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Protective effects of Coenzyme Q10 on dystrophic muscle cells
Author(s) -
Minatel Elaine,
Mizobuti Daniela Sayuri,
Macedo Aline Barbosa,
Moraes Luis Henrique Rapucci
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1022.2
Subject(s) - coenzyme q10 , duchenne muscular dystrophy , dystrophin , muscular dystrophy , oxidative stress , myocyte , mdx mouse , viability assay , lipid peroxidation , mtt assay , chemistry , reactive oxygen species , toxicity , antioxidant , skeletal muscle , cell , medicine , microbiology and biotechnology , endocrinology , biochemistry , biology
Duchenne muscular dystrophy (DMD) is a progressive and lethal X‐linked myopathy characterized by a deficiency of the dystrophin protein. Oxidative stress and abnormal production of reactive oxygen species (ROS) plays a key role in the pathophysiology of DMD. We investigated the effects of the antioxidant Coenzyme Q10 (CoQ10) on the primary cultures of dystrophic muscle cells from mdx mice, the experimental model of DMD. Mdx muscle cells were treated with CoQ10 (5 μM) for 24 h. The muscle cells of C57BL/10 mice were used as controls. Drug toxicity was assessed for using an MTT cell viability assay. H 2 O 2 (a marker of cellular ROS production) was measured by using the Amplex red assay kit. The levels of 4‐HNE (a lipid peroxidation marker) were analyzed by western blotting. The MTT results showed that CoQ10 not had cytotoxic effect on mdx and C57BL/10 muscle cells. H 2 O 2 production and 4‐HNE levels were significantly higher in mdx muscle cells compared to C57BL/10 muscle cells (P≤0.05, Student's t‐test). CoQ10 treatment decreased H 2 O 2 production by 51% and 4‐HNE levels by 18% in the dystrophic muscle cells. Based on the results, it can be seen that CoQ10 has protective effects on mdx muscle cells and this in turn would support further investigations for its use as a potential therapy for dystrophinopathies.