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Monensin has a relatively narrow therapeutic window, with episodes of severe and lethal intoxications reported in many animal species, e.g., cattle, poultry, sheep, horses, and dogs. One of the most striking findings of experimental or accidental monensin intoxication in animals is muscle necrosis and myoglobinuria. Target organs of monensin poisoning are skeletal and cardiac muscles.
Monensin may produce poor feathering when feeding diets with low energy and low sulphur-containing amino acids; tiamulin interfers with metabolism of monensin in chickens.At recommended doses MON may be toxic to guinea fowl and other avian species; horses are very sensitive to MON (LD 50%: horse 2-3 mg/kg b.w., cattle 25 mg/kg; chickens 200 mg/kg); Monensin will cause deaths in equines thet ingest feed containing it.
Toxicity of monensin is due primarily to its ability to increase intracellular sodium concentration. Monensin is a Na+-selective carboxylic ionophore which forms lipid-soluble cation complexes that can traverse cell membranes rapidly.
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