Abstract:
Carboxylic ionophores, such as monensin, salinomycin and lasalocid, are polyether antibiotics
used widely in production animals for the control of coccidiosis, as well as for the promotion
of growth and feed efficiency. Although the benefits of using ionophores are undisputed, cases of
ionophore toxicosis do occur, primarily targeting the cardiac and skeletal muscles of affected animals.
The 3-[4,5-dimethylthiazol-2yl]-2,5-diphenyl tetrazolium bromide (MTT) viability assay was used
to determine the cytotoxicity of monensin, salinomycin and lasalocid on mouse skeletal myoblasts
(C2C12). Immunocytochemistry and immunofluorescent techniques were, in turn, performed to
investigate the effects of the ionophores on the microfilament, microtubule and intermediate filament,
i.e., desmin and synemin networks of the myoblasts. Monensin was the most cytotoxic of
the three ionophores, followed by salinomycin and finally lasalocid. Monensin and salinomycin
exposure resulted in the aggregation of desmin around the nuclei of affected myoblasts. The synemin,
microtubule and microfilament networks were less affected; however, vesicles throughout the
myoblast’s cytoplasm produced gaps within the microtubule and, to a limited extent, the synemin
and microfilament networks. In conclusion, ionophore exposure disrupted desmin filaments, which
could contribute to the myofibrillar degeneration and necrosis seen in the skeletal muscles of animals
suffering from ionophore toxicosis.
