Q10 Levels Research Articles

Brain-derived neurotrophic factor and coenzyme Q10 levels in blood of children with learning disorder

Background Learning disorder (LD) is manifested by significant difficulties in the acquisition and use of reasoning, reading, writing, or mathematical abilities, despite average intelligence and proper education. Its etiological factors were suggested to be related to neurodevelopmental alterations. Measurement of the levels of brain-derived neurotrophic factor (BDNF) and coenzyme Q10 (CoQ10) was targeted in children with LD in comparison with typically developing (TD) ones. Materials and methods This study included 82 Egyptian Arabic-speaking children matched for age and sex and socioeconomic status, comprising 42 with specific LD (group I) and 40 TD children (group II). All participants were subjected to clinical and full neurological examination after reporting a full medical history. Furthermore, LD group was subjected to Stanford–Binet intelligence scale, dyslexia assessment test, and phonological awareness test, which evaluates cognitive and learning aptitudes. The levels of BDNF and CoQ10 were determined in serum by enzyme-linked immunosorbent assay. Results All children with LD obtained a score of 1 or more as at-risk quotient by the dyslexia assessment test, which indicated a specific reading disorder. The BDNF and CoQ10 levels in the LD group were significantly less than those in the TD group. No correlations were found between the measured markers and each other or between them and the measured factors of the used tests. Conclusion The detected low levels of BDNF and CoQ10 in children with specific LD with impairment in reading would be suspected to be related to etiological or exaggerating factors for the deficits in such children.

Feed quantitative restriction and coenzyme Q10 level on performance, plasma lipoproteins and organ weights of broiler chicks

An experiment was conduct in order to investigate the effects of feed restriction level and duration and dietary coenzyme Q10 level on growth performance, organ characteristics and plasma lipoproteins. A factorial arangment based on a completely randomized design was performed using two levels of feed restriction (10 and 20% less than the standard Ross strain 308 guidelines), two levels of restriction duration (7 and 14 days) and three levels of coenzyme Q10 (0, 20 and 40 mg/kg feed). The results of the experiment showed that restriction intensity had significant effect on feed intake in first, second and sixth weeks of age (P<0.05), body weight gain in second and sixth weeks of age (P<0.05), and feed conversion ratio in first week of age (P<0.05). Restriction duration had significant effect on feed intake in third week of age (P<0.05), and feed conversion ratio in third and sixth weeks of age (P<0.05). Coenzyme Q level had significant effect on feed intake in first and sixth weeks of age (P<0.05), body weight gain in second, fifth and sixth weeks of age (P<0.05), and feed conversion ratio in second and sixth weeks of age (P<0.05). In conclusion, considering the positive effects of feed restriction and coenzyme Q10 on broiler yield, the simaltaneous use of feed restriction strategy and dietary coenzyme Q10 can be considered as a management program in order to improvement of broiler productivity.

Mitochondrial Dysregulation and Impaired Autophagy in iPSC-Derived Dopaminergic Neurons of Multiple System Atrophy.

SummaryMultiple system atrophy (MSA) is a progressive neurodegenerative disease that affects several areas of the CNS, whose pathogenesis is still widely unclear and for which an effective treatment is lacking. We have generated induced pluripotent stem cell-derived dopaminergic neurons from four MSA patients and four healthy controls and from two monozygotic twins discordant for the disease. In this model, we have demonstrated an aberrant autophagic flow and a mitochondrial dysregulation involving respiratory chain activity, mitochondrial content, and CoQ10 biosynthesis. These defective mechanisms may contribute to the onset of the disease, representing potential therapeutic targets.

