Oxidative stress levels are raised in chronic fatigue syndrome and are associated with clinical symptoms

Vascular Diseases Research Unit, The Institute of Cardiovascular Research, Ninewells Hospital and Medical School, Dundee, Scotland DD1 9SY, UK.
Free Radical Biology and Medicine (Impact Factor: 5.71). 10/2005; 39(5):584-9. DOI: 10.1016/j.freeradbiomed.2005.04.020
Source: PubMed

ABSTRACT The aetiology of chronic fatigue syndrome (CFS) is unknown; however, recent evidence suggests excessive free radical (FR) generation may be involved. This study investigated for the first time levels of 8-iso-prostaglandin-F(2 alpha)-isoprostanes alongside other plasma markers of oxidative stress in CFS patients and control subjects. Forty-seven patients (18 males, 29 females, mean age 48 [19--63] years) who fulfilled the Centres for Disease Control classification for CFS and 34 healthy volunteers (13 males, 21 females, 46 [19--63] years) were enrolled in the study. The CFS patients were divided into two groups; one group had previously defined cardiovascular (CV) risk factors of obesity and hypertension (group 1) and the second were normotensive and nonobese (group 2). Patients had significantly increased levels of isoprostanes (group 1, P=0.007; group 2, P=0.03, unpaired t test compared to controls) and oxidised low-density lipoproteins (group 2, P=0.02) indicative of a FR attack on lipids. CFS patients also had significantly lower high-density lipoproteins (group 1, P=0.011; group 2, P=0.005). CFS symptoms correlated with isoprostane levels, but only in group 2 low CV risk CFS patients (isoprostanes correlated with; total symptom score P=0.005; joint pain P=0.002; postexertional malaise P=0.027, Pearson). This is the first time that raised levels of the gold standard measure of in vivo oxidative stress (isoprostanes) and their association with CFS symptoms have been reported.

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Available from: Vance Spence, Aug 21, 2015
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    • "As the prime source of reactive oxygen species (ROS) within the body, there may be a link between mitochondrial dysfunction and ME/CFS through oxidative stress (Morris and Maes 2014a; Meeus et al. 2013). Oxidative stress has been linked to ME/CFS through the detection of reduced antioxidant levels and increases in signals of oxidative damage including glutathione, peroxidated lipids and damaged tissue (Maes et al. 2011; Kennedy et al. 2005). Typically ROS production may be triggered by cytokines to attack pathogen but can create oxidative stress if production is too high, therefore linking a chronic inflammatory response to oxidative stress as proposed for ME/CFS (Morris and Maes 2014a). "
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    ABSTRACT: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating long-term multisystem disorder with a central and inexplicably persistent fatigue symptom that is unable to be relieved by rest. Energy metabolism and oxidative stress have been recent focal points of ME/CFS research and in this study we were able to elucidate metabolic pathways that were indicative of their dysfunction. Blood and urine samples were collected from 34 females with ME/CFS (34.9 ± 1.8 SE years old) and 25 non-ME/CFS female participants (33.0 ± 1.6 SE years old). All samples underwent metabolic profiling via 1D 1H Nuclear magnetic resonance spectroscopy and quantitated metabolites were assessed for significance. Blood glucose was elevated while blood lactate, urine pyruvate, and urine alanine were reduced indicating an inhibition of glycolysis that may potentially reduce the provision of adequate acetyl-CoA for the citric acid cycle. We propose that amino acids are being increasingly used to provide an adequate carbohydrate source for the citric acid cycle. We suggest that this is via glutamate forming 2-oxoglutarate through an enzyme that deaminates it and subsequently elevates blood aspartate. Dysfunctional energy metabolism appears to have impacted creatinine and its elevation in urine suggests that it may be used as an alternative for anaerobic ATP production within muscle. A decrease in blood hypoxanthine and an increase in urine allantoin further suggest the elevation of reactive oxygen species in ME/CFS patients. These findings bring new information to the research of energy metabolism, chronic immune activation and oxidative stress issues within ME/CFS.
    Metabolomics 05/2015; DOI:10.1007/s11306-015-0816-5 · 3.97 Impact Factor
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    • "ng HMGB1 , and indirectly stimu - late the production of secondary DAMP signaling ( Lotze et al . , 2007 ) . Interestingly , approximately 40% of all FDA - approved anticancer drugs have been shown to induce ROS ( Chen et al . , 2007 ) . Oxidative stress can produce behavioral toxicities , such as chronic fatigue syndrome ( Logan and Wong , 2001 ; Kennedy et al . , 2005 ) , mild cognitive impairment ( Fukui et al . , 2002 ; Pratico et al . , 2002 ) , and diabetic neuropathy ( Nagamatsu et al . , 1995 ; Low et al . , 1997 ; Vincent et al . , 2004 ) . Furthermore , there is evidence to suggest that chemotherapy - induced neuropathy ( Areti et al . , 2014 ) and cognitive impairment ( Aluise et al . , 2010"
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    Frontiers in Neuroscience 05/2015; 9. DOI:10.3389/fnins.2015.00131 · 3.70 Impact Factor
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    • "Increased levels of thiobarbituric acid reactive substances , isoprostane, protein carbonyl levels and 8-OH- deoxyguanosine were found indicating damage by O&NS to fatty acids, proteins and DNA (Vecchiet et al. 2003; Kennedy et al. 2005; Smirnova & Pall 2003; Maes et al. 2009b). Jammes et al. (2005) reported that O&NS pathways may be a causal factor in chronic fatigue. "
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    Neuro endocrinology letters 12/2014; 35(7):577-585. · 0.94 Impact Factor
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