Myopathies in broiler chickens: The roles of oxidative damage and vitamin E

Recent studies have shown that disruptions in intracellular calcium (Ca²⁺) homeostasis play a major role in the development of skeletal muscle damage (myopathy) in broilers. Elevations of intracellular free calcium result in Ca²⁺-activation of phospholipase A₂ (PLA₂) and the subsequent initiation of a cascade of pro-inflammatory mediators and oxygen-derived free radical generation. The ultimate consequence of free radical induced membrane lipid peroxidation is altered cell membrane integrity and thus pro-oxidative mechanisms may be central in the pathogenesis of myopathy. Vitamin E (α-tocopherol) plays an important role as a naturally occurring lipid soluble antioxidant acting as a free radical scavenger and may therefore prevent myopathy mediated by the above mechanisms. This study employed an isolated in vitro broiler chicken skeletal muscle preparation to examine the potential role of vitamin E in Ca²⁺-mediated oxidative membrane damage. Muscle damage was assessed by the measurement of CK in the incubation medium. Tissue calcium accumulation was estimated by ⁴⁵Ca uptake. Membrane lipid peroxidation was determined by malondialdehyde (MDA) measurement. Incubation with Ca²⁺-ionophore significantly (p<0.001) increased muscle ⁴⁵Ca²⁺ uptake (2.2-fold), MDA concentration (2.5-fold) and CK efflux (12-fold). Incubation with α-tocopherol (250 μM) significantly reduced MDA concentration (26%) and CK efflux (37%) but not ⁴⁵Ca²⁺ accumulation (18%; p=0.061). In a related in vivo study, broilers from fast (FG) and slow growing (SG) lines were reared with a dietary supplementation of vitamin E (500mg/kg) and subjected to acute oxidative stress (high thermal load-31°C/75%RH, 2h). FG birds exhibited a marked myopathic response, which was significantly reduced by vitamin E supplementation (p<0.05). It is suggested that vitamin E may exert protective actions in birds during spontaneous and stress induced myopathies. Its mechanism of action may involve inhibition of lipid peroxidation and/or PLA₂ activity.