Coenzyme Q10 Concentration Research Articles

CoenzymeQ10 localizations in model membranes. A Langmuir monolayer study

The interaction of coenzyme Q10 (CoQ10) in a monolayer of 1,2-dipalmitoyl-sn-glysero-3-phospho-L-choline (DPPC), in a monolayer of 1,2-dierucoyl-sn-glysero-3-phospho-L-choline (DEPC), in a monolayer of 1-palmitoyl-2-oleoyl-sn-glysero-3-phospho-L-serine (POPS) and in a monolayer of total lipid extract from pig brain (PB) has been investigated by using the Langmuir monolayer technique. Surface pressure (π)-mean molecular area (mma) isotherms have been measured for pure lipid monolayers and lipid monolayers with 0.5, 1.0, 2.0, 5.0 and 10.0 mol% CoQ10 concentrations. At the biological concentration (1.0-3.0 mol%) of CoQ10, intercalation of CoQ10 occurs in the lipid acyl chains of DPPC, POPS and PB monolayers. Above the biological concentration of CoQ10, the CoQ10 molecule induces domain formation in the monolayers of DPPC, POPS and PB lipids. The DEPC monolayer behavior deviates from the other lipids in this study. At 2.0 mol% the CoQ10 promotes very dense lipid packing, and the CoQ10 molecule is located parallel to the DEPC acyl chains at all concentrations.

Kolliphor® HS 15 Micelles for the Delivery of Coenzyme Q10: Preparation, Characterization, and Stability.

To enhance the stability of coenzyme Q10 (CoQ10), Kolliphor® HS 15 (HS15) was employed as a carrier to build up a stable CoQ10-loaded micelle delivery system. The impact of micellar compositions, the preparation condition, and the preparation method on size characteristics, the solubilization efficiency, and micellar stability were investigated. The optimal preparation conditions were 1:6, 4, 0.2%, 118°C, and 25min for CoQ10/HS15 mass ratio, pH value, the concentration of glucose, and the sterilization conditions. Upon these conditions, the particle size, polydispersity index (PDI), zeta potential, the entrapment efficiency, drug loading, and the critical micelle concentration (CMC) of CoQ10-loaded micelles were 19.76nm, 0.112, -3.405mV, 99.39%, 13.77%, and 5.623 × 10(-4)g/mL, respectively. Differential scanning calorimetry (DSC) analysis collectively corroborated that CoQ10 was entrapped into the micelles in amorphous form. The release pattern of drug was analyzed and proved to follow the first order. Additionally, the samples were exposed to the temperatures of 30°C for 6months with more significant impact on their stabilities as compared to 4 and 25°C based on particle size and PDI. Under constant humidity with light protection long-term (25 ± 2°C, relative humidity (RH) 60 ± 10%, 18months) conditions, there was no variation except minor changes of CoQ10 content of the samples. The shelf life of the micellar samples could be predicted as 24months based on the stability results. Consequently, the CoQ10-loaded micelles showed excellent stabilities below 25°C as a potential drug candidate for further clinical applications.

Coenzyme Q10 and oxidative stress, the association with peripheral sensory neuropathy and cardiovascular disease in type 2 diabetes mellitus

ObjectiveOur study aimed to explore associations between metabolic control, oxidative stress and coenzyme Q10 (CoQ10) in relation to diabetes complications in a representative population of type 2 diabetes. Research design and methodsA geographic cohort of 156 subjects was recruited. Serum concentrations of CoQ10 and vitamin E were measured by HPLC. ROS was determined by free oxygen radicals testing (FORT). Glutaredoxin (Grx) activity, oxidized LDL cholesterol (oxLDLc), high sensitive CRP (hsCRP), HbA1c, urine albumin, serum creatinine, serum cystatin C, and plasma lipids were assayed with routine laboratory protocols. ResultsSerum CoQ10 was higher than in nondiabetics. HbA1c, fP-glucose, hyperlipidemia, inflammation (hsCRP), and increased BMI were associated with signs of oxidative stress as increased levels of FORT, Grx activity and/or increased levels of oxLDLc Oxidative stress was found to be strongly correlated with prevalence of cardiovascular disease (CVD) and peripheral sensory neuropathy (PSN). In both gender groups there were positive correlations between CoQ10 and oxLDLc, and between BMI and the ratio CoQ10/chol. Grx activity was inversely correlated to oxLDLc and CoQ10. Women with CVD and PSN had higher waist index, oxLDLc, and FORT levels compared to men but lower CoQ10 levels. Men had worse kidney function and lower vitamin E. Multiple regression analysis showed increased levels of CoQ10 to be significantly correlated with increased levels of cholesterol, triglycerides, vitamin E, fB-glucose and BMI. ConclusionsHyperlipidemia, hyperglycemia and inflammation were associated with oxidative stress, which was correlated to the prevalence of diabetes complications. CoQ10 was increased in response to oxidative stress. There were gender differences in the risk factors associated with diabetes complications.

