Effect of monensin on the morphology of mitochondria in rodent and equine striated muscle.

Heart, diaphragm, and rear limb muscle from ponies and rats treated with monensin were examined by light and electron microscopy. In both species, mitochondrial aberrations were observed in selected muscle cells. The aberrations consisted of loss of matrix substance (vacuolization) usually accompanied by swelling. Vacuolated mitochondria were characterized by an almost total loss of matrix substance with retention of the rudimentary cristae form. In ponies, most vacuolated mitochondria were observed in heart muscle though some also were found in the diaphragm. In rats, most vacuolated mitochondria were observed in the diaphragm with lesser numbers in rear limb and heart muscles. Red and white muscle fibers were identified in the rat diaphragm based upon fiber size and mitochondrial content. About equal numbers of vacuolated mitochondria were seen in each type of fiber when the total number of vacuolated mitochondria was small. However, when large numbers of mitochondria were vacuolated, the majority of affected mitochondria were seen in white muscle fibers. The form and distribution of vacuolated mitochondria seem sufficiently characteristic to be useful as indicators of monensin poisoning. Mitochondrial vacuolation may be a secondary effect of monensin toxicity since mitochondrial vacuolation does not occur either in cultured cells (plant or animal) or in root plants exposed directly to monensin.