Coenzyme Q10 Concentration Research Articles

Coenzyme Q10 Treatment Monitoring in Different Human Biological Samples.

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.

CoQ10 improves meiotic maturation of pig oocytes through enhancing mitochondrial function and suppressing oxidative stress

Coenzyme Q10 (CoQ10) is essential to many fundamental biological processes. However, the effect of CoQ10 on meiotic maturation of pig oocytes still remains elusive. In the present study we aimed to understand the effects of CoQ10 on porcine oocyte maturation, by supplementing different concentrations of CoQ10 (25, 50 and 100 μM) into the maturation medium. We showed that CoQ10 at 50 μM had better capacity to promote the nuclear maturation of pig oocytes derived from both small and large antral follicles. Though the cleavage and blastocyst rates of parthenotes stayed stable, 50 μM CoQ10 treatment could accelerate the development of parthenotes to blastocyst stage, and increase the average cell number of blastocyst. For cumulus-oocyte complexes from large antral follicles categorized by the brilliant cresyl blue (BCB) test, 50 μM CoQ10 treatment could specifically promote the nuclear maturation of poor-quality oocytes in the BCB-negative group. Mitochondrial function of oocytes treated by 50 μM CoQ10 could be boosted, through increasing the levels of mitochondrial membrane potential, ATP production and CoQ6, and changing the pattern of mitochondrial distribution as well. Moreover, 50 μM CoQ10 treatment suppressed the level of reactive oxygen species and reduced the percentage of oocytes with early apoptosis signal. Taken together, CoQ10 could improve the meiotic maturation of pig oocytes, especially for poor-quality oocytes, mainly through enhancing mitochondrial function and suppressing oxidative stress to reduce apoptosis.

Effects of coenzyme Q10 on endothelial and cardiac function in patients undergoing haemodialysis: study protocol for a pilot randomised controlled trial

IntroductionEndothelial and cardiac dysfunction are highly prevalent and are associated with cardiovascular morbidity and mortality among patients undergoing dialysis. For patients undergoing dialysis, no study has explored the effect of...

Prolonged oral coenzyme Q10-β-cyclodextrin supplementation increases skeletal muscle complex I+III activity in young Thoroughbreds

Coenzyme Q10 (CoQ10) is an essential component of the mitochondrial electron transport chain (ETC). Decreased skeletal muscle CoQ10 content may result in decreased ETC activity and energy production. This study tested the hypotheses that supplementation with oral CoQ10 will increase plasma CoQ10 concentrations and that prolonged supplementation will increase skeletal muscle CoQ10 content in young, healthy untrained Thoroughbreds. Nineteen Thoroughbreds (27.5±9.7 months old; 11 males, eight females) from one farm and maintained on a grass pasture with one grain meal per day were supplemented daily with 1.5 mg/kg body weight of an oral CoQ10-β-cyclodextrin inclusion complex. Whole-blood and skeletal muscle biopsies were collected before (T0) and after (T1) nine weeks of supplementation. Plasma CoQ10 concentrations were determinedvia high-performance liquid chromatography. Skeletal muscle mitochondrial ETC combined complex I+III enzyme activity (indirect measurement of CoQ10 content) was assessed spectrophotometrically and normalised to mitochondrial abundance. Horses accepted supplementation with no adverse effects. Plasma CoQ10 concentration increased in all horses following supplementation, with mean plasma CoQ10 concentration significantly increasing from T0 to T1 (0.13±0.02 vs 0.25±0.03 μg/ml; mean difference 0.12±0.03;P=0.004). However, variability in absorbance resulted in a 58% response rate (i.e. doubling of T1 above T0 values). The mean skeletal muscle complex I+III activity significantly increased from T0 to T1 (0.36±0.04 vs 0.59±0.05 pmol/min/mg of muscle, mean difference 0.23±0.05;P=0.0004), although T1 values for three out of 19 horses decreased on average by 23% below T0 values. In conclusion, oral supplementation with CoQ10 in the diet of young, healthy untrained Thoroughbreds increased mean plasma CoQ10 concentration by 99% with prolonged daily supplementation increasing mean skeletal muscle complex I+III activity by 65%. Additional research is warranted investigating training and exercise effects on skeletal muscle CoQ10 content in CoQ10 supplemented and un-supplemented Thoroughbreds.

The Effect of Cellular Coenzyme Q10 Deficiency on Lysosomal Acidification.

