Role Of Coenzyme Q10 Research Articles

Role of Coenzyme Q10 in mitochondrial dysfunction and oxidative damage in RETT syndrome

Role of Coenzyme Q10 in mitochondrial dysfunction and oxidative damage in RETT syndrome

Multiple sclerosis: is there a role for coenzyme Q10?

Mitochondrial dysfunction, oxidative stress and inflammation have been implicated in the pathogenesis of multiple sclerosis (MS). Therefore, there is a rationale for the use of supplementary coenzyme Q10 (CoQ10) as a potential novel therapeutic agent for this disorder, based on the key roles of this vitamin-like substance in normal mitochondrial function, as an antioxidant and as an anti-inflammatory agent. In this article, the pre-clinical and clinical studies relating to the use of supplementary CoQ10 for the treatment of MS is reviewed.

Hepatoprotective effect of Co-enzyme Q10 in rats treated with Hydrogen Peroxide

This study was carried out to investigate the role of Co enzyme Q10 in ameliorating the deleterious effect of oxidative stress induced by a high dose of Hydrogen peroxide.Twenty four male rats were divided into three equal groups. One served as control and Group1 treated with 0.75% H2O2 in drinking water for one month, and Group2 adminstrated orally Co Q10 with daily dose 1 mg /rat for 30 days. To assess the effect of H2O2 in drinking water with Co Q10 on the lipid profile, ALT, AST and histological changes were recorded. The present study demonstrated a clear alteration in the lipid profile of G2 and significant (P<0.05) decrease in serum TC, TAG, LDL-c and VLDL-c and increase the HDL-c . also the result exhibit significant (P<0.05) reduction in serum ALT and AST concentration in animal treated with Co Q10 comparing with the values in G1.Histological section of liver revealed that H2O2 initiate pathological lesion such aggregation mononeuclear cell, infiltration of inflammatory cell, moderate fatty change and cytoplasmic vaculation ,on the other hand, oral administration of Co Q10 completely regressed these lesion. In conclusion, the result of this study clarified the possibility of induction oxidative stress in rats in 30 days provided by 0.75% H2O2, and ameliorating the oxidative stress effect of H2O2 by administration of Co Q10.

Multiple System Atrophy: Role Of Coenzyme Q10

Multiple system atrophy (MSA) is a progressive neurodegenerative disorder characterized by a variable combination of autonomic failure, Parkinsonism, and ataxia. There is currently no treatment available to halt or delay progression of this disorder. Biochemically, MSA is characterized by mitochondrial dysfunction, oxidative stress, and inflammation. In the present article we have therefore reviewed the potential role of coenzyme Q10 (CoQ10) in the pathogenesis and treatment of MSA, on the basis of its role in mitochondrial function, and its antioxidant and anti-inflammatory activities, as well as its reported depletion in blood and cerebellar tissue from MSA patients.

Coenzyme Q10 in the Treatment of Heart Failure with Preserved Ejection Fraction: A Prospective, Randomized, Double-Blind, Placebo-Controlled Trial.

BackgroundHeart failure with preserved ejection fraction (HFpEF) is common in elderly people and is increasing in prevalence. No specific treatment for this condition exists. Coenzyme Q10 (CoQ10) is an essential cofactor for energy production, with reduced levels being noted in HF. Previous studies have suggested a possible role for CoQ10 in the treatment of HF. This study examined the effect of CoQ10 supplementation on diastolic function in HFpEF patients.MethodsWe conducted a prospective, randomized, double-blind, placebo-controlled trial including patients aged > 55 years presenting with New York Heart Association class II–IV heart failure symptoms and left ventricular ejection fraction > 50%, with impaired diastolic function. Echocardiography and levels of serum N-terminal pro-B-type natriuretic peptide (NT-proBNP) were performed at baseline and following 4 months of CoQ10 or placebo supplementation.ResultsA total of 39 patients were enrolled—19 in the CoQ10 group and 20 in the placebo group. Baseline clinical characteristics were similar between groups, while compliance was high and also similar between the CoQ10 and placebo groups. There was no significant effect of treatment on indices of diastolic function (difference in the lateral E/e' ratio: −0.86 ± 6.57 in the CoQ10 group, +0.18 ± 3.76 in the placebo group; p = 0.561) or on serum NT-proBNP levels (− 72 pg/mL vs. − 42 pg/mL; p = 0.195).ConclusionsIn this pilot trial in elderly patients with HFpEF, treatment with CoQ10 did not significantly affect echocardiographic indices of diastolic function and serum NT-proBNP levels.Trial RegistrationThis trial was registered in the US National Institutes of Health Clinical Trials Registry (ClinicalTrials.gov identifier: NCT02779634).

