DEVELOPMENT OF AN L6 MYOBLAST IN-VITRO MODEL OF MONILIFORMIN TOXICOSIS

L6 myoblasts were used as an in vitro model to investigate the role of moniliformin and its interaction with monensin in turkey knockdown sy ndrome and sudden death syndromes in poultry. Cell viability and micro scopic and ultrastructural alterations noted in L6 myoblasts cultured in the presence of moniliformin (0.0-0.3 mu g/mu l) were compared to t hose observed in parallel cultures also containing one of the followin g compounds: selenium (0-0.004 ng/mu l), thiamine (0-0.3 mu g/mu l), o r pyruvate (0-0.46 mu g/mu l). Marked dilation of the RER, membranous whorls, glycogen deposition, membrane-bound cytoplasmic inclusions and necrosis were observed in myoblasts exposed to 0.03-0.30 mu g monilif ormin/mu l medium. Supplementation of medium with thiamine and pyruvat e, or selenium, provided significant protection to cells exposed to 0. 0-0.3 mu g/mu l or 0.0-0.15 mu g moniliformin/mu l, respectively. Dose -dependent differences in protein and ATP production were not detected . Myoblasts grown in medium containing 0-0.15 mu g moniliformin/mu l a nd 7.5-50.0 mu M A23187, beauvericin or monensin had degrees of cytoto xicity similar to parallel cultures receiving only an ionophere. L6 my oblasts were a useful model of moniliformin toxicosis. The findings of this study suggest cytotoxicity die to moniliformin in L6 myoblasts m ay be due in part to oxidative damage and altered pyruvate metabolism, and that moniliformin does not predispose myoblasts to ionophore toxi cosis. This study supports the results of in vivo investigations in po ultry that moniliformin and monensin do not act synergistically to ind uce knockdown or monensin toxicosis.