Coenzyme Q10 (CoQ10) deficiency currently represents the only treatable mitochondrial disorder, however, little is known about how it may affect other organelles. The lysosome has been found to have a large concentration of CoQ10 localised at its membrane; additionally, it has been suggested that it plays a role in the normal acidification of the lysosomal lumen. As a result, in this study we assessed the effect of CoQ10 deficiency on lysosomal acidification. In order to investigate this, a neuronal cell model of CoQ10 deficiency was established via the treatment of SH-SY5Y cells with para-aminobenzoic acid (PABA). This method works through the competitive inhibition of the CoQ10 biosynthetic pathway enzyme, CoQ2. A single 1 mM (5 days) treatment with PABA resulted in a decrease of up to 58% in cellular CoQ10 (p < 0.05). It was found that this resulted in a significant decrease in fluorescence of both the LysoSensor (23%) and LysoTracker (35%) probes used to measure lysosomal pH (p < 0.05). It was found that subsequent treatment with CoQ10 (5 µM, 3 days) was able to restore cellular CoQ10 concentration (p < 0.005), which was associated with an increase in fluorescence from both probes to around 90% of controls (p < 0.05), suggesting a restoration of lysosomal pH. This study provides insights into the association between lysosomal pH and cellular CoQ10 status and the possibility that a deficit in the status of this isoprenoid may result in an impairment of lysosomal acidification.

Systemic Redox Imbalance in Patients with Chronic Granulomatous Disease.

The aim of our study was to evaluate redox status, enzymatic and non-enzymatic antioxidant barriers, oxidative damage of proteins, lipids and DNA, as well as concentration of coenzyme Q10 and vitamins A and E in patients with chronic granulomatous disease (CGD). The study was performed on fifteen Caucasian individuals (median age 24 years and seven months) diagnosed with CGD. The mutation in the NCF1 gene was confirmed in ten patients, and in the CYBB gene in five patients. We demonstrated high levels of total oxidant status (TOS) and oxidative stress index (OSI), lipids (↑8-isoprostanes (8-isoP), ↑4-hydroxynonenal (4-HNE)), proteins (↑advanced oxidation protein products (AOPP)) and DNA (↑8-hydroxy-2’-deoxyguanosine (8-OHdG)) oxidation products in CGD individuals as compared to sex- and age-matched healthy controls. We showed enhanced serum enzymatic activity of catalase (CAT) and superoxide dismutase-1 (SOD) and significantly decreased coenzyme Q10 concentration. Our study confirmed redox disturbances and increased oxidative damage in CGD patients, and indicated the need to compare redox imbalance depending on the type of mutation and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity. The question regarding effectiveness of antioxidant therapy in patients with CGD is open, and the need to establish guidelines in this area remains to be addressed.

The therapeutic efficacy of water-soluble coenzyme Q10 in an experimental model of tacrolimus-induced diabetes mellitus.

Background/AimsCoenzyme Q10 (CoQ10) has antioxidant effects and is commercially available and marketed extensively. However, due to its low bioavailability, its effects are still controversial. We developed a water-soluble CoQ10-based micelle formulation (CoQ10-W) and tested it in an experimental model of tacrolimus (TAC)-induced diabetes mellitus (DM).MethodsWe developed CoQ10-W from a glycyrrhizic-carnitine mixed layer CoQ10 micelle preparation based on acyltransferases. TAC-induced DM rats were treated with either lipid-soluble CoQ10 (CoQ10-L) or CoQ10-W for 4 weeks. Their plasma and pancreatic CoQ10 concentrations were measured using liquid chromatography- tandem mass spectrometry. The therapeutic efficacies of CoQ10-W and CoQ10-L on TAC-induced DM were compared using functional and morphological parameters and their effects on cell viability and reactive oxygen species (ROS) production were also evaluated in cultured rat insulinoma cells.ResultsThe plasma CoQ10 level was significantly increased in the CoQ10-W group compared to that in the CoQ10-L group. Intraperitoneal glucose tolerance tests and glucose-stimulated insulin secretion revealed that CoQ10-W controlled hyperglycemia and restored insulin secretion significantly better than CoQ10-L. The TAC-mediated decrease in pancreatic islet size was significantly attenuated by CoQ10-W but not by CoQ10-L. TAC-induced oxidative stress and apoptosis were significantly more reduced by CoQ10-W than CoQ10-L. Electron microscopy revealed that CoQ10-W restored TAC-induced attenuation in the number of insulin granules and the average mitochondrial area, unlike CoQ10-L. In vitro studies showed that CoQ10-L and CoQ10-W both improved cell viability and reduced ROS production in TAC-treated islet cells to a similar extent.ConclusionsCoQ10-W has better therapeutic efficacy than CoQ10-L in TAC-induced DM.

