Development of an L6 myoblast in vitro model of moniliformin toxicosis

摘要: L6 myoblasts were used as an in vitro model to investigate the role of moniliformin and its interaction with monensin turkey knockdown syndrome sudden death syndromes poultry. Cell viability microscopic ultrastructural alterations noted cultured presence (0.0–0.3 μg/μl) compared those observed parallel cultures also containing one following compounds: selenium (0–0.004 ng/μl), thiamine (0–0.3 μg/μl), or pyruvate (0–0.46 μg/μl). Marked dilation RER, membranous whorls, glycogen deposition, membrane-bound cytoplasmic inclusions necrosis exposed 0.03/2-0.30 μg moniliformin/μl medium. Supplementation medium pyruvate, selenium, provided significant protection cells 0.0–0.3 μg/μl 0.0–0.15 moniliformin/μl, respectively. Dose-dependent differences protein ATP production not detected. Myoblasts grown 0–0.15 7.5–50.0 μM A23187, beauvericin had degrees cytotoxicity similar receiving only ionophore. a useful toxicosis. The findings this study suggest due may be part oxidative damage altered metabolism, that does predispose ionophore This supports results vivo investigations poultry do act synergistically induce