{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T19:41:53Z","timestamp":1789587713353,"version":"build-2803163510"},"reference-count":31,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2004,4,12]],"date-time":"2004-04-12T00:00:00Z","timestamp":1081728000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Muscle and Nerve"],"published-print":{"date-parts":[[2004,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>We analyzed the effects of corticosteroid on mitochondrial membrane potentials (\u0394\u03a8<jats:sub>m<\/jats:sub>), generation of reactive oxygen species (ROS), and apoptosis in a human rhabdomyosarcoma cell line, RD, and a dopaminergic neuroblastoma cell line, SH\u2010SY5Y. The cell lines were cultured in the presence or absence of dexamethasone and superoxide dismutase (SOD) for up to 1 week. Dexamethasone treatment increased \u0394\u03a8<jats:sub>m<\/jats:sub>, ROS generation, and apoptosis in proliferating RD cells. Treatment with SOD attenuated ROS generation and apoptosis, but not \u0394\u03a8<jats:sub>m<\/jats:sub>. The increase in \u0394\u03a8<jats:sub>m<\/jats:sub> seemed to be the primary effect of dexamethasone on proliferating RD cells, which is probably mediated by mitochondrial transcription. In differentiated RD cells, but not differentiated SH\u2010SY5Y cells, dexamethasone treatment showed a delayed effect of interfering with the \u0394\u03a8<jats:sub>m<\/jats:sub> and increasing ROS generation and apoptosis. Since these changes disappeared in the presence of SOD, dexamethasone primarily induced ROS generation, resulting in apoptosis. We speculate that this mechanism provides the basis of a pathophysiological model of corticosteroid myopathy. 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