The Imbalance among Oxidative Biomarkers and Antioxidant Defense Systems in Thromboangiitis Obliterans (Winiwarter-Buerger Disease).

(1) Background: Thromboangiitis obliterans or Winiwarter-Buerger disease (WBD), is an inflammatory, thrombotic occlusive, peripheral vascular disease, usually occurring in young smokers. The pathophysiological mechanisms underlying the disease are not clearly understood. The aim of this study is to investigate the imbalance between oxidants and antioxidants occurring in these patients. (2) Patients and Methods: In this cross-sectional study, 22 male patients with WBD and 20 healthy male smoking habit matched control group were included. To evaluate the possible sources of oxidative stress, the antioxidant biomarkers, and the markers of lipid peroxidation and protein oxidation, serum samples were analyzed for total oxidative status (TOS), total antioxidant capacity (TAC), myeloperoxidase (MPO), coenzyme Q10 (CoQ10), superoxide dismutase (SOD), glutathione reductase (GR), malondialdehyde (MDA), and protein carbonyl (PC) activity and/or content. (3) Results: The circulating levels of TOS, TAC, and CoQ10 were significantly higher in WBD patients, with respect to healthy smokers as controls. No significant difference was found among the serum level of PC, total cholesterol, MPO, and GR activity in WBD patients and healthy smoker controls. The activity of SOD and the mean serum level of MDA were significantly lower in WBD patients, with respect to healthy smoker controls. (4) Conclusion: Considerably high levels of oxidative stress were detected in WBD patients, which were greater than the antioxidant capacity. The low level of MDA may be associated with the enzymatic degradation of lipid peroxidation products. High levels of CoQ10 and low levels of SOD may be related to a harmful oxidative cooperation, leading to the vasoconstriction of WBD, representing a promising tool to discern possible different clinical risks of this poorly understood peripheral occlusive disease.

The Influence of Statins on the Aerobic Metabolism of Endothelial Cells

Endothelial mitochondrial dysfunction is considered to be the main cause of cardiovascular disease. The aim of this research was to elucidate the effects of cholesterol-lowering statins on the aerobic metabolism of endothelial cells at the cellular and mitochondrial levels. In human umbilical vein endothelial cells (EA.hy926), six days of exposure to 100 nM atorvastatin (ATOR) induced a general decrease in mitochondrial respiration. No changes in mitochondrial biogenesis, cell viability, or ATP levels were observed, whereas a decrease in Coenzyme Q10 (Q10) content was accompanied by an increase in intracellular reactive oxygen species (ROS) production, although mitochondrial ROS production remained unchanged. The changes caused by 100 nM pravastatin were smaller than those caused by ATOR. The ATOR-induced changes at the respiratory chain level promoted increased mitochondrial ROS production. In addition to the reduced level of mitochondrial Q10, the activity of Complex III was decreased, and the amount of Complex III in a supercomplex with Complex IV was diminished. These changes may cause the observed decrease in mitochondrial membrane potential and an increase in Q10 reduction level as a consequence, leading to elevated mitochondrial ROS formation. The above observations highlight the role of endothelial mitochondria in response to potential metabolic adaptations related to the chronic exposure of endothelial cells to statins.

Assembly and Characterization of Biocompatible Coenzyme Q10 -Enriched Lipid Nanoparticles.

