Age-related changes in plasma coenzyme Q(10) concentrations and redox state in apparently healthy children and adults

Department of Mathematical Sciences, University of Cincinnati, Cincinnati, Ohio, United States
Clinica Chimica Acta (Impact Factor: 2.76). 10/2004; 347(1-2):139-44. DOI: 10.1016/j.cccn.2004.04.003
Source: PubMed

ABSTRACT Coenzyme Q10 (CoQ) is an endogenous enzyme cofactor, which may provide protective benefits as an antioxidant. Because age-related CoQ changes and deficiency states have been described, there is a need to establish normal ranges in healthy children. The objectives of this study are to determine if age-related differences in reduced CoQ (ubiquinol), oxidized CoQ (ubiquinone), and CoQ redox state exist in childhood, and to establish reference intervals for these analytes in healthy children.
Apparently healthy children (n=68) were selected from individuals with no history of current acute illness, medically diagnosed disease, or current medication treatment. Self-reported healthy adults (n=106) were selected from the ongoing Princeton Follow-up Study in greater Cincinnati. Participants were assessed for lipid profiles, ubiquinol concentration, ubiquinone concentration, total CoQ concentration, and CoQ redox ratio.
Mean total CoQ and ubiquinol concentrations are similar in younger children (0.2-7.6 years) and adults (29-78 years); however, lipid-adjusted total CoQ concentrations are significantly increased in younger children. Also CoQ redox ratio is significantly increased in younger and older children compared with adults.
Elevated CoQ and redox ratios in children may be an indication of oxidative stress effects, which are associated with early development of coronary heart disease.


Available from: Peter Tang, May 28, 2015
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Redox status changes during an annual training cycle in young and adult track and field athletes and possible differences between the two age groups were assessed. Forty-six individuals (24 children and 22 adults) were assigned to four groups: trained adolescents, (TAD, ), untrained adolescents (UAD, ), trained adults (TA, ), and untrained adults (UA, ). Aerobic capacity and redox status related variables [total antioxidant capacity (TAC), glutathione (GSH), catalase activity, TBARS, protein carbonyls (PC), uric acid, and bilirubin] were assessed at rest and in response to a time-trial bout before training, at mid- and posttraining. TAC, catalase activity, TBARS, PC, uric acid, and bilirubin increased and GSH declined in all groups in response to acute exercise independent of training status and age. Training improved aerobic capacity, TAC, and GSH at rest and in response to exercise. Age affected basal and exercise-induced responses since adults demonstrated a greater TAC and GSH levels at rest and a greater rise of TBARS, protein carbonyls, and TAC and decline of GSH in response to exercise. Catalase activity, uric acid, and bilirubin responses were comparable among groups. These results suggest that acute exercise, age, and training modulate the antioxidant reserves of the body.
    Oxidative medicine and cellular longevity 01/2015; 2015:1-17. DOI:10.1155/2015/283921 · 3.36 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The bioavailability of a single, 100 mg, dose of reduced Coenzyme Q10 (CoQH-CF) and Coenzyme Q10 formulation was compared in individuals of >60 years. Significantly higher (P < 0.001) plasma concentrations were demonstrated for the CoQH-CF formulation at 5, 6, 8, 12, 24, 48 and 72 h post-dose compared to the CoQ10 formulation. The area under the curve (AUC) of reduced and total Coenzyme Q10 was significantly higher (P < 0.001) in subjects administered CoQH-CF resulting in 4.3-fold higher plasma AUC0–72 h (430% increase) in subjects receiving CoQH-CF compared to subjects receiving Coenzyme Q10. Oxidized Coenzyme Q10 in plasma was higher (P < 0.001) in subjects receiving CoQH-CF compared to subjects receiving Coenzyme Q10 resulting in a 3.3-fold higher plasma AUC0–72 h (329% increase). Total CoQ10 reached maximum plasma concentrations 15.5 ± 19.6 h after supplementation with CoQH-CF and 26.5 ± 25.8 h after supplementation with Coenzyme Q10, respectively. Thus, reduced Coenzyme Q10 liquid soft gel formulation was found to be superior to the commercial formulation of Coenzyme Q10 for bioavailability.
    Journal of Functional Foods 01/2009; 1(1):65-73. DOI:10.1016/j.jff.2008.09.010 · 4.48 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Ubiquinone and ubiquinol represent the oxidized and reduced forms of Coenzyme Q10 (CoQ10 ). CoQ10 is present in membranes of almost all human tissues and organs, with highest concentration in the heart. In patients with heart failure, serum levels of the N-terminal pro-brain natriuretic peptide (NT-proBNP) are an indicator of disease severity. Here, we investigated the relationship between serum levels of CoQ10 and NT-proBNP in healthy volunteers of an elderly study population (mean age 52 years, n = 871). We found a negative association between serum levels of ubiquinol and NT-proBNP (P < 0.001). Accordingly, the CoQ10 redox state (% oxidized form of CoQ10 ) is positively associated with serum NT-proBNP level (P < 0.001). Compared to patients who survived a myocardial infarction (n = 21), healthy subjects have lower NT-proBNP level (500.39 ± 631.28 pg/ml vs. 76.90 ± 120.27 pg/ml, P < 0.001), higher ubiquinol serum level (0.43 ± 0.19 µmol/L vs. 0.71 ± 0.32 µmol/L; P < 0.001), and a lower CoQ10 redox state (27.6 ± 13.8% vs. 17.6 ± 10.1%; P < 0.001). Interestingly, ubiquinol supplementation (150 mg/day; 14 day; n = 53) slightly reduces the expression of CLCN6, a gene related to NT-proBNP level. In summary, higher serum levels of ubiquinol are associated with lower serum NT-proBNP levels in healthy elderly subjects. However, to what extent a high serum level of ubiquinol is a protective factor for heart failure remains to be elucidated in prospective studies. © 2015 BioFactors, 41(1):35-43, 2015. © 2015 International Union of Biochemistry and Molecular Biology.
    BioFactors 01/2015; 41(1). DOI:10.1002/biof.1198 · 3.00 Impact Factor