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Letters to the Editor |
1 Biochemistry Department, Canterbury Health Laboratories, Christchurch, New Zealand
2 Department of Chemistry, University of Canterbury, Christchurch, New Zealand
aAddress correspondence to this author at: Sarah Molyneux, Biochemistry Unit, Canterbury Health Laboratories, P.O. Box 151, Christchurch 8140, New Zealand. Fax 64-3-3640889; e-mail sarah.molyneux{at}cdhb.govt.nz.
Coenzyme Q9 (CoQ9) in human plasma may originate as a product of incomplete CoQ10 biosynthesis or from the diet. The estimated dietary CoQ9 intake is 0–1.3 µmol/day, primarily from cereals and fats (1)(2), but this is unreliable because many food items contain levels below the detection limit (1).
Some methods for estimating human plasma CoQ10 use CoQ9 as an internal standard; thus, intraindividual variation in the concentration of endogenous CoQ9 is a potential source of error.
We measured total CoQ9 in human plasma, determined a reference interval, examined the biological variation, and documented the influence of CoQ10 supplementation on plasma CoQ9 concentrations.
Self-reportedly healthy volunteers (n = 193; men/women, 82/113) were enrolled for determination of a reference interval for CoQ9. Mean age of participants was 45 years (range 18–82). No participants reported taking CoQ10 supplements.
Biological variation of CoQ9 was determined in healthy adult male volunteers (n = 10) who did not smoke and did not take vitamin or CoQ10 supplements or medications in the 4 weeks before the study. Median age of the participants was 23.5 years (range 21–28). We took 7 blood samples from each participant in the morning after a 10-h overnight fast, at least 1 week apart, over a 2-month period.
We determined the effect of CoQ10 supplementation on plasma CoQ9 concentrations using the same 10 individuals. After baseline blood samples were taken, we administered a CoQ10 supplement (Q-Gel®, Tishcon USA) as a single, nominal 150-mg dose. A vegetarian breakfast and lunch were provided. We obtained a 2nd blood sample 6 h after administration of the supplement.
The plasma CoQ9 and CoQ10 assay, adapted from Tang et al. (3), measured total CoQ9 and CoQ10 simultaneously. We measured total cholesterol and direct LDL-cholesterol on all samples, using enzymatic methods (Aeroset, Abbott Laboratories), with coefficients of variation (CVs) of 1.6% and 1.2%, respectively.
Blood samples were collected in lithium heparin, centrifuged within 1 h of collection, and plasma was stored protected from light: at –30 °C until analysis (maximum storage time, 112 days) for the reference interval study; and at –80 °C until analysis (maximum storage time, 150 days) for the biological variation and effect of CoQ10 supplementation on plasma total CoQ9 concentration studies. These studies were approved by the Canterbury Ethics Committee, Christchurch, New Zealand, and written informed consent was obtained from all participants.
Statistical analysis was carried out using SigmaStat and SPSS software. Nonparametric statistics were used to determine the reference interval, and outliers were included in the analysis. Inter- and intraindividual variations were reported as CVs, correlation as the Pearson correlation coefficient, and comparisons by the Mann–Whitney rank-sum test. Statistical significance was inferred when P <0.05.
There was no significant difference in total CoQ9 between males and females (Table 1
).
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CoQ9 and CoQ10 were significantly correlated (r = +0.577; P <0.001) in the reference cohort, suggesting that CoQ9 could be made during CoQ10 biosynthesis by omission of 1 isoprenoid unit. However, the observed correlation was also consistent with a hypothesis that CoQ9 is a metabolite of CoQ10 catabolism.
The intra- and interindividual variations in CoQ9 were 20.9% and 35.5%, respectively. The index of individuality was 0.6 for CoQ9, calculated as within-subject variation/between-subject variation, whereas that for CoQ10 was 0.4 (4).
Plasma CoQ9 increased after supplementation with CoQ10, with the median (2.5–97.5 percentiles) CoQ9 concentration at baseline and after supplementation at 17.17 (9.23–36.81) and 26.94 (14.49–39.55) nmol/L, respectively (P = 0.052). The mean (SD) concentration of CoQ9 ingested with the CoQ10 supplements was 2.71 (0.99 µg; n = 6). The mean (SD) CoQ9 concentration of the vegetarian breakfast was approximately 134 (63 µg) (1)(2). This increase in plasma CoQ9 after supplementation with CoQ10 concurred with animal data in mice and rats (5).
The plasma ratio of CoQ9 to CoQ10 was significantly lower after CoQ10 supplementation (P = 0.022), with mean (SD) ratio before and after supplementation being 22.56 (4.88 mmol/mol) and 16.66 (5.66 mmol/mol), respectively.
Our confirmation that CoQ9 is a normal constituent of human plasma make it less than ideal for use as an internal standard, leading to underestimation of CoQ10 by 1% to 7%. This complicates the CoQ10 assay design and calls for further investigation.
Acknowledgments
The authors acknowledge Endolab for collaboration in the reference interval studies, Tishcon for donation of the Q-Gel® CoQ10 supplement, and the National Heart Foundation of New Zealand for funding.
References
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