Statin therapy and plasma coenzyme Q10 concentrations—A systematic review and meta-analysis of placebo-controlled trials

Statin therapy may lower plasma coenzyme Q10 (CoQ10) concentrations, but the evidence as to the significance of this effect is unclear. We assessed the impact of statin therapy on plasma CoQ10 concentrations through the meta-analysis of available RCTs. The literature search included selected databases up to April 30, 2015. The meta-analysis was performed using either a fixed-effects or random-effect model according to I2 statistic. Effect sizes were expressed as weighted mean difference (WMD) and 95% confidence interval (CI). The data from 8 placebo-controlled treatment arms suggested a significant reduction in plasma CoQ10 concentrations following treatment with statins (WMD: −0.44μmol/L, 95%CI: −0.52, −0.37, p<0.001). The pooled effect size was robust and remained significant in the leave-one-out sensitivity analysis. Subgroup analysis suggested that the impact of statins on plasma CoQ10 concentrations is significant for all 4 types of statins studied i.e. atorvastatin (WMD: −0.41μmol/L, 95%CI: −0.53, −0.29, p<0.001), simvastatin (WMD: −0.47μmol/L, 95% CI: −0.61, −0.33, p<0.001), rosuvastatin (WMD: −0.49μmol/L, 95%CI: −0.67, −0.31, p<0.001) and pravastatin (WMD: −0.43μmol/L, 95%CI: −0.69, −0.16, p=0.001). Likewise, there was no differential effect of lipophilic (WMD: −0.43μmol/L, 95%CI: −0.53, −0.34, p<0.001) and hydrophilic statins (WMD: −0.47μmol/L, 95%CI: −0.62, −0.32, p<0.001). With respect to treatment duration, a significant effect was observed in both subsets of trials lasting <12 weeks (WMD: −0.51μmol/L, 95%CI: −0.64, −0.39, p<0.001) and ≥12 weeks (WMD: −0.40μmol/L, 95%CI: −0.50, −0.30, p<0.001). The meta-analysis showed a significant reduction in plasma CoQ10 concentrations following treatment with statins. Further well-designed trials are required to confirm our findings and elucidate their clinical relevance.

Coenzyme Q10 consumption promotes ABCG1-mediated macrophage cholesterol efflux: a randomized, double-blind, placebo-controlled, cross-over study in healthy volunteers.

We have recently shown that coenzyme Q10 (CoQ10) enhances macrophage reverse cholesterol transport via activator protein-1/miRNA-378/ABCG1 signal pathway in vivo and in vitro. Whether CoQ10 exerts similar beneficial effects in human is currently unknown. The present study evaluated the effect of CoQ10 on ABCG1-mediated macrophage cholesterol efflux in 20 healthy volunteers. Participants were given 100 mg CoQ10 twice daily or placebo for 1 week with a 1-week washout period. Human monocyte-derived macrophages (MDMs) were differentiated under pooled sera obtained before (preCoQ10) or after CoQ10 (postCoQ10) consumption. The CoQ10-induced inhibition of MDMs foam cell formation was blocked by ABCG1 silencing in postCoQ10 MDMs incubated with postCoQ10 sera compared to preCoQ10 sera. The cholesterol efflux to HDL, and mRNA as well as protein expressions of ATP-binding cassette transporter G1 (ABCG1) were augmented in postCoQ10 MDMs incubated with postCoQ10 sera compared to preCoQ10 sera. The change in the serum CoQ10 concentration positively correlated with cholesterol efflux to HDL and ABCG1 mRNA level in the CoQ10 group. MDMs treated with purified CoQ10 had an enhanced cholesterol efflux to HDL. CoQ10 consumption may have an atheroprotective property by inducing ABCG1 expression and enhancing HDL-mediated macrophage cholesterol efflux in healthy individuals.