Coenzyme Q10 (CoQ10 ) is a strongly hydrophobic lipid that functions in the electron transport chain and as an antioxidant. CoQ10 was conferred with aqueous solubility by incorporation into nanoparticles containing phosphatidylcholine (PtdCho) and apolipoprotein (apo) A-I. These particles, termed CoQ10 nanodisks (ND), contain 1.0 mg CoQ10 /5 mg PtdCho/2 mg apoA-I (97% CoQ10 solubilization efficiency). UV/Vis absorbance spectroscopy of CoQ10 ND revealed a characteristic absorbance peak centered at 275 nm. Incorporation of CoQ10 into ND resulted in quenching of apoA-I tryptophan fluorescence emission. Gel filtration chromatography of CoQ10 ND gave rise to a single major absorbance peak and HPLC of material extracted from this peak confirmed the presence of CoQ10 . Incubation of cultured cells with CoQ10 ND, but not empty ND, resulted in a significant increase in the CoQ10 content of mitochondria as well as enhanced oxidative phosphorylation, as observed by a ~24% increase in maximal oxygen consumption rate. Collectively, a facile method to solubilize significant quantities of CoQ10 in lipid nanoparticles has been developed. The availability of CoQ10 ND provides a novel means to investigate biochemical aspects of CoQ10 uptake by cells and/or administer it to subjects deficient in this key lipid as a result of inborn errors of metabolism, statin therapy, or otherwise.

Short-term ubiquinol-10 supplementation alleviates tissue damage in muscle and fatigue caused by strenuous exercise in male distance runners.

Background: Coenzyme Q10 (CoQ10) is the electron transporter in oxidative phosphorylation and an endogenous antioxidant. Recent researches have indicated that doses of 200-300mg/day are needed to recognize effects to prevent oxidative damage in athletes, and the reduced form of CoQ10, ubiquinol-10, is more bioavailable than its oxidized form. Therefore, we hypothesized that higher doses of ubiquinol-10 could elevate plasma CoQ10 levels rapidly and exert physiological benefits in athletes. Therefore, a placebo controlled, double blinded test was carried out to determine the effects of ubiquinol-10 on the extravasate enzymes and fatigue levels of distance runners. Methods: Sixteen male collegiate distance runners were allocated to two groups receiving 300mg/day of ubiquinol-10 (19.8±1.7 years) or a placebo (20.1±1.6years) for 12 days during summer training that comprised 25- and 40-km runs on days 7 and 9, respectively. Results: Ubiquinol-10 elevated plasma CoQ10 concentration to 5.62μg/mL and significantly decreased activities of the serum extravasate enzymes, CK, ALT, LDH (P<0.01), and AST (P<0.05) on day 6. Subjective fatigue status was significantly elevated on day 10 (the day after the 45-km run) in the placebo group (P<0.001), but did not significantly change in the group given ubiquinol-10. Therefore, ubiquinol-10 could mitigate tissue damage and alleviate fatigue status in distance runners during summer training. Conclusions: Ubiquinol-10 (300mg/day) supplementation elevated plasma CoQ10 concentrations almost to plateau levels, decreased extravasate enzymes within six days, and suppressed the subjective fatigue in male distance runners.

Effects of non-caloric ultrashort wave on the expression of CoQ10 and C1GALT1C1 in rats with cerebral ischemia reperfusion injury.

To examine the changes of coenzyme Q10 (CoQ10) and β1,3-galactosyl transferase specific chaperone 1 (C1GALT1C1) in brain of rats with ischemic injury at different time points and to explore the protective mechanism of ultrashort wave (USW) on ischemic brain injury. Fifty SD rats were randomly divided into 5 groups (n=10 per group): a sham group (control group) and 4 experimental group (ischemia for 2 h). The 4 experimental groups were set as a model 1 d group, a USW 1 d group, a model 3 d group and a USW 3 d group, respectively. Five rats were randomly selected for 2,3,5-triphenyltetrazoliumchloride (TTC) staining in each experimental group, and the remaining 5 rats were subjected to Western blotting and real-time PCR. The percentage of cerebral infarction volume and the relative expression level of CoQ10 and C1GALT1C1 in the brain were examined and compared. The infarct volume percentage after TTC staining was zero in the sham group. With the progress of disease and USW therapy, the infarct volume percentage was decreased in the experimental groups (all P<0.05); Western blotting and real-time PCR showed that the relative expression level of CoQ10 in the sham group was the highest, while in the experimental groups, the content of CoQ10 showed a upward trend with the extension of disease and USW therapy, with significant difference (all P<0.05). The relative expression level of C1GALT1C1 in the sham group was the lowest, but in the experimental groups, they showed a downward trend with the extension of disease and USW therapy, with significant difference (all P<0.05). Non-caloric USW therapy may upregulate the expression of CoQ10 to suppress the expression of C1GALT1C1 in rats, leading to alleviating cerebral ischemic reperfusion injury.

