Ultrastructural changes in muscle mitochondria during cell damage

During rapid cellular damage, the organelles frequently undergo major ultrastructural pathological changes which are shown most dramatically in the mitochondria. In particular, the mitochondria undergo apparent septation and subdivision, this phenomenon being most commonly seen in skeletal and cardiac muscle cells (Duncan, 1988). Are these ultrastructural changes in muscle mitochondria perhaps triggered by changes in the intracellular concentration of Ca2+ ([Ca2+]i) or by active oxygen radicals?

Lipid bodies, lipofuscin granules and myelin-like figures (or membrane whorls) are regarded as late-stage products of lysosomal digestion or as lysosome-derived elements in mammalian skeletal muscle; they occur rarely in human healthy muscle but are much more common in diseased muscle and in old age (Mastaglia & Walton, 1982; Dubowitz, 1985; Walton, 1988). Lipid droplets are present in many cells and are considered to lack a limiting membrane (Threadgold, 1976), but lipid bodies with a bounding membrane are clearly evident in the electronmicrographs of skeletal muscles of neonatal kittens (Tomanek, 1976), rats (Nag & Cheng, 1982) and dystrophic hamsters (Caulfield, 1966) as well as in ischaemic canine muscle (Stenger et al., 1962). Ultrastructural studies of mammalian skeletal muscle undergoing rapid cellular damage that is experimentally-induced in vitro, with a time-course of minutes (Duncan, 1988), show that lipid bodies develop quickly in association with the muscle mitochondria.