Oxidative stress-associated mitochondrial dysfunction in corticosteroid-treated muscle cells

We analyzed the effects of corticosteroid on mitochondrial membrane potentials (ΔΨm), 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...

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Bibliographic Details
Published in:Muscle & nerve 2004-07, Vol.30 (1), p.49-54
Main Authors: Oshima, Yasushi, Kuroda, Yukiko, Kunishige, Makoto, Matsumoto, Toshio, Mitsui, Takao
Format: Article
Language:English
Subjects:
apoptosis
Apoptosis - drug effects
Biological and medical sciences
Cell Differentiation
Cell Line, Tumor
corticosteroid myopathy
dexamethasone
Dexamethasone - pharmacology
Diseases of striated muscles. Neuromuscular diseases
Dose-Response Relationship, Drug
Fundamental and applied biological sciences. Psychology
Glucocorticoids - pharmacology
Humans
In Vitro Techniques
Medical sciences
Mitochondrial Diseases - chemically induced
Mitochondrial Diseases - metabolism
mitochondrial membrane potentials
Muscle Cells - drug effects
Muscle Cells - metabolism
Neuroblastoma
Neurology
Oxidative Stress
reactive oxygen species
Reactive Oxygen Species - metabolism
Rhabdomyosarcoma
Striated muscle. Tendons
superoxide dismutase
Vertebrates: osteoarticular system, musculoskeletal system
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Summary:We analyzed the effects of corticosteroid on mitochondrial membrane potentials (ΔΨm), 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 ΔΨm, ROS generation, and apoptosis in proliferating RD cells. Treatment with SOD attenuated ROS generation and apoptosis, but not ΔΨm. The increase in ΔΨm 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 ΔΨm 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
ISSN:0148-639X
1097-4598
DOI:10.1002/mus.20036