Myeloid bodies

The morphological alterations induced by aminoglycosides in LLC-PKi cells correlated well with in vivo histological findings in the kidney, including the formation of secondary lysosomal inclusions referred to as myeloid bodies. 

Figure 29.10. Postulated pathways of aminoglycoside-induced cellular injury. On the left, aminoglycoside (AG) enters the cell by pinocytosis and endocytosis, subsequently fusing with a primary lysosome (L). Aminoglycosides may interfere with normal lysosomal function, forming myeloid bodies (center). Additionally, aminoglycosides may destabilize lysosomes, leading to release of intralysosomal enzymes (lower left). Intracellular aminoglycosides may produce direct injury to intracellular organelles such as mitochondria. (Adapted from G.J. Kaloyanides and E. Pastoriza-Munoz, Kidney Int. 18, 571-582,1980.)...

Aminoglycoside binding to membrane acidic phospholipids Changes in content and metabolism of membrane phospholipids Displacement of calcium bound to phospholipids Formation of myeloid bodies... 

VPA. Histologically, microvesicular steatosis induced by 4-en-VPA is accompanied by ultrastructural changes characterized by myeloid bodies, hpid vacuoles and mitochondrial abnormalities. An enhanced excretion of Cg to Cio dicarboxylic acids by patients and rats indicates an interference with mitochondrial P-oxidation as an important pathogenesis. If the normal pathway of fatty acid oxidation is disrupted by VPA, it results in reduced ketone body formation and decrease of free coenzyme-A (CoA) in the liver. Especially, decreased CoA would limit the activities of one or more enzymes in the pathway of fatty acid oxidation. 

Nonakal, Sunohara N, Ishiura S, SatoyoshiB. (1981) Familial distal myopathy with rimmed vacuole and lamellar (myeloid) body formation. J Neurol Sci 51, 141-155. 

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