Journal
ANTIOXIDANTS & REDOX SIGNALING
Volume 18, Issue 7, Pages 800-807Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2012.4892
Keywords
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Funding
- Fondo Europeo de Desarrollo Regional (FEDER-Union Europea)
- Servicio Andaluz de Salud-Junta de Andalucia
- Proyecto de Investigacion de Excelencia de la Junta de Andalucia [CTS-5725]
- Federacion Andaluza de Fibromialgia y Fatiga Cronica (ALBA Andalucia)
- [FIS PI10/00543]
- [SAS 111242]
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Fibromyalgia (FM) is a complex disorder that affects up to 5% of the general population worldwide. Both mitochondrial dysfunction and inflammation have been implicated in the pathophysiology of FM. We have investigated the possible relationship between mitochondrial dysfunction, oxidative stress, and inflammation in FM. We studied 30 women diagnosed with FM and 20 healthy women. Blood mononuclear cells (BMCs) from FM patients showed reduced level of coenzyme Q(10) (CoQ(10)) and mtDNA contents and high level of mitochondrial reactive oxygen species (ROS) and serum tumor necrosis factor (TNF)-alpha and transcript levels. A significant negative correlation between CoQ(10) and TNF-alpha levels (r=-0.588; p < 0.01), and a positive correlation between ROS and TNF-alpha levels (r=0.791; p < 0.001) were observed accompanied by a significant correlation of visual analogical scale with serum TNF-alpha and transcript levels (r =0.4507; p < 0.05 and r=0.7089; p < 0.001, respectively). TNF-alpha release was observed in an in vitro (BMCs) and in vivo (mice) CoQ(10) deficiency model. Oral CoQ(10) supplementation restored biochemical parameters and induced a significant improvement in clinical symptoms (p < 0.001). These results lead to the hypothesis that inflammation could be a mitochondrial dysfunction-dependent event implicated in the pathophysiology of FM in several patients indicating at mitochondria as a possible new therapeutic target. Antioxid. Redox Signal. 18, 800-807.
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