Optimization of coenzyme Q10 encapsulation in liposomes using supercritical carbon dioxide

Coenzyme Q10 (CoQ10)-loaded liposomes were prepared with soy lecithin utilizing a single step supercritical carbon dioxide (SCCO2) method, which did not require the use of organic solvents, buffers or surfactants. The effects of pressure, temperature, pressurization rate and CoQ10-to-lecithin ratio on bioactive loading (BL), particle size (Ps) and polydispersity index (PdI) were investigated and modeled by response surface methodology (RSM). Pressure and concentration of CoQ10 had a great influence on the three responses. High pressures led to lower BLs, but also particles with smaller Ps and PdI. High concentrations of CoQ10 allowed obtaining higher BLs and lower PdI, but also higher Ps. High pressurization rates were needed to obtain high BLs, but, in contrast, it also led to higher PdIs. Temperature had a positive influence only on the PdI. The optimum conditions predicted by the model to simultaneously maximize the BL and minimize the Ps and PdI were 30 MPa, 40 °C, 6 MPa∙min−1 and 17 mol% CoQ10 (BL of 4.2 %, Ps of 177 nm and PdI of 0.313). Furthermore, encapsulation efficiencies between 87.6–99.7 % were achieved and semi-spherical stable particles (zeta potential ≈ −70 mV) were formed. Differential scanning calorimetry indicated a potential loss of crystallinity upon the encapsulation of CoQ10 into the liposomes. The findings reveal the great potential of this SCCO2 method for the encapsulation of CoQ10 in liposomes.

Miso Soup Consumption Enhances the Bioavailability of the Reduced Form of Supplemental Coenzyme Q10.

Coenzyme Q10 (CoQ10) is an essential compound that is involved in energy production and is a lipid-soluble antioxidant. Although it has been proposed as an antiaging and a health-supporting supplement, its low bioavailability remains a significant issue. Concurrent food intake enhances the absorption of orally administered CoQ10, but it has not been fully established whether specific food substances affect intestinal CoQ10 absorption. Therefore, to determine whether the bioavailability of supplemental CoQ10 is affected by diet, P30, a granulated and reduced form of CoQ10, was dispersed in four different foods, clear soup, miso soup, milk soup, and raw egg sauce. Those foods which contained CoQ10 were consumed on different occasions at intervals of 6–14 weeks by the same participants. Thirteen participants were recruited in the single-dose and repeated clinical study. When miso soup containing P30 was provided, the serum CoQ10 concentration increased faster than when participants consumed other P30-containing soups or a P30-containing raw egg sauce. The area under the curve for serum CoQ10 during the first 5 h after consumption of the P30-containing miso soup was approximately 1.5 times larger than those after the consumption of other P30-containing meals. These data imply that the absorption of CoQ10 supplements can be enhanced by consuming them with food and in particular with specific food substances, such as miso soup.

Coenzyme Q10 Improves Sperm Parameters, Oxidative Stress Markers and Sperm DNA Fragmentation in Infertile Patients with Idiopathic Oligoasthenozoospermia.

PurposeOxidative stress and sperm DNA fragmentation (SDF) are potential contributing factors for idiopathic male infertility. Coenzyme Q10 (CoQ10) have been reported to be effective in the treatment of idiopathic male infertility, in general, owing to its antioxidant properties. Thus, the present study intends to investigate the effects of CoQ10 therapy on semen parameters, oxidative stress markers and SDF in infertile men, specifically with idiopathic oligoasthenozoospermia (OA).Materials and MethodsIn this case-control study, sixty-five infertile patients with idiopathic OA and forty fertile men (control) were included. All participants underwent semen analysis based on the World Health Organization guidelines (5th edition, 2010). Patients received CoQ10 at the dose of 200 mg/d orally for three months. Seminal plasma CoQ10, total antioxidant capacity (TAC), total reactive oxygen species (ROS), glutathione peroxidase (GPx), and SDF levels were measured in controls (baseline) and infertile patients pre- and post-CoQ10 treatment.ResultsCoQ10 treatment for three months significantly improved sperm concentration (p<0.05), progressive motility (p<0.05), total motility (p<0.01), seminal fluid CoQ10 concentration (p<0.001), TAC (p<0.001), and GPx (p<0.001) levels in infertile men with OA. Further, ROS level (p<0.05) and SDF percentage (p<0.001) were reduced in OA patients as compared to the baseline. CoQ10 levels also correlated positively with sperm concentration (r=0.48, p=0.01) and total motility (r=0.59, p=0.003) while a negative correlation was recorded between SDF and sperm motility (r=−0.54, p=0.006).ConclusionsCoQ10 supplementation for three months could improve semen parameters, oxidative stress markers and reduce SDF in infertile men with idiopathic OA.

