Mitochondrial Dysfunction in Chronic Fatigue Syndrome

Chazotte, Brad

doi:10.1007/0-306-46835-2_21

Cited by 4 publications

(6 citation statements)

References 50 publications

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“…Several studies have demonstrated muscle tissue damage after sternness physical exercise, as well as muscle damage regardless of the cause will induce an inflammatory response ( Tidball, 1995 ; Huard et al, 2002 ; Sugama et al, 2015 ). Moreover administration of cytokines to smooth muscle cells reportedly inhibits mitochondrial respiration causing mitochondrial dysfunction ( Chazotte, 2001 ). This evidence suggested that cytokines may affect mitochondrial function during chronic fatigue.…”

Section: Discussionmentioning

confidence: 99%

“…Fatigue is a complex phenomenon determined by several factors, including psychological health but at the biochemical level fatigue is related to the metabolic energy available to tissues and cells, mainly through mitochondrial electron transport ( Chazotte, 2001 ; Finsterer, 2012 ). Fatigue is the most common symptom of poorly functioning mitochondria; the classic symptoms of persistent and debilitating fatigue, chronic muscle weakness, and myalgia are consistent with mitochondrial dysfunction in other diseases of known mitochondrial etiology ( Chazotte, 2001 ; Nicolson and Ellithorpe, 2006 ). Most fatigue patients report mental concentration impairment and cognitive deficits, which are also seen in mitochondrial dysfunctions ( Nicolson and Ellithorpe, 2006 ).…”

Section: Introductionmentioning

confidence: 99%

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Placenta Peptide Can Protect Mitochondrial Dysfunction through Inhibiting ROS and TNF-α Generation, by Maintaining Mitochondrial Dynamic Network and by Increasing IL-6 Level during Chronic Fatigue

et al. 2016

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Background: Level of fatigue is related to the metabolic energy available to tissues and cells, mainly through mitochondrial respiration, as well fatigue is the most common symptom of poorly functioning mitochondria. Hence, dysfunction of these organelles may be the cause of the fatigue seen in Chronic fatigue (CF). Placenta has been used for treatment of fatigue and various disease, moreover peptides has known protect mitochondrial viability, and alleviate fatigue. These properties of placenta and peptides may link with its effect on mitochondria; therefore, it is highly important to investigate the effectiveness of placenta peptide on fatigue and mitochondrial dysfunction.Methods: After administration of sheep placenta peptide (SPP) for 1 month, mice’s were forced to swim till exhaustion for 90 min to induce chronic fatigue. Electron microscopic examination of skeletal muscle mitochondrial structure, tissue Malondialdehyde (MDA), mitochondrial SOD and serum inflammatory cytokines level were investigated in order to determine the potential effect of SPP on mitochondria during CF. Rat skeletal muscle (L6 cell) were also treated with different concentration of SPP to determine the effect of SPP on cell viability using Thiazoyl blue tetrazolium assay.Results: Our finding revealed that forced swimming induced fatigue model can cause mitochondrial damage through Reactive oxygen species (ROS) mediated lipid peroxidation and Tumor Necrosis factor alpha (TNF-α) elevation. Whereas SPP protected fatigue induced mitochondrial dysfunction through preventing ROS and TNF-α generation, by maintaining mitochondrial dynamic network and by increasing serum IL-6 level.Conclusion: SPP can protect damage in mitochondrial components which will allow proper functioning of mitochondria that will in turn inhibit progression of chronic fatigue. Therefore, SPP may represent a novel therapeutic advantage for preventing mitochondrial dysfunction in patients with chronic fatigue.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Placenta Peptide Can Protect Mitochondrial Dysfunction through Inhibiting ROS and TNF-α Generation, by Maintaining Mitochondrial Dynamic Network and by Increasing IL-6 Level during Chronic Fatigue

et al. 2016

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“…Related evidence suggests that cytokine imbalances occur in chronic fatigue and other chronic diseases [29,64,65]. Studies by Chazotte showed cytokine can lower mitochondrial membrane potential in human cells [2].…”

