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Oxidative stress–associated mitochondrial dysfunction in corticosteroid‐treated muscle cells
Author(s) -
Oshima Yasushi,
Kuroda Yukiko,
Kunishige Makoto,
Matsumoto Toshio,
Mitsui Takao
Publication year - 2004
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.20036
Subject(s) - oxidative stress , mitochondrion , medicine , corticosteroid , oxidative phosphorylation , reactive oxygen species , mitochondrial dna , endocrinology , biology , microbiology and biotechnology , biochemistry , gene
We analyzed the effects of corticosteroid on mitochondrial membrane potentials (ΔΨ m ), generation of reactive oxygen species (ROS), and apoptosis in a human rhabdomyosarcoma cell line, RD, and a dopaminergic neuroblastoma cell line, SH‐SY5Y. The cell lines were cultured in the presence or absence of dexamethasone and superoxide dismutase (SOD) for up to 1 week. Dexamethasone treatment increased ΔΨ m , ROS generation, and apoptosis in proliferating RD cells. Treatment with SOD attenuated ROS generation and apoptosis, but not ΔΨ m . The increase in ΔΨ m 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‐SY5Y cells, dexamethasone treatment showed a delayed effect of interfering with the ΔΨ m 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. Muscle Nerve 30:49–54,2004