Phosphate limitation increases coenzyme Q10 production in industrial Rhodobacter sphaeroides HY01

Coenzyme Q10 (CoQ10) is an important component of the respiratory chain in humans and some bacteria. As a high-value-added nutraceutical antioxidant, CoQ10 has excellent capacity to prevent cardiovascular disease. The content of CoQ10 in the industrial Rhodobacter sphaeroides HY01 is hundreds of folds higher than normal physiological levels. In this study, we found that overexpression or optimization of the synthetic pathway failed CoQ10 overproduction in the HY01 strain. Moreover, under phosphate- limited conditions (decreased phosphate or in the absence of inorganic phosphate addition), CoQ10 production increased significantly by 12% to220 mg/L, biomass decreased by 12%, and the CoQ10 productivity of unit cells increased by 27%. In subsequent fed-batch fermentation, CoQ10 production reached 272 mg/L in the shake-flask fermentation and 1.95 g/L in a 100-L bioreactor under phosphate limitation. Furthermore, to understand the mechanism associated with CoQ10 overproduction under phosphate- limited conditions, the comparatve transcriptome analysis was performed. These results indicated that phosphate limitation combined with glucose fed-batch fermentation represented an effective strategy for CoQ10 production in the HY01. Phosphate limitation induced a pleiotropic effect on cell metabolism, and that improved CoQ10 biosynthesis efficiency was possibly related to the disturbance of energy metabolism and redox potential.

Use of supplemental dietary coenzyme Q10 to improve testicular function and fertilization capacity in aged broiler breeder roosters

In numerous studies it has been suggested that targeting mitochondria with specific compounds could efficiently inhibit various conditions associated with oxidative stress. The treatment of aged roosters with compounds such as coenzyme Q10 (CoQ10), may improve their reproductive performance by providing protection from oxidative stress. Therefore, this study was performed to assess the effect of supplemental dietary CoQ10 on the testicular function and fertility of aged broiler breeder roosters. A total of 36 roosters)47 weeks of age) were randomly divided into dietary treatments containing either 0, 300 or 600 mg CoQ10/kg diet. Three birds were allocated to each of four replicate groups in each dietary treatment. Between 47 and 54 weeks of age, ejaculates were obtained weekly from the three roosters in each replicate group. Samples in a replicate were pooled and analyzed as a single sample. Between 51 and 54 weeks of age, seminal plasma total antioxidant capacity (TAC), alanine amino transferase (ALAT) and aspartate amino transferase (ASAT) levels were assessed. Fertility, hatchability, and sperm penetration (SP) rates were likewise evaluated. Seminal volume, sperm concentration, sperm plasma membrane functionality, sperm plasma membrane integrity, seminiferous tubule diameter and seminiferous epithelium thickness exhibited quadratic increases in response to increasing levels of dietary CoQ10. Respectively, the 429.19, 433.33, 464.50, 613.50, 392.78 and 447.99 mg/kg dietary concentrations of CoQ10 provided the best results for each of the aforementioned variables. Also, other seminal traits, as well as testosterone concentration, fertility, and SP rates, displayed linear increases in response to the increasing levels of CoQ10. Dietary supplementation of CoQ10 linearly decreased seminal plasma ALAT and ASAT and linearly increased seminal plasma TAC. In conclusion, CoQ10 supplementation in the diet (a minimum of 300 mg CoQ10/kg diet) has the potential to improve the reproductive performance of aged broiler breeder roosters.

Coenzyme Q10 Upregulates Platelet cAMP/PKA Pathway and Attenuates Integrin αIIbβ3 Signaling and Thrombus Growth.