Role of Coenzyme Q10 in Health and Disease: An Update on the Last 10 Years (2010–2020)

The present review focuses on preclinical and clinical studies conducted in the last decade that contribute to increasing knowledge on Coenzyme Q10’s role in health and disease. Classical antioxidant and bioenergetic functions of the coenzyme have been taken into consideration, as well as novel mechanisms of action involving the redox-regulated activation of molecular pathways associated with anti-inflammatory activities. Cardiovascular research and fertility remain major fields of application of Coenzyme Q10, although novel applications, in particular in relation to topical application, are gaining considerable interest. In this respect, bioavailability represents a major challenge and the innovation in formulation aspects is gaining critical importance.

Impact of Coenzyme Q10 on Hormonal Profile in Male Sprague-Dawley Rat Exposed to Sub-Chronic Concentrations of Cypermethrin

Aim: This study was aimed at evaluating the impact of Coenzyme Q10 on hormonal profile in male Sprague-Dawley rat exposed to sub-chronic concentrations of Cypermethrin.
 Experimental Design: A completely randomized experimental design using standard methods for analysis. Hormonal assay was carried out by Microplate Enzyme Immunoassay using their respective test kits. Including AccuBindTM Microplate EIA Test system from Monobind Inc. Lake Forest CA 92630 USA while statistical analysis was carried out using one-way Analysis of Variance (ANOVA); where significant differences were found, Pair-wise comparisons conducted with Tukey test using SPSS 20 software.
 Location and Duration of Study: This study was carried out in the Department of Biology, Ignatius Ajuru University of Education Rumuolumeni, Port Harcourt, Rivers State, Nigeria. GPS 4o48ʹ14ʹʹ N 6o59ʹ12ʹʹ E. The study lasted for 28days.
 Methodology: Thirty male Sprague-Dawley rats were randomly assigned to five groups, A-E(n=6/group).Group A was given cool clean water and standard rat pellet ad libitum. Group B,C and D were administered Cypermethrin @ 10mg/kg/bw,20mg/kg/bw,30mg/kg/bw respectively along with 10mg/kg/bw of coenzyme Q10 (CoQ10). Group E received 30mg/kg/bw of cypermethrin only without Coenzyme Q10. All animals were allowed access to cool clean water and standard rat pellet ad libitum. Bodyweight of the animals were taken twice a week and recorded in grams. Twenty-four hours before the animals were euthanized with ethyl ether inhalation, feed was withdrawn from the animals. Blood samples were collected by cardiac puncture between the hours of 7:00 and 9:00am into plain sample tubes according to the approved protocol of blood collection techniques. Analysis for the quantitative determination of all androgens was by Microplate Enzyme Immunoassay using the AccuBindTM Microplate EIA Test system from Monobind Inc. Lake Forest CA 92630 USA and expressed as their respective units. The animals were latter dissected and the vital organs harvested and weighed. The values were subjected to statistical analysis using SPSS software 20.
 Results: Results showed that there was no significant difference between the bodyweight and organ weight of animals in the treatment group compared with the control. Also, treatment with Cypermethrin only in group E, reduced the level of all the androgens considered in exposed animals. However, with concurrent administration of coenzyme Q10, the production of all androgens especially the production of Follicle Stimulating Hormone, Luteinizing Hormone and Progesterone in groups B,C,D and Estrogen in group B were significantly (P=.05) increased to values higher than the control.
 Conclusion: This elevation indicates the role of Coenzyme Q10 as an effective antioxidant to boost hormonal level production especially the level of androgens.

Coenzyme Q10 and Immune Function: An Overview.