Section: Effect Of Inflammatory Cytokines On Mitochondria During Chromentioning

confidence: 99%

“…Fatigue is a complex phenomenon determined by several factors, including psychological health but at the biochemical level fatigue is related to the metabolic energy available to tissues and cells, mainly through mitochondrial electron transport [36], Fatigue is the most common symptom of poorly functioning mitochondria, The classic symptoms of persistent and debilitating fatigue, chronic muscle weakness, and myalgia are consistent with mitochondrial dysfunction in other diseases of known mitochondrial etiology [2]. Most fatigue patients report mental concentration impairment and cognitive deficits, which are also seen in mitochondrial dysfunctions [36,37].…”

Section: Chronic Fatigue and Mitochondrial Dysfunctionmentioning

confidence: 99%

“…The plasma concentration of TNF-α has been reported to rise several hours later after the finishing of intensive exercise though significant increases immediately after exercise were absent [29,59,67]. TNF-alpha have showed effect on membrane potentials of human cell lines was examined in relation to a possible role in CFS [2].…”

Section: Tumor Necrosis Factor α (Tnf-α)mentioning

confidence: 99%

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Mechanism of Mitochondrial Dysfunction during Chronic Fatigue

Muluye¹,

Bian²

2017

Int J Phys Med Rehabil

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A clinically defined condition characterized by persistent, severe, disabling fatigue lasting more than six months that is not reversed by sleep is regarded as chronic fatigue (CF). Fatigue is a complex phenomenon determined by several factors, including psychological health but at the biochemical level fatigue is related to the metabolic energy available to tissues and cells, mainly through mitochondrial respiration. Fatigue is the most common symptom of poorly functioning mitochondria. therefore dysfunction of these organelles may be the cause of the fatigue seen in CF. There is a great progress in the molecular understanding of mitochondrial disorder but the relation of mitochondrial dysfunction with CF and the underlying mechanism is not identified well in addition treatment of fatigue is still inadequate. In this review we try to summarize the relation between CF with mitochondrial dysfunction and determine the underline mechanism.

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Metabolomic fingerprinting for biomarker discovery in renal amyloidosis

Ghosh

Singh

Govil

et al. 2022

Preprint

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Background Minimal change disease (MCD), a glomerular disease subtype is characterised by no visible change in the glomerulus upon light microscopy except for the urinary excretion of excess proteins. The symptoms of minimal change disease and renal amyloidosis are mostly overlapping and thereby misdiagnosed. However, the possible linkage between these two disease types has not been documented. We hypothesised that amyloid formation could be one of the players promoting the pathology associated with minimal change disease, resulting in perturbations of the downstream cellular pathways. Methods One hundred glomerular diseased patients were identified in a two-year study, based on symptoms and biochemical markers. Histopathological analysis showed predominance of minimal change disease in twenty patients. Further, gold standard Congo red staining was performed in these patients to detect amyloid deposition followed by tracking its downstream effects on cellular pathways using mass-spectrometry-based untargeted approach. Results Congo red staining showed presence of amyloid deposits in eleven minimal change diseased patients. Further, plasma metabolomic fingerprinting revealed a total of fifteen biologically important metabolites altered in minimal change diseased patients having renal amyloidosis as compared to controls. Different classes of lipids, carnitines and amino acids were found to be dysregulated in these patients. Conclusion In the present study we have shown the onset of renal amyloidosis and associated pathogenesis in minimal change diseased patients. Additionally, we have identified novel altered metabolic signatures in these patients as compared to controls. This is the first study in context to the Indian population, depicting the potential of metabolomic fingerprinting to identify novel markers for early diagnosis of amyloid formation in minimal change disease, a glomerular disease type.

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Mitochondrial Dysfunction in Chronic Fatigue Syndrome

Cited by 4 publications

References 50 publications

Placenta Peptide Can Protect Mitochondrial Dysfunction through Inhibiting ROS and TNF-α Generation, by Maintaining Mitochondrial Dynamic Network and by Increasing IL-6 Level during Chronic Fatigue

Placenta Peptide Can Protect Mitochondrial Dysfunction through Inhibiting ROS and TNF-α Generation, by Maintaining Mitochondrial Dynamic Network and by Increasing IL-6 Level during Chronic Fatigue

Mechanism of Mitochondrial Dysfunction during Chronic Fatigue

Metabolomic fingerprinting for biomarker discovery in renal amyloidosis

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