Coenzyme Q10 in human blood: Native levels and determinants of oxidation during processing and storage

Abstract

Coenzyme Q10 (Q10) is present in the circulation mainly in its reduced form (ubiquinol-10; UL10), but oxidizes quickly ex vivo to ubiquinone-10 (UN10). Therefore, native UL10:UN10 ratios, used as markers of redox status and disease risk, are difficult to measure. We established an RP-(U)HPLC method with coulometric detection to measure natively circulating UL10 and UN10 concentrations by adding a ubiquinol/ubiquinone mixture as an internal standard immediately after plasma preparation. This allowed adjustment for unavoidable artificial UL10 oxidation as well as for total losses (or gains) of analytes during sample storage, processing, and analysis because the internal standards exactly paralleled the chemical behavior of Q10. This technique applied to blood (n = 13) revealed Q10 levels of 680–3300 nM with a mean UL10:UN10 ratio of 95:5, which was inversely associated with total Q10 (r=−0.69; p=0.004). The oxidation of UL10 to UN10 was equimolar, increased by O2, and decreased by lower temperatures or various degassing methods. Although UL10 was stable in blood or when pure in organic solvents at 22 °C, its oxidation was catalyzed dose dependently by α-tocopherol and butylated hydroxytoluene, particularly when present in combination. Key structural features for the catalytic pro-oxidant properties of phenolic antioxidants included two substituents vicinal to the phenolic hydroxyl group.

New insights into the chemistry of Coenzyme Q-0: A voltammetric and spectroscopic study

“…The redox features of many hydrophilic and lipophilic Q and HQ have been intensively studied by various electrochemical methods [4,19,20,[24][25][26][27][28][29], but surprisingly, there are only few reports related to the electrochemical features of the simplest CoQ member, i.e. CoQ-0 [21][22][23].…”

Coenzyme Q10 prevented full blown splenomegaly and decreased melarsoprol-induced reactive encephalopathy in mice infected with Trypanosoma brucei rhodesiense

“…Previously it has been demonstrated that extracellular supply of coenzyme Q 10 through the circulation influences coenzyme Q 10 levels in blood cells [21] . This may indicate an underlying possibility that coenzyme Q 10 prevents splenomegaly through other mechanism other than its antioxidant capabilities.…”

“…Mice in the second and third groups were infected with T. b. rhodesiense for 21 and 57 d post infection (dpi) respectively, while those in the first group were uninfected and served as health control for the second and third group. Animals in the third group were projected to survive for 60 dpi after which they were sacrificed at termination of experiment.…”

“…Mice in the second, third and fourth group were infected with T. b. rhodesiense for 21 Gray, 1983) and thus is used to induce severe late CNS infection that closely mirrors PTRE in human subjects. Thereafter, mice were monitored for relapse of parasitaemia after which they were treated with melarsoprol at a dosage of 3.6 mg/kg for 4 d and sacrificed 24 h post the last dosage to obtain brain samples.…”

“…On the other hand, infected mice orally administered with coenzyme Q 10 treated with DA and melarsoprol after relapse showed less of these lesions (Figure 2). The sections show different neuro-inflammation at different stages of the disease, and also with different treatments: (1) uninfected (control), (2) early-CNS stage (21 dpi), (3) severe late-CNS stage, (4) uninfected melarsoprol treated, (5) infected melarsoprol treated 21 dpi, (6) infected CoQ 10 melarsoprol treated 21 dpi, (7) infected CoQ 10 , PTRE-induced and melarsoprol treated with less marked cellular infiltration and perivascular cuffing, and infected, PTRE-induced and melarsoprol treated, (8a & 8b) increasing development of the perivascular cuffs, cellular infiltration and encephalitis as demonstrated. …”