Dataset Information

Coenzyme Q10 Treatment Monitoring in Different Human Biological Samples.

ABSTRACT: Coenzyme Q10 (CoQ) treatment monitoring is a matter of debate since CoQ distribution from plasma to blood cells and tissues is not fully understood. We aimed to analyze the CoQ levels in a wide set of human biological samples (plasma, blood mononuclear cells (BMCs), platelets, urinary cells, and skeletal muscle) from a group of 11 healthy male runners before and after CoQ supplementation. The CoQ content in the different samples was analyzed by HPLC coupled to electrochemical detection. No significant differences were observed in the CoQ levels measured in the BMCs, platelets, and urine after the one-month treatment period. Plasma CoQ (expressed in absolute values and values relative to total cholesterol) significantly increased after CoQ supplementation (p = 0.003 in both cases), and the increase in CoQ in muscle approached significance (p = 0.074). CoQ levels were increased in the plasma of all supplemented subjects, and muscle CoQ levels were increased in 8 out of 10 supplemented subjects. In conclusion, the analysis of CoQ in plasma samples seems to be the best surrogate biomarker for CoQ treatment monitoring. Moreover, oral CoQ administration was effective for increasing muscle CoQ concentrations in most subjects.

SUBMITTER: Paredes-Fuentes AJ

PROVIDER: S-EPMC7601005 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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Coenzyme Q<sub>10</sub> Treatment Monitoring in Different Human Biological Samples.

Paredes-Fuentes Abraham J AJ Montero Raquel R Codina Anna A Jou Cristina C Fernández Guerau G Maynou Joan J Santos-Ocaña Carlos C Riera Joan J Navas Plácido P Drobnic Franchek F Artuch Rafael R

Antioxidants (Basel, Switzerland) 20201013 10

Coenzyme Q<sub>10</sub> (CoQ) treatment monitoring is a matter of debate since CoQ distribution from plasma to blood cells and tissues is not fully understood. We aimed to analyze the CoQ levels in a wide set of human biological samples (plasma, blood mononuclear cells (BMCs), platelets, urinary cells, and skeletal muscle) from a group of 11 healthy male runners before and after CoQ supplementation. The CoQ content in the different samples was analyzed by HPLC coupled to electrochemical detectio ...[more]

PMID: 33066002

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Project description:Coenzyme Q10 (CoQ10) deficiency syndrome is a rare condition that causes mitochondrial dysfunction and includes a variety of clinical presentations as encephalomyopathy, ataxia and renal failure. First, we sought to set up what all have in common, and then investigate why CoQ10 supplementation reverses the bioenergetics alterations in cultured cells but not all the cellular phenotypes. DESIGN MODELLING STUDY: This work models the transcriptome of human CoQ10 deficiency syndrome in primary fibroblast from patients and study the genetic response to CoQ10 treatment in these cells.Four hospitals and medical centres from Spain, Italy and the USA, and two research laboratories from Spain and the USA.Primary cells were collected from patients in the above centres.We characterised by microarray analysis the expression profile of fibroblasts from seven CoQ10-deficient patients (three had primary deficiency and four had a secondary form) and aged-matched controls, before and after CoQ10 supplementation. Results were validated by Q-RT-PCR. The profile of DNA (CpG) methylation was evaluated for a subset of gene with displayed altered expression.CoQ10-deficient fibroblasts (independently from the aetiology) showed a common transcriptomic profile that promotes cell survival by activating cell cycle and growth, cell stress responses and inhibiting cell death and immune responses. Energy production was supported mainly by glycolysis while CoQ10 supplementation restored oxidative phosphorylation. Expression of genes involved in cell death pathways was partially restored by treatment, while genes involved in differentiation, cell cycle and growth were not affected. Stably demethylated genes were unaffected by treatment whereas we observed restored gene expression in either non-methylated genes or those with an unchanged methylation pattern.CoQ10 deficiency induces a specific transcriptomic profile that promotes cell survival, which is only partially rescued by CoQ10 supplementation.

Dataset Information

Coenzyme Q10 Treatment Monitoring in Different Human Biological Samples.

Publications

Coenzyme Q<sub>10</sub> Treatment Monitoring in Different Human Biological Samples.

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