홍국발효가 백태와 서리태의 생리활성 성분에 미치는 영향

Changes in the contents of mevinolins (natural statins, 0-568.18 ㎍), coenzyme Q10 (CoQ10, 26.41-65.59 ㎍), and tocopherols (232.80-312.87 ㎍/g dry weight) in Monascus-fermented soybean were determined using HPLC. Significant increases (p＜0.05) in mevinolins and CoQ10 were obtained in Monascus-fermented soybean after 20 days of fermentation compared with unfermented soybean (0 days), whereas no significant change (p＞0.05), or a slight decrease, in tocopherols was observed. The results indicate that Monascus-fermentation has great potential for enriching mevinolin and CoQ10 in soybeans.

Oxidized proportion of muscle coenzyme Q10 increases with age in healthy children.

Coenzyme Q10 (CoQ10) is synthesized in most human tissues, with high concentration in the skeletal muscle. CoQ10 functions in the mitochondrial respiratory chain and serves as a potent liphophilic antioxidant in membranes. CoQ10 deficiency impairs mitochondrial ATP synthesis and increases oxidative stress. It has been suggested that plasma CoQ10 status is not a robust proxy for the diagnosis of CoQ10 deficiency. We determined the concentration and redox-status of CoQ10 in plasma and muscle tissue from 140 healthy children (0.8-15.3 y) by high-performance liquid chromatography (HPLC) with electrochemical detection. There was no correlation between CoQ10 concentration or redox status between plasma and muscle tissue. Lipid-related CoQ10 plasma concentrations showed a negative correlation with age (Spearman's, P ≤ 0.02), but there was no significant age-related correlation for muscle concentration. In muscle tissue, we found a distinct shift in the redox status in favor of the oxidized proportion with increasing age (Spearman's, P ≤ 0.00001). Reference values for muscle CoQ10 concentration (40.5 ± 12.2 pmol/mg wet tissue) and CoQ10 redox status (46.8 ± 6.8% oxidized within total) were established for healthy children. The age-related redox shift in muscle tissue suggests changes in antioxidative defense during childhood. The reference values established here provide a necessary prerequisite for diagnosing early CoQ10 deficiency.

The role of mitochondria in statin-induced myopathy.

Statins inhibit hydroxymethylglutaryl-coenzyme A reductase, decrease plasma low-density lipoprotein cholesterol and reduce cardiovascular morbidity and mortality. They can also exert adverse effects, mostly affecting skeletal muscle, ranging from mild myalgia to rhabdomyolysis. Based on a PubMed search until December 2014, this review summarizes studies on statin effects on muscle mitochondrial morphology and function in the context of myopathy. Possible mechanisms of statin-induced myopathy include lower cholesterol synthesis and production of prenylated proteins, reduced dolichols and increased atrogin-1 expression. Statin-treated patients frequently feature decreased muscle coenzyme Q10 (CoQ10) contents, suggesting that statins might impair mitochondrial function. In cell cultures, statins diminish muscle oxygen consumption, promote mitochondrial permeability transient pore opening and generate apoptotic proteins. Animal models confirm the statin-induced decrease in muscle CoQ10, but reveal no changes in mitochondrial enzyme activities. Human studies yield contradictory results, with decreased CoQ10, elevated lipids, decreased enzyme activities in muscle and impaired maximal oxygen uptake in several but not all studies. Some patients are susceptible to statin-induced myopathy due to variations in genes encoding proteins involved in statin uptake and biotransformation such as the solute carrier organic anion transporter family member 1B1 (SLCO1B1) or cytochrome P450 (CYP2D6, CYP3A4, CYP3A5). Carriers for carnitine palmitoyltransferase II deficiency and McArdle disease also present with higher prevalence of statin-induced myopathy. Despite the widespread use of statins, the pathogenesis of statin-induced myopathy remains unclear, requiring prospective randomized controlled trials with intensive phenotyping also for identifying strategies for its risk assessment, prevention and treatment.

