Arthritis Research & Therapy 2010, 12:R17doi:10.1186/ar2918
Research article
* Contributed equally
Article URL : http://arthritis-research.com/content/12/1/R17
Published: 28 January 2010
© 2010 Cordero et al. , licensee BioMed Central Ltd.
This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0/),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Fibromyalgia is a chronic pain syndrome with unknown etiology. Recent studies have shown some evidence demonstrating that oxidative stress may have a role in the pathophysiology of fibromyalgia. However, it is still not clear whether oxidative stress is the cause or the effect of the abnormalities documented in fibromyalgia. Furthermore, the role of mitochondria in the redox imbalance reported in fibromyalgia is also controversial. We undertook this study to investigate the role of mitochondrial dysfunction, oxidative stress and mitophagy in fibromyalgia.
We studied 20 patients (2 males and 18 females) recruited from the database of the Sevillian Fibromyalgia Association and 10 healthy controls. We evaluated mitochondrial function in blood mononuclear cells from fibromyalgia patients measuring coenzyme Q10 levels by high performance liquid chromatography (HPLC), and mitochondrial membrane potential by flow cytometry. Oxidative stress was determined by measuring mitochondrial superoxide production by MitoSOXTM, and lipid peroxidation in blood mononuclear cells and plasma from fibromyalgia patients. Autophagy activation was evaluated by quantifying the fluorescence intensity of LysoTrackerTM Red staining of blood mononuclear cells. Mitophagy was confirmed by measuring citrate synthase activity and electron microscopy examination of blood mononuclear cells.
We found reduced levels of coenzyme Q10, decreased mitochondrial membrane potential, increased level of mitochondrial superoxide in blood mononuclear cells, and increased levels of lipid peroxidation in both blood mononuclear cells and plasma from fibromyalgia patients. Mitochondrial dysfunction was also associated with increased expression of autophagic genes and the elimination of dysfunctional mitochondria by mitophagy.
These findings may support the role of oxidative stress and mitophagy in the pathophysiology of fibromyalgia.
Full Text article at : http://arthritis-research.com/content/12/1/R17
Also available as PDF document
Disclaimer:
Information on this site is provided for educational purposes only and
is not meant to substitute the advice provided by your own physician or other
medical professionals.
Consult your own physician regarding the applicability of any information
listed on this website with respect to your symptoms or medical condition