Effect of Oral Coenzyme Q10 Supplementation on the Oxidation Resistance of Human VLDL+LDL Fraction: Absorption and Antioxidative Properties of Oil and Granule-Based Preparations

Coenzyme Q10 (Q10) is supposed to be an important endogenous lipid-soluble antioxidant. We studied 60 healthy 46 ± 7 (mean ± SD)-year-old smoking men. They were randomized into three groups to receive oil-based or granular Q10 (90 mg/d) or placebo for 2 months. Oil-based capsule elevated Q10 in plasma by 178% and in VLDL+LDL fraction by 160%. The granular preparation increased Q10 in plasma by 168% and in VLDL+LDL by 127%. However, the 2-month Q10 supplementation did not increase the oxidation resistance of VLDL+LDL fraction, as assessed by copper induced VLDL+LDL oxidation, haemin+H₂O₂-induced VLDL+LDL oxidation, total antioxidative capacity of LDL, and plasma malondialdehyde measurements. The first and the last dose was used to carry out a 12 h pharmacokinetic study (five subjects per group), which indicated that only a small part of supplemented Q10 was absorbed to the circulation in 12 h and that the absorption varied extensively between subjects. Our results suggest that at least among smoking men, 90 mg of orally supplemented Q10 daily does not increase the oxidation resistance of VLDL+LDL. Bioavailability of both the granular and the oil-based Q10 preparation was similar during the long-term supplementation, but one dose of 30 mg had only a marginal effect on the plasma levels of Q10. © 1997 Elsevier Science Inc.     

Coenzyme Q10: absorption, antioxidative properties, determinants, and plasma levels

The purpose of this article is to summarise our studies, in which the main determinants and absorption of plasma coenzyme Q10 (Q10, ubiquinone) have been assessed, and the effects of moderate dose oral Q10 supplementation on plasma antioxidative capacity, lipoprotein oxidation resistance and on plasma lipid peroxidation investigated. All the supplementation trials carried out have been blinded and placebo-controlled clinical studies. Of the determinants of Q10, serum cholesterol, serum triglycerides, male gender, alcohol consumption and age were found to be associated positively with plasma Q10 concentration. A single dose of 30 mg of Q10, which is the maximum daily dose recommended by Q10 producers, had only a marginal elevating effect on plasma Q10 levels in non-Q10-deficient subjects. Following supplementation, a dose-dependent increase in plasma Q10 levels was observed up to a daily dose of 200 mg, which resulted in a 6.1-fold increase in plasma Q10 levels. However, simultaneous supplementation with vitamin E resulted in lower plasma Q10 levels. Of the lipid peroxidation measurements, Q10 supplementation did not increase LDL TRAP, plasma TRAP, VLDL+LDL oxidation resistance nor did it decrease LDL oxidation susceptibility ex vivo. Q10 with minor vitamin E dose neither decreased exercise-induced lipid peroxidation ex vivo nor muscular damage. Q10 supplementation might, however, decrease plasma lipid peroxidation in vivo , as assessed by the increased proportion of plasma ubiquinol (reduced form, Q10H 2 ) of total Q10. High dose vitamin E supplementation decreased this proportion, which suggests in vivo regeneration of tocopheryl radicals by ubiquinol.     

NMR structure of the LCCL domain and implications for DFNA9 deafness disorder

The LCCL domain is a recently discovered, conserved protein module named after its presence in Limulus factor C, cochlear protein Coch-5b2 and late gestation lung protein Lgl1. The LCCL domain plays a key role in the autosomal dominant human deafness disorder DFNA9. Here we report the nuclear magnetic resonance (NMR) structure of the LCCL domain from human Coch-5b2, where dominant mutations leading to DFNA9 deafness disorder have been identified. The fold is novel. Four of the five known DFNA9 mutations are shown to involve at least partially solvent-exposed residues. Except for the Trp91Arg mutant, expression of these four LCCL mutants resulted in misfolded proteins. These results suggest that Trp91 participates in the interaction with a binding partner. The unexpected sensitivity of the fold with respect to mutations of solvent-accessible residues might be attributed to interference with the folding pathway of this disulfide-containing domain.     

Coenzyme Q10: Absorption,Antioxidative Properties,Determinants, and Plasma Levels

The purpose of this article is to summarise our studies, in which the main determinants and absorption of plasma coenzyme Q10 (Q10, ubiquinone) have been assessed, and the effects of moderate dose oral Q10 supplementation on plasma antioxidative capacity, lipoprotein oxidation resistance and on plasma lipid peroxidation investigated. All the supplementation trials carried out have been blinded and placebo-controlled clinical studies. Of the determinants of Q10, serum cholesterol, serum triglycerides, male gender, alcohol consumption and age were found to be associated positively with plasma Q10 concentration. A single dose of 30 mg of Q10, which is the maximum daily dose recommended by Q10 producers, had only a marginal elevating effect on plasma Q10 levels in non-Q10-deficient subjects. Following supplementation, a dose-dependent increase in plasma Q10 levels was observed up to a daily dose of 200 mg, which resulted in a 6.1-fold increase in plasma Q10 levels. However, simultaneous supplementation with vitamin E resulted in lower plasma Q10 levels. Of the lipid peroxidation measurements, Q10 supplementation did not increase LDL TRAP, plasma TRAP, VLDL+LDL oxidation resistance nor did it decrease LDL oxidation susceptibility ex vivo. Q10 with minor vitamin E dose neither decreased exercise-induced lipid peroxidation ex vivo nor muscular damage. Q10 supplementation might, however, decrease plasma lipid peroxidation in vivo, as assessed by the increased proportion of plasma ubiquinol (reduced form, Q10H 2 ) of total Q10. High dose vitamin E supplementation decreased this proportion, which suggests in vivo regeneration of tocopheryl radicals by ubiquinol.     

Changes in maximal cardiorespiratory capacity and submaximal strain while exercising in cold

Sixteen subjects were exposed to varying climatic conditions (20 to −20 °C) while exercising with different intensities from light to maximal. The results indicate that maximal cardiorespiratory capacity is lowered and submaximal strain is increased when ambient working temperature decreases. This means that the individual strain caused by a given submaximal workload may be significantly higher in cold as compared to thermoneutral environment due to cooling, use of additional clothing or their combination.     

High-intensity endurance training increases nocturnal heart rate variability in sedentary participants

The effects of endurance training on endurance performance characteristics and cardiac autonomic modulation during night sleep were investigated during two 4-week training periods. After the first 4-week training period (3 x 40 min per week, at 75% of HRR) the subjects were divided into HIGH group (n = 7), who performed three high-intensity endurance training sessions per week; and CONTROL group (n = 8) who did not change their training. An incremental treadmill test was performed before and after the two 4-week training periods. Furthermore, nocturnal RR-intervals were recorded after each training day. In the second 4-week training period HIGH group increased their VO₂max (P = 0.005) more than CONTROL group. At the same time, nocturnal HR decreased (P = 0.039) and high-frequency power (HFP) increased (P = 0.003) in HIGH group while no changes were observed in CONTROL group. Furthermore, a correlation was observed between the changes in nocturnal HFP and changes in VO₂max during the second 4-week training period (r = 0.90, P < 0.001). The present study showed that the increased HFP is related to improved VO₂max in sedentary subjects suggesting that nocturnal HFP can provide a useful method in monitoring individual responses to endurance training.