GLUCOCORTICOID LONG-TERM TREATMENT INDUCES OXIDATIVE STRESS, MITOCHONDRIAL DYSFUNCTION AND ATROPHY OF SKELETAL MUSCLES

• DOI: 10.18143/jwms_v2i2_1919
• Publication Date: 2016-09-09
• Authors: Elisa Balboa; Fujiko Saavedra; Tomás Regueira; Juan C. Sáez
• Keywords: Muscle Atrophy; Mitochondrial ROS

The mechanism of glucocorticoid-induced atrophy remains unclear. Objectives: to evaluate the involvement oxidative stress, connexin hemichannels (Cx HCs) and mitochondrial dysfunction in dexamethasone (DEX)-induced muscle atrophy. Methods: We used specific Cx43/Cx45 expression deficient wild-type mice treated with DEX or DEX+vitaminE. Atrophy was evaluated by atrogin-1 reactivity (immunofluorescense) cross sectional area (CSA) myofibers. functional state mitochondria measuring oxygen consumption rate (OCR), membrane potential (MMP) superoxide production (mtROS). Cx immunofluorescence. Results: At day 7th treatment myofibers showed reduced MMP, increased mtROS, OCR, CSA.These changes were absent muscles with + vitaminE Cx43/45 mice.Moreover, induced de novo mice, which prevented vitaminE. Conclusions: induces stress expression, have a negative impact on function leading Consequently, these side effects chronic glucocorticoid might be avoided co-administration antioxidant agents such as HC blocker.