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Title: DEVELOPMENT OF AN L6 MYOBLAST IN VITRO MODEL OF MONILIFORMIN TOXICOSIS

Author
item REAMS, R - PURDUE UNIV, W LAF, IN
item THACKER, H - PURDUE UNIV, W LAF, IN
item NOVILLA, M - ELI LILLY, GREENFIELD, IN
item LASKA, D - ELI LILLY, GREENFIELD, IN
item HORN, J - ELI LILLY, GREENFIELD, IN
item HARRINGTON, D - PURDUE UNIV, W LAF, IN
item GREENLEE, W - PURDUE UNIV, W LAF, IN
item Vesonder, Ronald

Submitted to: Mycopathologia
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/23/1996
Publication Date: N/A
Citation: N/A

Interpretive Summary: A toxin often found in the USA corn crop is called moniliformin. Many scientific investigators studying poultry diseases think moniliformin causes chickens to die because of its effect on their muscles and heart. This disease is called sudden death syndrome in chickens. This study established a model using cells of skeletal and heart muscle that can be studied in the laboratory for the involvement of moniliformin toxic effect in chickens. This information would be useful for those working on the sudden death syndrome in chickens.

Technical Abstract: 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 ug/ul) were compared to those observed in parallel cultures also containing one of the following compounds: selenium (0-0.004 ng/ul), thiamine (0-0.3 ug/ul), or pyruvate (0-0.46 ug/ul). 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 ug moniliformin/ul medium. Supplementation of medium with thiamine and pyruvate, or selenium, provided significant protection to cells exposed to 0.0-0.3 ug/ul or 0.0-0.15 ug moniliformin/ul, respectively. Dose-dependent differences in protein and ATP production were not detected. Myoblasts grown in medium containing 0-0.15 ug moniliformin/ul and 7.5-50.0 uM 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.