Aim: The present study was conducted to define the relationship between the anti-aging effect of ubiquinol-10 supplementation and mitochondrial activation in senescence-accelerated mouse prone 1 (SAMP1) mice.
Results: Here, we report that dietary supplementation with ubiquinol-10 prevents age-related decreases in the expression of sirtuin gene family members, which results in the activation of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a major factor that controls mitochondrial biogenesis and respiration, as well as superoxide dismutase 2 (SOD2) and isocitrate dehydrogenase 2 (IDH2), which are major mitochondrial antioxidant enzymes. Ubiquinol-10 supplementation can also increase mitochondrial complex I activity and decrease levels of oxidative stress markers, including protein carbonyls, apurinic/apyrimidinic sites, malondialdehydes, and increase the reduced glutathione/oxidized glutathione ratio. Furthermore, ubiquinol-10 may activate Sirt1 and PGC-1α by increasing cyclic adenosine monophosphate (cAMP) levels that, in turn, activate cAMP response element-binding protein (CREB) and AMP-activated protein kinase (AMPK).
Innovation And Conclusion: These results show that ubiquinol-10 may enhance mitochondrial activity by increasing levels of SIRT1, PGC-1α, and SIRT3 that slow the rate of age-related hearing loss and protect against the progression of aging and symptoms of age-related diseases.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4025630 | PMC |
| http://dx.doi.org/10.1089/ars.2013.5406 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Plasma CoQ10 Status in Patients with Propionic Acidaemia and Possible Benefit of Treatment with Ubiquinol.
Antioxidants (Basel)
August 2022
Unidad de Enfermedades Metabólicas, Hospital Universitario Ramón y Cajal, Crta de Colmenar Viejo, km 9, 100, PC 28034 Madrid, Spain.
Article Synopsis
- Propionic acidaemia (PA) is a metabolic disorder caused by a lack of the enzyme propionyl-CoA carboxylase, leading to acute decompensation and potential long-term complications from mitochondrial dysfunction.
- A study involving seven PA patients aged 2.5 to 20 years examined the effects of Coenzyme Q10 (CoQ10) supplementation in the form of ubiquinol, showing that it corrected initially low plasma CoQ10 levels and was well tolerated.
- Supplementation resulted in significant increases in urinary citrate and the citrate/methylcitrate ratio, indicating potential improvements in mitochondrial function and anaplerosis, warranting further investigation for preventing chronic complications in PA.
Bioavailability of Reduced Coenzyme Q10 (Ubiquinol-10) in Burn Patients.
Metabolites
July 2022
Department of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, 149 Thirteenth Street, Charlestown, MA 02129, USA.
Mitochondrial dysfunction has been implicated in the pathogenesis of inflammation and multi-organ dysfunction in major trauma, including burn injury. Coenzyme Q10 (CoQ10) is a metabolite of the mevalonate pathway and an essential cofactor for the electron transport in the mitochondria. In addition, its reduced form (ubiquinol) functions as an antioxidant.
View Article and Find Full Text PDFShort-term ubiquinol-10 supplementation alleviates tissue damage in muscle and fatigue caused by strenuous exercise in male distance runners.
Int J Vitam Nutr Res
June 2021
Juntendo University Faculty of Health and Sports Science, Hiragagakuendai, Inzai, Chiba, Japan.
Coenzyme Q10 (CoQ10) is the electron transporter in oxidative phosphorylation and an endogenous antioxidant. Recent researches have indicated that doses of 200-300 mg/day are needed to recognize effects to prevent oxidative damage in athletes, and the reduced form of CoQ10, ubiquinol-10, is more bioavailable than its oxidized form. Therefore, we hypothesized that higher doses of ubiquinol-10 could elevate plasma CoQ10 levels rapidly and exert physiological benefits in athletes.
View Article and Find Full Text PDFPET imaging of C-labeled coenzyme Q: Comparison of biodistribution between [C]ubiquinol-10 and [C]ubiquinone-10.
Biochem Biophys Res Commun
May 2019
RIKEN Center for Life Science Technologies, Japan; RIKEN Center for Biosystems Dynamics Research, Japan; RIKEN Compass to Healthy Life Research Complex Program, Kobe, Hyogo, Japan. Electronic address:
Coenzyme Q (CoQ) plays a key role not only as an essential electron carrier in the mitochondrial electron transport chain, but also as an antioxidant to protect cells from oxidative stress. CoQ supplementation is expected to be effective for a variety of diseases. The predominant forms of CoQ are the ubiquinol-10 (reduced form) and ubiquinone-10 (oxidized form).
View Article and Find Full Text PDFCombination of Coenzyme Q Intake and Moderate Physical Activity Counteracts Mitochondrial Dysfunctions in a SAMP8 Mouse Model.
Oxid Med Cell Longev
January 2019
Polytechnic University of Marche, Department of Life and Environmental Sciences (DISVA), via Brecce Bianche, Ancona, Italy.
Aging skeletal muscles are characterized by a progressive decline in muscle mass and muscular strength. Such muscular dysfunctions are usually associated with structural and functional alterations of skeletal muscle mitochondria. The senescence-accelerated mouse-prone 8 (SAMP8) model, characterized by premature aging and high degree of oxidative stress, was used to investigate whether a combined intervention with mild physical exercise and ubiquinol supplementation was able to improve mitochondrial function and preserve skeletal muscle health during aging.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!