Rapid and sensitive analysis of reduced and oxidized coenzyme Q10 in human plasma by ultra performance liquid chromatography-tandem mass spectrometry and application to studies in healthy human subjects

Coenzyme Q10 is an endogenous antioxidant as well as a popular dietary supplement. In blood circulation, coenzyme Q10 exists predominantly as its reduced ubiquinol-10 form, which readily oxidizes to ubiquinone-10 ex vivo. Plasma concentrations of coenzyme Q10 reflect net overall metabolic demand, and the ratio of ubiquinol-10:ubiquinone-10 has been established as an important biomarker for oxidative stress. However, the lability of ubiquinol-10 makes accurate determination of both forms of coenzyme Q10 difficult. Ex vivo oxidation of ubiquinol-10 to ubiquinone-10 during sample collection, processing and analysis may obfuscate the invivo ratio. We developed a rapid and sensitive method for the determination of ubiquinol-10 and ubiquinone-10 in human plasma, using coenzyme Q9 analogues as internal standards. Single-step protein precipitation in 1-propanol, a lipophilic and water-soluble alcohol, allowed for rapid extraction. Analysis by ultra performance liquid chromatography-tandem mass spectrometry provided rapid run-time and high sensitivity, with lower limits of quantitation for ubiquinol-10 and ubiquinone-10 of 5 μg/L and 10 μg/L, respectively. This method is suitable for clinical studies with coenzyme Q10 supplementation in various disease states where this lipid-antioxidant may be beneficial. We have applied this method to >300 plasma samples from coenzyme Q10 research studies in chronic haemodialysis patients and postsurgical patients.

Coenzyme Q10 and statin-related myopathy

Statins inhibit the enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, which is involved in the production of mevalonic acid in the cholesterol biosynthesis pathway.1 This pathway also results in the production...

Therapeutic targeting of oxidative stress with coenzyme Q10 counteracts exaggerated diabetic cardiomyopathy in a mouse model of diabetes with diminished PI3K(p110α) signaling

Diabetes-induced cardiac complications include left ventricular (LV) dysfunction and heart failure. We previously demonstrated that LV phosphoinositide 3-kinase p110α (PI3K) protects the heart against diabetic cardiomyopathy, associated with reduced NADPH oxidase expression and activity. Conversely, in dominant negative PI3K(p110α) transgenic mice (dnPI3K), reduced cardiac PI3K signaling exaggerated diabetes-induced cardiomyopathy, associated with upregulated NADPH oxidase. The goal was to examine whether chronic supplementation with the antioxidant coenzyme Q10 (CoQ10) could attenuate LV superoxide and diabetic cardiomyopathy in a setting of impaired PI3K signaling. Diabetes was induced in 6-week-old nontransgenic and dnPI3K male mice via streptozotocin. After 4 weeks of diabetes, CoQ10 supplementation commenced (10mg/kg ip, 3 times/week, 8 weeks). At study end (12 weeks of diabetes), markers of LV function, cardiomyocyte hypertrophy, collagen deposition, NADPH oxidase, oxidative stress (3-nitrotyrosine), and concentrations of CoQ9 and CoQ10 were determined. LV NADPH oxidase (Nox2 gene expression and activity, and lucigenin-enhanced chemiluminescence), as well as oxidative stress, were increased by diabetes, exaggerated in diabetic dnPI3K mice, and attenuated by CoQ10. Diabetes-induced LV diastolic dysfunction (prolonged deceleration time, elevated end-diastolic pressure, impaired E/A ratio), cardiomyocyte hypertrophy and fibrosis, expression of atrial natriuretic peptide, connective tissue growth factor, and β-myosin heavy chain were all attenuated by CoQ10. Chronic CoQ10 supplementation attenuates aspects of diabetic cardiomyopathy, even in a setting of reduced cardiac PI3K protective signaling. Given that CoQ10 supplementation has been suggested to have positive outcomes in heart failure patients, chronic CoQ10 supplementation may be an attractive adjunct therapy for diabetic heart failure.