Coenzyme Q10 (CoQ10) has a number of important roles in the cell that are required for optimal functioning of the immune system. These include its essential role as an electron carrier in the mitochondrial respiratory chain, enabling the process of oxidative phosphorylation to occur with the concomitant production of ATP, together with its role as a potential lipid-soluble antioxidant, protecting the cell against free radical-induced oxidation. Furthermore, CoQ10 has also been reported to have an anti-inflammatory role via its ability to repress inflammatory gene expression. Recently, CoQ10 has also been reported to play an important function within the lysosome, an organelle central to the immune response. In view of the differing roles CoQ10 plays in the immune system, together with the reported ability of CoQ10 supplementation to improve the functioning of this system, the aim of this article is to review the current literature available on both the role of CoQ10 in human immune function and the effect of CoQ10 supplementation on this system.

Coenzyme Q10 in Male Infertility

Currently the male factor is frequently encountered in the infertility problem. Basically, the factors that cause sperm dysfunction and male infertility are environmental, physiological and genetic. Excessive amount of reactive oxygen species and other oxidant radicals have been associated with male infertility. In addition, although semen analysis parameters appear normal in idiopathic male infertility, it is suggested that the possible cause of infertility is oxidative stress. Antioxidants in foods that are protective against oxidative stress increase the success of assisted reproductive techniques by protecting spermatozoa from free oxygen radicals, preventing DNA breaks caused by free oxygen radicals, and supporting the sperm maturation process. Coenzyme Q10 (CoQ10), which is found in every cell and has the ability to dissolve in oil, is a vitamin-like compound that acts as a coenzyme in key enzymatic reactions in energy production in the cell. Endogenous CoQ10, is significantly associated with sperm count and motility and is shown as one of the most important antioxidants in seminal plasma. Exogenous CoQ10 administration can be explained by its positive effects on sperm motility, its effectiveness in mitochondria and its antioxidant effects. In this review, articles investigating the effect of oxidative stress on infertility and the role of CoQ10, a natural antioxidant vitamin in the treatment of infertility, were presented. As a result, the positive effects of using CoQ10 as a supportive treatment in male infertility have been shown in studies. However, more comprehensive, long-term and pregnancy-related studies are needed.

The effect of CO-Q10 on the testicular histological changes in rats induced by imatinib

The safety zone of imatinib, and specifically its relevancy to organ toxicity, has been discussed dialectically in current years. Oxidative stress may be one of the causes of imatinib -mediated toxicity. This study aimed to examine the possible role of co-enzyme Q10 in ameliorating the adverse effect of imatinib on the testicular histology of male albino rats -if it is present. Twenty-eight male Albino rats were used randomly assigned to 4 experimental groups: Group 1 includes 40-45 days aged rats (n=8) which were gavage a dose of 200 mg/kg/day/30 days of imatinib mesylate. Group 2 includes age matched control rats which were administered with distilled water(n=4). Group 3 includes eight rats were received Q10, 50mg/kg, alone, Q10-sorb capsule of 50 mg given with the same schedule. Group 4. Includes eight rats were co administrated orally with 50 mg/kg of Q10+200 mg/kg of imatinib (once/day/30days). Euthanizing of animals with ether 24 hours after the final dose was done. Testes of rats from each experimental group were obtained. The tissues processed and stained by routine histological method. Histological sections of testes's rats treated with 200mg/Kg of imatinib revealed different testicular lesions compared to those of control group (P<0.05). Six 6(75%) of these sections revealed degenerated tubules, detached Sertoli cells, and apoptosis. These histological sections also showed thick tunica albuginea, seminiferous tubules with thick basement membrane. sometimes only a few of Sertoli cells were appeared in histological sections of imatinib treated rats. Mean Johnsen’s scores in these sections was 5.1±0.1 (P˂0.001). Features of retained spermatid were also noticed in some sections. There was significant reduction in both seminiferous tubular diameter and the epithelial height of histological sections of group 2(P˂0.001) with mean of 140.2±3.2µm and 14.8±1.1 µm respectively. Moreover, the number of Sertoli cells/ seminiferous tubule were significantly increased (P˂0.001), with mean of 27.4±0.2 and Leydig cell number is also significantly raised with mean of 7.5±0.5. In conclusion, treatment of peripubertal rats with imatinib induced several testicular alterations (including Sertoli cells) in comparison to control rats indicated that this drug is a gonadotoxic agent as it affects the quality and quantity of spermatogenesis. An Ameliorating effect of co-enzyme Q10 co-administration on imatinib-induced testicular toxicity was concluded.

