Chronic corticosteroid administration causes mitochondrial dysfunction in skeletal muscle
| Autor: | Masaaki Odomi, Masashi Akaike, Toshio Matsumoto, Hiroyuki Azuma, Takao Mitsui, Takahiko Iuchi, Masakazu Nagasawa |
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| Rok vydání: | 2002 |
| Předmět: |
Male
medicine.medical_specialty Time Factors medicine.drug_class Physical exercise medicine.disease_cause Pathogenesis Electron Transport Complex III Adrenal Cortex Hormones Multienzyme Complexes Internal medicine Pyruvic Acid medicine Aerobic exercise Humans NADH NADPH Oxidoreductases Lactic Acid Myopathy Muscle Skeletal Electron Transport Complex I Dose-Response Relationship Drug business.industry Electron Transport Complex II Skeletal muscle Deoxyguanosine Middle Aged Muscle atrophy Mitochondria Succinate Dehydrogenase Oxidative Stress Endocrinology medicine.anatomical_structure Neurology 8-Hydroxy-2'-Deoxyguanosine Case-Control Studies Exercise Test Corticosteroid Female Neurology (clinical) medicine.symptom business Oxidoreductases Oxidative stress DNA Damage |
| Zdroj: | Journal of neurology. 249(8) |
| ISSN: | 0340-5354 |
| Popis: | Corticosteroid myopathy is a major clinical problem in patients undergoing chronic corticosteroid treatment and shows insidious and progressive muscle atrophy in proximal limbs. Although several mechanisms underlying the pathophysiology of muscle injury have been postulated, precise pathogenesis is still not clear. We evaluated the mitochondrial functions in patients receiving corticosteroids compared with those in healthy controls or patients not receiving corticosteroids. The serum levels and total production of lactate were investigated by an aerobic exercise test using a bicycle ergometer. Mitochondrial respiratory activities and oxidative damage in biopsied skeletal muscles were also studied. The results of aerobic exercise tests revealed a significant overproduction of lactate in patients treated with corticosteroids (p < 0.005), which was positively correlated with total corticosteroid doses administered (p < 0.0001). In these patients, mitochondrial enzyme activity in complex I was significantly decreased (p < 0.05) and oxidative damage of biopsied skeletal muscle was remarkable both in mitochondrial and nuclear DNAs (p < 0.001). The results suggest that chronic corticosteroid administration induces mitochondrial dysfunction and oxidative damage in skeletal muscles, which may be the pathogenesis, at least in part, of corticosteroid-induced myopathy. |
| Databáze: | OpenAIRE |
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