The Effect of Bisphosphonate Use on Coenzyme Q10 Serum Levels

BackgroundIt has been proposed in the literature that the nitrogen‐containing bisphosphonates bind to and inhibit the activity of farnesyl pyrophosphate synthase (FPPS), a key enzyme in the mevalonate pathway for cholesterol and coenzyme Q10 (CoQ10) synthesis. This suggests that bisphosphonate use may decrease serum levels of CoQ10.Objective:The aim of this case report analysis is to assess the effect of a bisphosphonate, alendronate sodium, on serum CoQ10 levels.Methods:7 participants diagnosed with osteoporosis were administered a single tablet of alendronate sodium 70mg once per week for 8 weeks. Assessment of serum CoQ10 concentrations were conducted at baseline, day 14, day 30 and day 60.Results:Statistical analysis was conducted for the 6 completing participants. Compared to baseline, there was a non‐significant mean decrease of 0.1400 mcg/ml in the CoQ10 level at day 14, a non‐significant mean increase of 0.1250 mcg/ml at day 30, and a statistically significant mean increase of 0.1900 mcg/ml at day 60.ConclusionThe results indicate that there was no decrease in the CoQ10 level as a result of bisphosphonate ingestion from day 1 to day 60. These results suggest inhibition of farnesyl pyrophosphate synthase by a nitrogen containing bisphosphonate (alendronate sodium) is limited in its inhibitory effect upon the pathway that leads to the synthesis of CoQ10.

Semiquinone oscillations as a tool for investigating the ubiquinone binding to photosynthetic reaction centers.

Semiquinone oscillations induced by light pulses in the presence of exogenous electron donors are a valuable source of information on the kinetics and thermodynamics of ubiquinone chemistry relevant to the QB site of the photosynthetic reaction center (RC). In previous attempts to achieve the quantitative interpretation of data, the ubiquinone concentration was considered constant during the experiment since it was much bigger than that of RC. In this work, we extended existing models to low ubiquinone concentrations revealing several hidden processes taking place during the ubiquinone photoreduction and enabling the evaluation of the ubiquinone binding constant K Q at the QB site. The proposed approach provides for the first time the evaluation of K Q without any preliminary treatment of ubiquinone extraction from the binding site, thereby better preserving its native structure.

Biochemical features in rats with different behavioral activity under conditions of emotional stress.

Adaptive capacities of the organism under conditions of emotional stress are determined by individual complex of anti-stress protective mechanisms. We studied the content of coenzyme Q10 and the spectrum of polyunsaturated fatty acids omega-3 and omega-6 in the serum, liver, and brain, and LPO intensity in the serum and liver of behaviorally active and passive rats under conditions of acute emotional stress. The differences in the formation of adaptive responses in animals with various behavioral activities were demonstrated.

Determination by UPLC/MS-MS of Coenzyme Q10 (CoQ10) in Plasma of Healthy Volunteers before and after Oral Intake of Food Supplements Containing CoQ10

To evaluate CoQ10 concentration a UPLC/MS-MS method for its analysis in plasma samples was developed. Before validation, the choice of the anticoagulant, of the Internal Standard (CoQ9; IS) and the stability of CoQ10 in plasma were evaluated. These determinations were necessary to assess the effect of the oral intake of CoQ10 in nine healthy volunteers after 10 days of treatment with a food supplement containing it. The basal levels of CoQ10 were determined and the analyses were repeated after four days to take into account the variability of endogenous substances. After oral intake, the increase in plasma concentration of CoQ10 resulted statistically significant (P<0.05), indicating that the assumption of food supplements containing this ubiquinone could be of help to increase its concentration, thus exploiting the its beneficial properties.

Coenzyme Q10 and Pyridoxal Phosphate Deficiency Is a Common Feature in Mucopolysaccharidosis Type III.

Mucopolysaccharidoses (MPS) are a group of lysosomal storage disorders caused by deficiencies of lysosomal enzymes catalyzing degradation of glycosaminoglycans (GAGs). Previously, we reported a secondary plasma coenzyme Q10 (CoQ) deficiency in MPS patients. For this study, nine MPS patients were recruited in the Hospital Sant Joan de Déu (HSJD, Barcelona) and two patients in the Neurometabolic Unit, National Hospital (NMU, London), to explore the nutritional status of MPS type III patients by analyzing several vitamins and micronutrients in blood and in cerebrospinal fluid. Plasma CoQ and plasma and cerebrospinal fluid pyridoxal phosphate (PLP) content were analyzed by high-pressure liquid chromatography (HPLC) with electrochemical and fluorescence detection, respectively. We found that most MPS-III patients disclosed low plasma pyridoxal phosphate (PLP) values (seven out of nine) and also low plasma CoQ concentrations (eight out of nine). We observed significantly lower median values of PLP, tocopherol, and CoQ (Mann-Whitney U test, p = 0.006, p = 0.004, and p = 0.001, respectively) in MPS patients when compared with age-matched controls. Chi-square test showed a significant association between the fact of having low plasma PLP and CoQ values in the whole cohort of patients. Cerebrospinal fluid PLP values were clearly deficient in the two patients studied. In conclusion, we report a combined CoQ and PLP deficiency in MPS-III patients. These observations could be related to the complexity of the physiopathology of the disease. If our results are confirmed in larger series of patients, CoQ and PLP therapy could be trialed as coadjuvant therapy with the current MPS treatments.