Abstract 12897: Coenzyme Q10 in the Treatment of Heart Failure With Preserved Ejection Fraction: A Prospective, Randomized, Double-blind Trial

Background: Heart failure with preserved ejection fraction (HFpEF) is the most common form of heart failure (HF) in the elderly and is increasing in prevalence. No specific treatment for this condition appears to be effective. Coenzyme Q10 (CoQ10) is an essential cofactor for energy production and reduced levels have been noted in HF. Previous studies have suggested a possible role for CoQ10 in the treatment of HF in particular in the elderly. Aim: To evaluate the effect of CoQ10 supplementation on diastolic function in patients with HFpEF. Methods: A prospective, randomized, double-blind, placebo-controlled trial. Inclusion criteria were age &gt; 50 years, New York Heart Association class II-IV, ejection fraction &gt; 50%, and evidence of impaired diastolic function defined as lateral e' &lt; 0.09 cm/sec, average E/e' &gt; 13 or average E/e' &gt; 8 with additional markers of impaired diastolic function such as delayed relaxation (E/A &lt; 0.5), elevated left atrial volume index (&gt; 40ml / m 2 ) elevated left ventricular mass index ( &gt; 122 gr/ m 2 ♀ or 149 gr/ m 2 ♂) or pulmonary hypertension. Patients with other forms of cardiomyopathies or treated with chronic renal replacement therapy were excluded. Echocardiographic studies and levels of N-terminal pro-B type natriuretic peptide (NT-proBNP) were completed at baseline and following 4 months of CoQ10 (300 mg daily) or placebo supplementation. Results: A total of 39 patients were enrolled, 19 patients in the CoQ10 and 20 patients in the placebo group. Groups were similar in baseline clinical characteristics. Compliance was high and similar between groups (average 208 ± 108 mg/day for the CoQ10 versus 212 ± 95 mg/day for the placebo group). No significant effect was observed on indices of diastolic function or NT-proBNP levels following 4 months of CoQ10 use. Conclusions: Treatment with CoQ10 did not affect indices of diastolic function or NT-proBNP levels in patients with HFpEF. Our study does not support the routine use of CoQ10 in patients with HFpEF.

Coenzyme Q10 nullified khat-induced hepatotoxicity, nephrotoxicity and inflammation in a mouse model

Ethnopharmacological relevanceThe consumption of khat (Catha Edulis, Forsk) is on the rise despite the much publicized associated deleterious health effects. How chemicals present in khat, affect various physiological and biochemical processes requires further scrutiny. A clear understanding of these processes will provide an avenue for countering khat-driven negative effects using appropriate pharmacological and/or nutritional interventions. Aim of the studyThe current study investigated the effect of khat on vital physiological and biochemical processes such as oxidative stress, inflammation and immune responses and the role of Coenzyme-Q10 (CoQ10), a potent antioxidant and anti-inflammatory, in modulating any negative effects due to khat exposure. MethodologyThree (3) weeks old forty (40) Swiss albino mice were randomly assigned into four treatment groups (n = 10). The first group was the control that was not administered with khat or CoQ10. The second group received 200 mg/kg body weight (b/w) of CoQ10, while the third group received 1500 mg/kg b/w of khat extract and finally the forth group was co-treated with 200 mg/kg b/w of CoQ10 and 1500 mg/kg b/w of khat extract. The experiment was conducted for 90 days after which samples were collected for physiological and biochemical analyses. ResultsThe effects of khat and CoQ10 on the weights of brain, liver, kidney and spleen was determined. Administration of khat decreased the levels of RBCs and its subtypes (MCV, MCH, RDW-SD and RDW-CV), a clear indicator of khat-induced normochromic microcytic anemia. White blood cells (lymphocytes, monocytes, neutrophils and eosinophil) which are vital in responding to infections were markedly elevated by khat. Moreover, these results provide evidence for khat-induced liver and kidney injury as shown by increased biomarkers; AST, ALT, GGT and creatinine respectively. Standard histopathological analysis confirmed this finding for khat-driven liver and kidney injury. Further studies showed evidence for khat-induced inflammation and oxidative stress as depicted by increased levels of the pro-inflammatory cytokine TNF-alpha and elevation of GSH in the brain, liver and spleen. Remarkably, this is the first study to demonstrate the potential of CoQ10 in ameliorating khat-induced negative effects as outlined. CoQ10 supplementation restored the khat-induced reduction in RBC subtypes, and was protective against liver and kidney injury as shown by the appropriate biomarkers and standard histopathology analysis. The other significant finding was the CoQ10-driven normalization of GSH and TNF-α levels, indicating a protective effect from khat-driven oxidative stress and inflammation respectively. ConclusionFrom this study, we conclude that CoQ10 may be useful in nullifying khat-driven deleterious events among chronic khat users.

