Can Coenzyme Q₁₀ Improve Clinical and Molecular Parameters in Fibromyalgia?

Lipophilic antioxidants prevent lipopolysaccharide-induced mitochondrial dysfunction through mitochondrial biogenesis improvement

“…This is interesting because NAC has a very evident antioxidant effect which has been described to be involved in the positive effect of mitochondrial respiration compared with CoQ analogs [4]. In this regard, a possible explanation of the more significant effect in the other parameters of CoQ 10 compared with NAC is the induction of mitochondrial biogenesis of CoQ 10 observed and demonstrated by us after oral CoQ 10 treatment [3]. This effect on mitochondrial biogenesis was found in NAC treatment.…”

“…The mitochondrial production of superoxide has been ascribed to several electron transport chain enzymes, including Complex I and Complex III. These complexes along with Coenzyme Q 10 (CoQ 10 ) may leak electrons which in turn may interact with oxygen, thus forming ROS [2,3]. All conditions able to alter mitochondria efficiency can enhance ROS production, having a direct and critical effect on oxidative stress.…”

Fibromyalgia Syndrome: Novel Therapeutic Targets

“…A more recent study has reported on coenzyme Q deficiency as well as increased oxidative stress among juvenile FMS patients [101], with amelioration of both fatigue as well as hypercholesterolemia under coenzyme Q treatment. Coenzyme Q treatment has been associated with diverse metabolic effects such as antioxidant enzymes, mitochondrial biogenesis and AMPK geneexpression levels as well as with salutary clinical effects on pain and fatigue [102]. Thus, exploring the metabolic and energy-related effects of coenzyme Q and similar substances may pose another direction to look at in the treatment of FMS.…”

Could Mitochondrial Dysfunction Be a Differentiating Marker Between Chronic Fatigue Syndrome and Fibromyalgia?

“…Inclusion criteria were to fulfill the classification criteria for CFS and FM that had been diagnosed in the previous 2-3 years based on the current diagnostic criteria (2,5). Exclusion criteria for patients were acute infection diseases in the previous 3 weeks; past/present neurological, psychiatric, metabolic (diabetes), autoimmune diseases, allergy-related, dermal or chronic inflammatory disorders, undesired habits (e.g., smoking, alcohol abuse), oral diseases (e.g., periodontitis), medical conditions that required glucocorticoids treatment, use of statins, analgesics, antioxidants therapy or antidepressant/anxiolytics drugs, past or current substance abuse or dependence, as well as pregnancy or current breastfeeding.…”

“…Increasing evidence implicates mitochondrial dysfunction and metabolic/bioenergetics impairment in the pathogenesis of CFS and FM. In particular, peroxisome proliferator-activated receptor gammacoactivator 1-alpha (PGC-1a) and transcription factor A, mitochondrial (TFAM) are key transcriptional co-regulators that are important in protecting mitochondria against oxidative damage (2), and which appear to be involved in the pathogenesis of immune-inflammatory conditions (4). Both PGC-1a and TFAM induce the transcription of cellular programs, regulating mitochondrial respiration, oxidative stress defense, and adaptive thermogenesis (2).…”