Platelet integrin αIIbβ3 is the key mediator of atherothrombosis. Supplementation of coenzyme Q10 (CoQ10), a fat-soluble molecule that exists in various foods, exerts protective cardiovascular effects. This study aims to investigate whether and how CoQ10 acts on αIIbβ3 signaling and thrombosis, the major cause of cardiovascular diseases. Using a series of platelet functional assays in vitro, it is demonstrated that CoQ10 reduces human platelet aggregation, granule secretion, platelet spreading, and clot retraction. It is further demonstrated that CoQ10 inhibits platelet integrin αIIbβ3 outside-in signaling. These inhibitory effects are mainly mediated by upregulating cAMP/PKA pathway, where CoQ10 stimulates the A2A adenosine receptor and decreases phosphodiesterase 3A phosphorylation. Moreover, CoQ10 attenuates murine thrombus growth and vessel occlusion in a ferric chloride (FeCl3 )-induced thrombosis model in vivo. Importantly, the randomized, double-blind, placebo-controlled clinical trial in dyslipidemic patients demonstrates that 24 weeks of CoQ10 supplementation increases platelet CoQ10 concentrations, enhances the cAMP/PKA pathway, and attenuates αIIbβ3 outside-in signaling, leading to decreased platelet aggregation and granule release. Through upregulating the platelet cAMP/PKA pathway, and attenuating αIIbβ3 signaling and thrombus growth, CoQ10 supplementation may play an important protective role in patients with risks of cardiovascular diseases.

Evaluation of Coenzyme Q10 Redox Status as a Biomarker of Oxidative Stress

The article examines the role of ubiquinone as a redox molecule whose functions consist in electron transport in the mitochondrial respiratory chain and regeneration of endogenous antioxidants. Changes in electron redox pathways cause uncontrolled release of reactive oxygen species, which leads to oxidative stress and development of pathologies. The objective of the study was to determine the content of coenzyme Q10 and its redox status in the human body as a biomarker of oxidative stress in various pathologies. This was achieved by assessing and consolidating data on changes in concentrations of the oxidized, reduced ubiquinone forms and total ubiquinone in various pathologies. Total serum ubiquinone was reduced in patients with chronic heart failure (0.68 μmol/L) compared with the control group (0.97 μmol/L). The redox status, expressed as the [ubiquinol]/ [ubiquinone] concentration ratio, decreased in patients with coronary heart disease (0.49 ± 0.34), diabetes (0.26 ± 0.16) compared with the healthy subjects (1.23–1.41). A negative correlation with malonic dialdehyde was observed. The authors analysed the possibility of assessing the efficacy of statin therapy by plasma ubiquinone concentration in patients. Patients with hyperlipidemia who received statins showed a statistically significant reduction in ubiquinol concentration after taking the drug (from 0.81 to 0.46 μg/mL) and the [ubiquinone]/[total ubiquinone] ratio (from 11 to 10 %), which confirms the potential mechanism of statinassociated muscle injury development. Thus, coenzyme Q10 redox status, as well as the concentrations of oxidized, reduced and total ubiquinone can be effective biomarkers of oxidative stress in cardiovascular diseases, diabetes, as well as an important indicator in evaluating the efficacy of hyperlipidemia treatment.

Extracellular coenzyme Q10 (CoQ10) is reduced to ubiquinol-10 by intact Hep G2 cells independent of intracellular CoQ10 reduction

Coenzyme Q10 (CoQ10) is an essential factor in the mitochondrial respiratory chain and is closely associated with ATP production in humans. It is known that orally administered CoQ10 in humans is rapidly reduced, and most is detected as a reduced form, ubiquinol-10 (CoQ10H2), in serum. However, the mechanism of exogenous CoQ10 reduction in vivo is unclear. Therefore, in order to clarify how CoQ10 is reduced to CoQ10H2, we conducted a study using human liver cancer cell line Hep G2 cells, which show strong intracellular CoQ10-reducing activity. When intact cells were incubated with CoQ10, the exogenously added CoQ10 was incorporated into the cells, time-, concentration-, and temperature-dependently, and 50–80% of that was detected as CoQ10H2. On the other hand, a part of the extracellular CoQ10 was also detected as CoQ10H2, and the amount was greater than that of the intracellular CoQ10H2. Furthermore, the CoQ10-loaded cells did not leak the intracellular CoQ10H2 (or CoQ10) to the outside of the cells, and modulation of the extracellular CoQ10H2 amount had little effect on the intracellular CoQ10 or CoQ10H2 contents, suggesting the existence of an individual mechanism of CoQ10 reduction inside and outside the cells. Moreover, intact cells could reduce CoQ10 in low-density lipoprotein to CoQ10H2. Therefore, we concluded that a novel CoQ10-reducing mechanism may exist in the plasma membrane, probably the outer surface, of Hep G2 cells, and it may work to reduce extracellular CoQ10 and/or maintain extracellular CoQ10H2.