The importance of coenzyme Q10 and its ratio to cholesterol in the progress of chronic kidney diseases linked to non- -communicable diseases.

The mortality of patients with chronic kidney diseases (CKD) increases with thedecrease in glomerular filtration rate (eGFR). In the progress of CKD that is closely linked to non-communicable diseases (NCDs), the role of coenzyme Q10 (CoQ10) is not fully evaluated. We aimed to evaluate the importance of CoQ10, CoQ10/cholesterol ratio, and oxidative stress in the progress of CKD. The control group was constituted of 19 healthy subjects who volunteered to enrol in the study, CKD group consisted of 58 patients with CKD, of whom 54 had CKD combined with hypertension, 22 had CKD combined with hypertension and diabetes type 2 , and 18 had CKD combined with hypertension and statin therapy. We observed age, BMI, creatinine, uric acid, eGFR, hemoglobin, CRP, glucose, lipids fraction, and liver enzymes. Coenzyme Q10-TOTAL (ubiquinol+ubiquinone) in platelets and plasma were determined using HPLC method with UV detection. Indexed of CoQ10/lipid fractions were evaluated. Oxidative stress was determined as thiobarbituric acid‑reactive substances (TBARS). With increased stages of CKD, eGFR and CoQ10 as well as its ratio to lipids were significantly reduced while TBARS increased. We assume that lower endogenous CoQ10 level may be one of the reasons of kidney dysfunction. CoQ10/lipids ratio and increase in oxidative stress can predict the progression of CKD in patients with arterial hypertension, diabetes mellitus and dyslipidemia (Tab. 2, Fig. 4, Ref. 49).

Abstract 595: Circulating levels of coenzyme Q10 and lung cancer risk

Abstract Background: Coenzyme Q10 (CoQ10) is an ubiquitous molecule in living organisms that serves as a cofactor in energy production via the electron-transport chain (ETC). Research has previously shown that deficiencies in CoQ10 can result in a variety of detrimental outcomes including cardiovascular disease and neurological disorders. More recently, epidemiological studies have reported low CoQ10 levels being associated with increased risk of breast, ovarian, and skin cancers. However, studies exploring the link between CoQ10 and lung cancer risk are largely lacking. Methods: A nested case-control study including 201 lung cancer cases and 395 matched controls from the Southern Community Cohort Study (SCCS) was conducted. Plasma CoQ10 levels were measured using high-performance liquid chromatography (HPLC). A conditional logistic regression model was applied to estimate the odds ratio (OR) and 95% confidence interval (CI) for the association between plasma CoQ10 concentrations and lung cancer risk. CoQ10 level was categorized by tertile distribution among controls. Results: Plasma CoQ10 concentration was inversely associated with risk of lung cancer. Compared to the first tertile, the ORs (95% CI) were 0.82 (0.52-1.31) and 0.57 (0.34-0.96) for the second and third tertile, respectively, (P for trend=0.038), after adjusting for age, smoking status and pack-years of smoking. Additional adjustment for alcohol consumption, education, income, history of COPD and BMI slightly attenuated the association (OR=0.60, 95% CI=0.34-1.08, comparing third to first tertile). No notable difference was found between African Americans and European Americans. Stratified analysis identified a significant association between CoQ10 and lung cancer in current smokers (OR=0.47, 95% CI=0.26-0.87, third vs. first tertile), but not in former/never smokers (OR=0.84, 95% CI=0.35-2.03). The significant associations between CoQ10 and lung cancer risk were more evident in cases who were diagnosed within one year of blood draw (OR=0.17, 95% CI=0.04-0.73, third vs. first tertile, P for trend=0.023) than in cases diagnosed after one year following blood draw (OR=0.72, 95% CI=0.36-1.41). Conclusions: Findings from this study suggest that Coenzyme Q10 may be a potential marker for lung cancer, although the stronger effect shortly after diagnosis indicates the association may be related to dietary or other changes associated with the cancer diagnosis rather than CoQ10 being a causal risk biomarker. Further studies exploring the link between CoQ10 and lung cancer risk are necessary to better understand the role of CoQ10 in lung carcinogenesis. Citation Format: Chris Shidal, Hyung-Suk Yoon, Wei Zheng, Jie Wu, Adrian A. Franke, William J. Blot, Xiao-Ou Shu, Qiuyin Cai. Circulating levels of coenzyme Q10 and lung cancer risk [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 595.