Ultra-small lipid nanoparticles promote the penetration of coenzyme Q10 in skin cells and counteract oxidative stress

UV irradiation leads to the formation of reactive oxygen species (ROS). An imbalance between the antioxidant system and ROS can lead to cell damage, premature skin aging or skin cancer. To counteract these processes, antioxidants such as coenzyme Q10 (CoQ10) are contained in many cosmetics. To improve and optimize cell/tissue penetration properties of the lipophilic CoQ10, ultra-small lipid nanoparticles (usNLC) were developed. The antioxidant effectiveness of CoQ10-loaded usNLC compared to conventional nanocarriers was investigated in the human keratinocyte cell line HaCaT. Using confocal laser scanning microscopy investigations of the carriers additionally loaded with nile red showed a clear uptake into cells and their distribution within the cytoplasm. By use of the XTT cell viability test, CoQ10 concentrations of 10–50μg/ml were shown to be non-toxic, and the antioxidant potential of 10μg/ml CoQ10 loaded usNLC in the HaCaT cells was analyzed via electron paramagnetic resonance spectroscopy after cellular exposure to UVA (1J/cm2) and UVB (18mJ/cm2) irradiation. In comparison with the CoQ10-loaded conventional carriers, usNLC-CoQ10 demonstrated the strongest reduction of the radical formation; reaching up to 23% compared to control cells without nanocarrier treatment. Therefore, usNLC-CoQ10 are very suitable to increase the antioxidant potential of skin.

Molecular, Physiological and Phenotypic Characterization of Paracoccus denitrificans ATCC 19367 Mutant Strain P-87 Producing Improved Coenzyme Q10.

Coenzyme Q10 (CoQ10) is a blockbuster nutraceutical molecule which is often used as an oral supplement in the supportive therapy for cardiovascular diseases, cancer and neurodegenerative diseases. It is commercially produced by fermentation process, hence constructing the high yielding CoQ10 producing strains is a pre-requisite for cost effective production. Paracoccus denitrificans ATCC 19367, a biochemically versatile organism was selected to carry out the studies on CoQ10 yield improvement. The wild type strain was subjected to iterative rounds of mutagenesis using gamma rays and NTG, followed by selection on various inhibitors like CoQ10 structural analogues and antibiotics. The screening of mutants were carried out using cane molasses based optimized medium with feeding strategies at shake flask level. In the course of study, the mutant P-87 having marked resistance to gentamicin showed 1.25-fold improvements in specific CoQ10 content which was highest among all tested mutant strains. P-87 was phenotypically differentiated from the wild type strain on the basis of carbohydrate assimilation and FAME profile. Molecular differentiation technique based on AFLP profile showed intra specific polymorphism between wild type strain and P-87. This study demonstrated the beneficial outcome of induced mutations leading to gentamicin resistance for improvement of CoQ10 production in P. denitrificans mutant strain P-87. To investigate the cause of gentamicin resistance, rpIF gene from P-87 and wild type was sequenced. No mutations were detected on the rpIF partial sequence of P-87; hence gentamicin resistance in P-87 could not be conferred with rpIF gene. However, detecting the mutations responsible for gentamicin resistance in P-87 and correlating its role in CoQ10 overproduction is essential. Although only 1.25-fold improvement in specific CoQ10 content was achieved through mutant P-87, this mutant showed very interesting characteristic, differentiating it from its wild type parent strain P. denitrificans ATCC 19367, which are presented in this paper.

