that monensin-induced myopathy (MIM) may be caused in part by Na⁺-mediated disturbances in muscle intracellular calcium (Ca²⁺) homeostasis. These disturbances lead to an elevation in myoplasmic Ca²⁺ concentration and the activation of several Ca²⁺-dependent degradative processes, resulting in tissue degeneration and the loss of intracellular constituents such as creatine kinase (CK), a recognised indicator of myopathy. The present study investigated the effects of monensin treatment upon CK loss from the muscles of broiler chickens selected for fast (FG) and slow growth rates (SG) using a previously described isolated skeletal muscle preparation.