Mitochondria and Coenzyme Q10 in the Pathogenesis of Preeclampsia

Hypertensive disorders during pregnancy constitute one of the main causes of maternal and perinatal morbidity and mortality across the world and particularly in developing countries such as Ecuador. However, despite its impact on public health, the primary pathophysiological processes involved are yet to be elucidated. It has been proposed, among other theories, that an abnormal placentation may induce an endothelial dysfunction, which is ultimately responsible for the final clinical manifestations. Mitochondria, particularly from trophoblastic cells, are responsible for the production of energy, which is extremely important for normal placentation. The malfunction in this supply of energy may produce higher levels of free radicals. In both production of energy and free radicals, coenzyme Q10 (CoQ10) plays a crucial role in electron transport. As such, the role of CoQ10 in the genesis and prevention of preeclampsia has become the focus of a number of research groups, including that of the authors. Developing an in-depth understanding of these mechanisms might allow us to design new and feasible strategies with which we can reduce preeclampsia, particularly in the Latin-American countries.

Interaction of Coenzyme Q10 with Liposomes and its Impact on Suppression of Selenite - Induced Experimental Cataract.

Purpose: To stress the influence of Coenzyme Q10 (CoQ10) on the structural properties of liposomes as model membranes and to investigate the possible role of CoQ10 or CoQ10 doped in liposomes when topically instilled as eye drops, in preventing cataract.Methods: The molecular interaction between liposomes and Coenzyme Q10 was examined using differential scanning calorimetry (DSC) and Fourier transform infrared spectroscopy (FTIR). Rat pups were randomly divided into six groups comprising 15 pups. Group (1), control group. Group (2), untreated model of cataract, received a single subcutaneous injection of sodium selenite. Instillation of pure CoQ10 (Group 3), CoQ10 encapsulated into neutral (Group 4), positive (Group 5) and negative (Group 6) Dipalmitoyl phosphatidylcholine (DPPC) liposomes on the opacification of lenses in rat pups after sodium selenite injection was topically received.Results: The incorporated CoQ10 is probably associated with lipid bilayers where it interacts to a large extent and perturbs them. This results in strong broadening and shift to lower temperature (94°C) of the major characteristic endothermic peak of pure DPPC at 105°C. FTIR showed that the incorporation of CoQ10 into DPPC induces a conformational change in the polar region of DPPC. Ophthalmological and Biochemical studies revealed that CoQ10 alone followed by negatively charged liposomes doped with CoQ10 are more effective in reducing the progress of cataract as well as improving the lens soluble proteins levels and total antioxidant capacity.Conclusion: The interactions of CoQ10 with membrane systems may contribute to a better understanding of CoQ10 physiological properties and the development of therapeutically advanced systems.

Mitochondrial Dysfunctions and Role of Coenzyme Q10 in Patients with Glaucoma

Mitochondrial function is closely linked to numerous aspects of eye health. Imbalance between the creation of energy and the development of reactive oxygen species (ROS) seems to be the cause of the development of mitochondrial dysfunctions. As a result of this energy deficit, the level of oxidative stress in the eye tissues increases, leading to numerous ophthalmic impairments. It is important to distinguish between primary mitochondrial eye diseases and secondary mitochondrial changes. Primary mitochondrial eye diseases, for example Leber's hereditary optic atrophy (LHON), retinitis pigmentosa and chronic progressive external ophthalmoplegia are caused by direct damage to mitochondrial function induced by defective genes, either located on mitochondrial DNA (mtDNA) or the DNA of the nucleus (nDNA). In contrast, secondary mitochondrial dysfunctions are caused by environmental factors. In recent years, there has been growing evidence that mitochondrial dysfunctions play an important role in many common eye diseases, such as glaucoma, dry eye, diabetic retinopathy, cataract and age-related macular degeneration (AMD). This article summarises current knowledge of mitochondrial dysfunctions and the role of coenzyme Q10 (CoQ10) as a possible treatment option - with a special focus on glaucoma.

