Coenzyme Q10 Long-Term Supplementation

Coenzyme Q10 Long-Term Supplementation May Result in Withdrawal Effect in Myocardium 

Authors: Meredith Spindler, M Flint Beal, Claire Henchcliffe

Published Date November 2009 , Volume 2009:5 Pages 597 - 610 DOI 10.2147/NDT.S5212

Meredith Spindler, M Flint Beal, Claire Henchcliffe

Department of Neurology, ²Department of Neuroscience, Weill Medical College of Cornell University, New York, NY, USA

Coenzyme Q10 (CoQ10) is an essential co-factor in the mitochondrial respiratory chain, and as a dietary supplement it has recently gained attention for its potential role in the treatment of neurodegenerative disease. Evidence for mitochondrial dysfunction in neurodegenerative disorders derives from animal models, studies of mitochondria from patients, identification of genetic defects in patients with neurodegenerative disease, and measurements of markers of oxidative stress.

Studies of in vitro models of neuronal toxicity and animal models of neurodegenerative disorders have demonstrated potential neuroprotective effects of CoQ10. With this data in mind, several clinical trials of CoQ10 have been performed in Parkinson’s disease and atypical Parkinson’s syndromes, Huntington’s disease, Alzheimer disease, Friedreich’s ataxia, and amyotrophic lateral sclerosis, with equivocal findings.

CoQ10 is widely available in multiple formulations and is very well tolerated with minimal adverse effects, making it an attractive potential therapy. Phase III trials of high-dose CoQ10 in large sample sizes are needed to further ascertain the effects of CoQ10 in neurodegenerative diseases.

Journals: Withdrawal Effect in Myocardium

CoQ10 Long-Term Supplementation

May Result in Withdrawal Effect in Myocardium

Author: Kalenikova, E;   Pp.13.492

Lomonosov Moscow State University, Faculty of Basic Medicine,

Department of Pharmacology, Moscow, Russia

Cardiology Research Center, Moscow, Russia

Abstract

Objective: Coenzyme Q10 (CoQ10) is used as cardioprotector. CoQ10 is endogenous substance and long-term administration of exogenous CoQ10 can influence on its tissue biosynthesis. The aim of the study was to examine the possibility of replenishment of coenzymes Q myocardial level by long-term supplementation with solubilized CoQ10 and to estimate myocardial CoQ content after discontinuation of supplementation.

Design and Methods: Male conscious Wistar rats (n = 30) were supplemented with solubilized CoQ10 (10 mg/kg/day per os; Kudesan solution, “Akvion”, Russia). Serum and myocardial levels of CoQ9, CoQ10 were measured after 3 weeks (n = 6), 6 weeks (n = 8) of administration and 2 weeks (n = 8), 6 weeks (n = 8) after discontinuation. Tissue samples were collected 3–4 h after the last administration. Age-matched rats served as control. Myocardial levels of CoQ were estimated in supernatants of homogenates. Assay carried out using HPLC with electrochemical detection after liquid extraction with ethanol-hexane mixture. Statistical analysis was performed with two-tailed t-test.

Results: Serum CoQ10 level after 3 and 6 weeks of supplementation was 10 time higher than in control rats. 2 weeks after discontinuation serum CoQ10 level was 3 time higher than in control group and 6 weeks after discontinuation CoQ10 level was not different from control values. CoQ9 serum concentration did not differ between groups. Myocardial content of CoQ10 increased by 40% and 60%, CoQ9 – by 75% and 50% after 3 and 6 weeks of treatment, correspondently. Discontinuation of CoQ10 supplementation evoked the fall of CoQ9 (by 50%) and CoQ10 (by 60%) levels below the control values in 2 weeks; recovery to the control levels was detected in 6 weeks.

Conclusion: Results demonstrate CoQ10 withdrawal effect in rat myocardium. These data have to take account of long-term treatment the patients with cardiovascular diseases.