Objectives: Coenzyme Q(10) (CoQ(10)) is an essential electron carrier in the mitochondrial respiratory chain and a strong antioxidant. Signs associated with skin alteration and mitochondrial dysfunction have been observed in patients with fibromyalgia (FM). The aim of this study was to analyze CoQ(10) levels, mitochondrial dysfunction, and oxidative stress in plasma, blood mononuclear cells, and skin biopsies from FM patients.
Methods: We studied CoQ(10) level by HPLC in plasma, blood mononuclear cells, and skin obtained from patients with FM and healthy control subjects. Oxidative stress markers and mitochondrial respiratory chain enzyme activities were analysed in both plasma, blood mononuclear cells, and skin biopsies from FM patients.
Results: Oxidative stress, mitochondrial dysfunction, and CoQ(10) deficiency have been observed in blood mononuclear cells and skin biopsies.
Conclusions: In our patients, mitochondrial dysfunction and CoQ(10) deficiency are present in several tissues. These results may contribute to the understanding of the pathophysiology of FM, and, moreover, CoQ(10) deficiency could represent a good marker for the diagnosis of FM.
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http://dx.doi.org/10.1016/j.clinbiochem.2010.06.013 | DOI Listing |
Sci Transl Med
January 2025
Graduate Program in Human Genetics, University of Miami Miller School of Medicine, 1501 NW 10th Avenue (M-860), Miami, FL 33136, USA.
Primary mitochondrial disorders are most often caused by deleterious mutations in the mitochondrial DNA (mtDNA). Here, we used a mitochondrial DddA-derived cytosine base editor (DdCBE) to introduce a compensatory edit in a mouse model that carries the pathological mutation in the mitochondrial transfer RNA (tRNA) alanine (mt-tRNA) gene. Because the original m.
View Article and Find Full Text PDFSci Adv
January 2025
Department of Molecular Biology and Microbiology, Tufts University, Boston, MA 02111, USA.
The Epstein-Barr virus (EBV) infects nearly 90% of adults globally and is linked to over 200,000 annual cancer cases. Immunocompromised individuals from conditions such as primary immune disorders, HIV, or posttransplant immunosuppressive therapies are particularly vulnerable because of EBV's transformative capability. EBV remodels B cell metabolism to support energy, biosynthetic precursors, and redox equivalents necessary for transformation.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
February 2025
Princess Margaret Cancer Centre, University Health Network, Toronto, ON M5G 1L7, Canada.
ClpXP is a two-component mitochondrial matrix protease. The caseinolytic mitochondrial matrix peptidase chaperone subunit X (ClpX) recognizes and translocates protein substrates into the degradation chamber of the caseinolytic protease P (ClpP) for proteolysis. ClpXP degrades damaged respiratory chain proteins and is necessary for cancer cell survival.
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Key Laboratory of Longevity and Aging-Related Disease of Chinese Ministry of Education, Center for Translational Medicine, School of Basic Medical Sciences, Guangxi Medical University, Nanning, Guangxi, China.
2-dodecyl-6-methoxycyclohexa-2,5-diene-1,4-dione (DMDD) is a cyclohexanedione compound extracted from the roots of Averrhoa carambola L. Several studies have documented its beneficial effects on diabetes, Alzheimer's disease, and cancer. However, its potential neuroprotective effects on Parkinson's disease (PD) have not yet been explored.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Huai'an Hospital Affiliated to Yangzhou University, The Fifth People's Hospital of Huai'an), 1 Huaihe East Road, Huaiyin District, Huai'an City, Jiangsu Province, China.
Ginkgolide B (GB) is a bioactive constituent found in Ginkgo biloba leaves that has been long recognized as a protective agent against many neurological disorders. Our study aimed to examine the effect of GB in an in vitro Parkinson's disease (PD) model and to investigate its neuroprotective mechanism as a primary objective. SK-N-SH cells were challenged with 1-methyl-4-phenylpyridinium (MPP) to act as a PD-like model of neuronal damage.
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