To Determine the Role of Co-Enzyme Q10 and Trace Elements in Patient with Pre-Eclampsia-A Cross Sectional Study in Hyderabad

To Determine the Role of Co-Enzyme Q10 and Trace Elements in Patient with Pre-Eclampsia-A Cross Sectional Study in Hyderabad

Coenzyme Q10 Status as a Determinant of Muscular Strength in Two Independent Cohorts.

Aging is associated with sarcopenia, which is a loss of skeletal muscle mass and function. Coenzyme Q10 (CoQ10) is involved in several important functions that are related to bioenergetics and protection against oxidative damage; however, the role of CoQ10 as a determinant of muscular strength is not well documented. The aim of the present study was to evaluate the determinants of muscular strength by examining hand grip force in relation to CoQ10 status, gender, age and body mass index (BMI) in two independent cohorts (n = 334, n = 967). Furthermore, peak flow as a function of respiratory muscle force was assessed. Spearman’s correlation revealed a significant positive association between CoQ10/cholesterol level and hand grip in the basic study population (p<0.01) as well as in the validation population (p<0.001). In the latter, we also found a negative correlation with the CoQ10 redox state (p<0.01), which represents a lower percentage of the reduced form of CoQ10 (ubiquinol) in subjects who exhibit a lower muscular strength. Furthermore, the age of the subjects showed a negative correlation with hand grip (p<0.001), whereas BMI was positively correlated with hand grip (p<0.01), although only in the normal weight subgroup (BMI <25 kg/m2). Analysis of the covariance (ANCOVA) with hand grip as the dependent variable revealed CoQ10/cholesterol as a determinant of muscular strength and gender as the strongest effector of hand grip. In conclusion, our data suggest that both a low CoQ10/cholesterol level and a low percentage of the reduced form of CoQ10 could be an indicator of an increased risk of sarcopenia in humans due to their negative associations to upper body muscle strength, peak flow and muscle mass.

Plasma Coenzyme Q10 Levels in Patients With Multiple System Atrophy

Multiple system atrophy (MSA) is an intractable neurodegenerative disease characterized by autonomic failure in addition to various combinations of parkinsonism, cerebellar ataxia, and pyramidal dysfunction. It has recently been reported that functionally impaired variants of COQ2, which encodes an essential enzyme in the biosynthetic pathway of coenzyme Q10 (CoQ10), are associated with MSA. However, little is known about the role of CoQ10 in the pathogenesis of MSA. To compare the levels of plasma CoQ10 in patients with MSA with those in age-, sex-, and COQ2 genotype-matched controls. We enrolled 44 Japanese patients with MSA and 39 Japanese controls from September 1, 2012, to December 31, 2015. Patients with MSA were diagnosed on the basis of the second consensus criteria by at least 2 neurologists. Plasma CoQ10 levels were measured by high-performance liquid chromatography with electrochemical detection. Sanger sequencing of COQ2 was performed to determine the COQ2 genotypes. Multiple logistic regression analysis was performed to determine the association between MSA and the plasma CoQ10 level. Plasma CoQ10 levels in patients with MSA were compared with those in controls after adjusting for age, sex, and COQ2 genotype. Among 44 patients with MSA (mean [SD] age, 63.7 [8.3] years) and 39 controls (mean [SD] age, 60.3 [13.0] years), the mean (SD) plasma level of CoQ10 in patients with MSA was lower than that in controls (0.51 [0.22] vs 0.72 [0.42] µg/mL; P = .01) (difference between medians: -0.14; 95% CI, -0.25 to -0.03). The mean (SD) plasma levels of CoQ10 in patients with the cerebellar variant of MSA and those with the parkinsonian variant of MSA were 0.58 (0.19) and 0.49 (0.26) µg/mL, respectively. After adjusting for age, sex, and COQ2 genotype, the levels of plasma CoQ10 were significantly associated with MSA (95% CI, 0.10; range, 0.02 to 0.66) (P = .02). Our data showed decreased levels of plasma CoQ10 in patients with MSA regardless of the COQ2 genotype, supporting a hypothesis that supplementation with CoQ10 is beneficial for patients with MSA.