CoQ10-containing eye drops prevent UVB-induced cornea cell damage and increase cornea wound healing by preserving mitochondrial function.

We evaluated the potential protective effects of Coenzyme Q10 (CoQ10) on human corneal cells and rabbit eyes after ultraviolet B (UVB) exposure and a model of wound healing in rabbit eyes after corneal epithelium removal. Human corneal epithelium cells (HCE) were exposed to a source of UVB radiation (312 nM) in the presence of different CoQ10 concentrations or vehicle. The mitochondrial function and cell survival were evaluated by means of 3-(4,5-dimethylthiazole-2-yl)2,5-diphenyl-tetrazolium (MTT) reduction and lactic dehydrogenase (LDH) release. Furthermore, quantitation of oxygen consumption and mitochondrial membrane potential were conducted. In vivo rabbit models were adopted to evaluate the effect of CoQ10 on UVB-induced conjunctival vessel hyperemia and corneal recovery after ethanol induced corneal lesion. In UVB-exposed HCE cells, CoQ10 addition led to an increased survival rate and mitochondrial function. Furthermore, oxygen consumption was maintained at control levels and adenosine triphosphate (ATP) decline was completely prevented in the CoQ10-treated cells. Interestingly, in an in vivo model, CoQ10 was able dose-dependently to reduce UVB-induced vessel hyperemia. Finally, in a model of corneal epithelium removal, 12 hours from surgery, animals treated with CoQ10 showed a reduction of damaged area in respect to vehicle controls, which lasted until 48 hours. We demonstrated that CoQ10 reduces corneal damages after UVB exposure in vivo and in vitro by preserving mitochondrial function. Also, for the first time to our knowledge we showed that the administration of CoQ10 after corneal epithelium removal promotes corneal wound healing.

Effects of coenzyme q10 supplementation on serum lipoproteins, plasma fibrinogen, and blood pressure in patients with hyperlipidemia and myocardial infarction.

Background:Low plasma concentrations of coenzyme Q10 (CoQ10) have been associated with concentration of lipoproteins and other factors contributing to coronary heart diseases.Objectives:The present investigation aimed to improve the blood pressure and serum lipoproteins concentration in patients with myocardial infarction (MI) by CoQ10 supplementation.Patients and Methods:In this randomized double-blinded controlled clinical trial, 52 Iranian patients with hyperlipidemia and MI were recruited to examine the effect of CoQ10 on serum total cholesterol (TC), LDL-C, HDL-C, triglyceride (TG), LDL-C/HDL-C ratio, TC/HDL-C ratio, fibrinogen, systolic blood pressure (SBP) and diastolic blood pressure (DBP). Individuals were randomly allocated to two groups for receiving either 200 mg/d of CoQ10 or placebo for 12 weeks.Results:There were not significant differences in serum LDL-C (2.70 ± 0.31 vs. 2.70 ± 0.35 mmol/L), TC (4.47 ± 0.33 vs. 4.93 ± 0.57 mmol/L), TG (2.48 ± 0.12 vs. 2.25 ± 0.69 mmol/L), and fibrinogen (2.08 ± 0.99 vs. 38.7 ± 0.64 mg/dL) between CoQ10 and placebo groups. After 12 weeks, a significant enhancement in serum HDL-C (1.44 ± 0.18 vs. 1.14 ± 0.18 mmol/L) level was observed between groups after the supplementation (P < 0.001). A significant reduction of TC, LDL-C, and fibrinogen and a significant increase in HDL-C concentration was observed in CoQ10 group after intervention (P < 0.001). Our assessment demonstrated statistically significant differences between the two groups in SBP and DBP after intervention (P < 0.001). ANCOVA also revealed significant differences in the ratio of LDL-C/HDL-C and TC/HDL-C between the two groups (1.89 ± 0.42 vs. 2.39 ± 0.38, P = 0.002; and 3.2 ± 0.5 vs. 4.24 ± 0.66, P = 0.01, respectively). A significant reduction of LDL-C/HDL-C and TC/HDL-C was observed in CoQ10 group (P < 0.001).Conclusions:Twelve-week supplementation with CoQ10 in patients with hyperlipidemia and MI can improve blood pressure, serum HDL-C as well as LDL-C/HDL-C and TC/HDL-C ratios; therefore, it might decrease the risk of frequent MI.