calcimycin and Poultry-Diseases

The role of Ca(2+)-dependent phospholipase A2 (PLA2) in the mechanism of skeletal muscle damage in broiler chickens was examined in vitro using a novel, synthetic, PLA2-specific inhibitor Ro31-499/001 (Ro31). Muscle damage was assessed by measurement of creatine kinase (CK) efflux from isolated muscles into the incubation medium. Treatment with the specific Ca(2+)-ionophore 4-Br-A23187 (5 microM) caused a 72% elevation (P<0.05) in muscle 45Ca2+ accumulation, which was associated with a marked increase (P<0.001) in muscle CK efflux (7.6-fold). Incubation with Ro31 (50 microM) reduced (P<0.001) CK efflux from muscles treated with ionophore (45%) but was without effect on 45Ca accumulation. Treatment with the Na+ ionophore monensin (100 microM) induced 55% (P< 0.05) elevation in 45Ca2+ accumulation with a concomitant 2.5-fold increase (P<0.001) in CK loss. Muscles incubated with monensin in the presence of Ro31 exhibited a 49% reduction (P<0.001) in CK leakage but showed no change in 45Ca2+ uptake. The results indicate that increasing external Ca2+ entry, directly or indirectly, and elevation of intracellular Ca2+, significantly alters sarcolemmal integrity resulting in increased CK efflux from broiler skeletal muscle. This process is, at least in part, dependent upon activation of PLA2 activity and thus inhibitable by Ro31. It is further proposed that muscle damage in poultry induced by a range of stresses, and insults may also be mediated by a Ro31 sensitive, PLA2-dependent component. The findings have implications for strategies to reduce or prevent myopathies in poultry affecting bird welfare and product quality.

Topics: Animals; Calcimycin; Calcium; Chickens; Creatine Kinase; Enzyme Activation; Enzyme Inhibitors; Female; Ionophores; Muscle, Skeletal; Muscular Diseases; Phospholipases A; Phospholipases A2; Poultry Diseases

The formation of lactic acid and consumption of adenosine triphosphate (ATP) were measured in erythrocytes from broiler and White Leghorn chickens with the goal of providing further evidence that lactic acid, a metabolite from glycolysis, is an etiological factor for sudden death syndrome (SDS) in broiler chickens. When loaded with Ca2+, erythrocytes exhibited increased lactic acid concentrations. The effect of Ca2+ loading was significantly faster in broiler erythrocytes. In the absence of adenosine used as an energy-yielding substrate, Ca2+ loading was followed by a reduction in ATP concentrations. The effect was also significantly faster in broiler erythrocytes. Intravenous injection of a 20% lactate solution at 0.1 mL/kg produced SDS-like death of broilers but not White Leghorns. The results obtained in erythrocytes indicate that, in broilers, a greater amount of energy is required for regulation of intracellular Ca2+ concentrations, and, thereby, formation of lactic acid is more accelerated. In addition to the result that intravenous lactate injection caused death in broilers, an elevation of lactic acid concentrations in blood, arising from operation of Ca2+ regulation mechanisms, may predispose broilers to incidence of SDS.

Topics: Adenosine Triphosphate; Animals; Calcimycin; Calcium; Chickens; Death, Sudden; Erythrocytes; In Vitro Techniques; Lactic Acid; Poultry Diseases