The role of sodium ions in the pathogenesis of skeletal muscle damage in broiler chickens.
The effect of sodium ions (Na+) on calcium (Ca2+)-mediated muscle damage in broiler chickens was investigated using an in vitro muscle preparation. Muscle Ca2+ accumulation was determined by 45Ca2+ uptake. Muscle damage was assessed by measurement of the efflux of the intracellular enzyme creatine kinase (CK) into the incubation medium. Loading muscle cells with Na+ by means of the sodium ionophore monensin led to concentration-dependent (25 to 200 microM) increases in 45Ca2+ uptakes and corresponding and proportional CK losses. The greatest responses occurred at 100 microM ionophore or greater, reflected in a 49% increase (P < 0.05) in 45Ca2+ uptake and an associated 140%-fold increase (P < 0.001) in CK efflux. Inhibition of muscle Na+/K+-ATPase activity with ouabain (2 mM) induced a 56% increase in 45Ca2+ uptake and a 60%-fold increase (P < 0.001) in total CK loss. The combined use of ionophore and ouabain resulted in 90 and 130%-fold elevations in 45Ca2+ uptake and CK loss, respectively. In monensin-treated muscles, inhibition of external Ca2+ influx from the incubation medium by chelation with 1,2 bis(2-aminophenoxy)ethane-N,N,N',N' tetracetic acid (5 mM) markedly reduced 45Ca2+ uptake (38%: P < 0.05) but increased CK release by 85% (P < 0.001). The results demonstrate that initial elevations in muscle Na+ can facilitate increases in muscle Ca2+ and lead to alterations in muscle cell membrane integrity and CK loss. The Na+-induced increases in myocellular Ca2+ may be mediated via direct extracellular Ca2+ entry or redistribution from internal Ca2+ stores. It is proposed that in order to reduce or prevent myopathies in poultry, exposure to conditions that may lead to elevations in muscle Na+ (e.g., increased muscle activity and stress or accidental ionophore toxicosis) should be avoided. The findings of this study have implications for management strategies of bird welfare, muscle pathology, and product quality.
Sandercock
D A
DA
Roslin Institute, Division of Integrative Biology, Roslin, Midlothian, EH25 9PS, United Kingdom. dale.sandercock@bbsrc.ac.uk
Mitchell
M A
MA
D000818:Animals; D001682:Biological Availability; D002118:Calcium / Q000378:metabolism; D002132:Calcium Radioisotopes; D002645:Chickens; D005260:Female; D008985:Monensin / Q000494:pharmacology; D018482:Muscle, Skeletal / Q000187:drug effects / Q000473:pathology*; D009135:Muscular Diseases / Q000139:chemically induced / Q000662:veterinary*; D010042:Ouabain / Q000494:pharmacology; D011201:Poultry Diseases / Q000139:chemically induced*; D012964:Sodium / Q000009:adverse effects*; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors
D002132:Calcium Radioisotopes; D010042:Ouabain; D008985:Monensin; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D002118:Calcium