L6 myoblasts were used as an in vitro model to investigate the role of
moniliformin and its interaction with
monensin in turkey knockdown syndrome and
sudden death syndromes in poultry. Cell viability and microscopic and ultrastructural alterations noted in L6 myoblasts cultured in the presence of
moniliformin (0.0-0.3 microgram/microliter) were compared to those observed in parallel cultures also containing one of the following
compounds: selenium (0-0.004 ng/microliter),
thiamine (0-0.3 microgram/microliter), or
pyruvate (0-0.46 microgram/microliter). 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 microgram
moniliformin/microliter medium. Supplementation of medium with
thiamine and
pyruvate, or
selenium, provided significant protection to cells exposed to 0.0-0.3 microgram/microliter or 0.0-0.15 microgram
moniliformin/microliter, respectively. Dose-dependent differences in
protein and
ATP production were not detected. Myoblasts grown in medium containing 0-0.15 microgram
moniliformin/microliter and 7.5-50.0 microM
A23187,
beauvericin or
monensin had degrees of cytotoxicity similar to parallel cultures receiving only an
ionophore. L6 myoblasts were a useful model of
moniliformin toxicosis. The findings of this study suggest cytotoxicity due to
moniliformin in L6 myoblasts may be due in part to oxidative damage and altered
pyruvate metabolism, and that
moniliformin does not predispose myoblasts to
ionophore toxicosis. This study supports the results of in vivo investigations in poultry that
moniliformin and
monensin do not act synergistically to induce knockdown or
monensin toxicosis.