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Related Experiment Videos

Chronic corticosteroid administration causes mitochondrial dysfunction in skeletal muscle.

Takao Mitsui1, Hiroyuki Azuma, Masakazu Nagasawa

  • 1First Department of Internal Medicine, School of Medicine, The University of Tokushima, Kuramoto-3-18-15, Tokushima 770-8503, Japan. tmitsui@clin.med.tokushima-u.ac.jp

Journal of Neurology
|August 27, 2002
PubMed
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Corticosteroid treatment causes muscle atrophy by impairing mitochondrial function and increasing oxidative damage in skeletal muscles. This study reveals mitochondrial dysfunction and lactate overproduction in patients undergoing corticosteroid therapy.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Clinical Medicine

Background:

  • Corticosteroid myopathy is a significant clinical issue in patients on long-term corticosteroid therapy, characterized by progressive muscle atrophy.
  • The exact mechanisms driving corticosteroid-induced muscle injury remain unclear, necessitating further investigation into cellular and molecular pathways.

Purpose of the Study:

  • To investigate mitochondrial function and oxidative stress markers in skeletal muscles of patients receiving corticosteroids.
  • To compare mitochondrial function and lactate production between corticosteroid-treated patients, healthy controls, and non-corticosteroid-treated patients.

Main Methods:

  • Aerobic exercise testing using a bicycle ergometer to assess serum lactate levels and production.
  • Analysis of mitochondrial respiratory activities and oxidative damage in skeletal muscle biopsies.

Related Experiment Videos

  • Evaluation of mitochondrial and nuclear DNA integrity.

    • Main Results:

    • Patients treated with corticosteroids exhibited significant lactate overproduction during exercise, correlating positively with cumulative corticosteroid dosage.
    • A notable decrease in mitochondrial enzyme activity (Complex I) was observed in corticosteroid-treated patients.
    • Skeletal muscle biopsies revealed substantial oxidative damage to both mitochondrial and nuclear DNA in these patients.

    Conclusions:

    • Chronic corticosteroid administration leads to mitochondrial dysfunction in skeletal muscles.
    • Increased oxidative damage in skeletal muscles contributes to the pathogenesis of corticosteroid-induced myopathy.
    • Mitochondrial impairment and oxidative stress are key factors in corticosteroid myopathy development.