The pathogenesis linked to coenzyme Q10 insufficiency in iPSC-derived neurons from patients with multiple-system atrophy

Multiple-system atrophy (MSA) is a neurodegenerative disease characterized by autonomic failure with various combinations of parkinsonism, cerebellar ataxia, and pyramidal dysfunction. We previously reported that functionally impaired variants of COQ2, which encodes an essential enzyme in the biosynthetic pathway of coenzyme Q10, are associated with MSA. Here, we report functional deficiencies in mitochondrial respiration and the antioxidative system in induced pluripotent stem cell (iPSC)-derived neurons from an MSA patient with compound heterozygous COQ2 mutations. The functional deficiencies were rescued by site-specific CRISPR/Cas9-mediated gene corrections. We also report an increase in apoptosis of iPSC-derived neurons from MSA patients. Coenzyme Q10 reduced apoptosis of neurons from the MSA patient with compound heterozygous COQ2 mutations. Our results reveal that cellular dysfunctions attributable to decreased coenzyme Q10 levels are related to neuronal death in MSA, particularly in patients with COQ2 variants, and may contribute to the development of therapy using coenzyme Q10 supplementation.

Dietary supplementation with MicroActive Coenzyme Q10 increases plasma and skeletal muscle Coenzyme Q10 levels in Thoroughbred horses that are genetically variable for basal Coenzyme Q10 activity levels

Dietary supplementation with MicroActive Coenzyme Q10 increases plasma and skeletal muscle Coenzyme Q10 levels in Thoroughbred horses that are genetically variable for basal Coenzyme Q10 activity levels

The effect of coenzyme Q10 on cognitive status in chronic hemodialysis patients; a double-blind, randomized, clinical trial

Introduction: Renal failure is a stressful process that has several complications, including neurological disorders such as cognitive disorder, which can lead to the incidence of psychological disorders. Objectives: Given the reduced coenzyme Q10 levels in patients with chronic renal failure and the known role of this coenzyme in cognitive disorders, the present study was conducted to assess the effect of CoQ10 supplementation in the treatment of cognitive disorder in hemodialysis patients in Semnan, Iran. Patients and Methods: The present double-blind, randomized, clinical trial was conducted on patients with chronic renal failure undergoing hemodialysis at Kosar Hospital of Semnan. The participants underwent a cognitive assessment using the Mini-Mental State Examination (MMSE). They were then randomly divided into two groups; group one received CoQ10 supplement and group two received placebo for 90 days, after which period they underwent another cognitive assessment using the MMSE. The Kolmogorov-Smirnov test and Levene’s test were used to verify the normal distribution of the data. Data were analyzed using the t test and Mann–Whitney U test at a significance level of P<0.05. Results: There were no statistically significant differences between the two groups in terms of their personal details. The mean (± standard deviation) of the MMSE1 score was 21.29±6.5 in the control group and 21.09±5.4 in the case group. The mean (± standard deviation) of the MMSE2 score was 20.62±6.5 in the control group and 23.29±5.8 in the case group. A significant difference between the two groups in terms of their pre- and post-intervention MMSE scores was observed, suggesting the positive effect of the medication (P<0.001). Conclusion: The daily intake of CoQ10 100-mg led to a significant change in the cognitive status of chronic hemodialysis patients compared to the group that received only the placebo. Conducting a similar study but with the addition of a healthy control group is recommended in order to establish a base measure for the healthy population and to thus enable the better interpretation of the effect of this supplement.

Clinical correlates of decreased plasma coenzyme Q10 levels in patients with multiple system atrophy

IntroductionMultiple system atrophy (MSA) is a progressive neurodegenerative disease. Recent studies revealed decreased coenzyme Q10 (COQ10) levels in the cerebellum and blood samples of MSA patients. But few studies focused on the associations of COQ10 with the clinical symptoms of MSA. In this study, we aimed to quantify plasma COQ10 and characterize its association with clinical features. MethodsWe recruited 40 patients with MSA, 30 patients with Parkinson's disease (PD), and 30 healthy participants. Plasma COQ10 was quantified by UPLC-MS. The basic demographic data, motor symptoms, and non-motor symptoms were also assessed. ResultsPlasma COQ10 levels were significantly different in MSA, PD, and controls (P = 0.001). Post-hoc analysis revealed plasma COQ10 levels in MSA patients were lower than that in controls after adjusting for age, gender, and total cholesterol (P = 0.001). COQ10 levels differentiated MSA patients from controls with modest accuracy (P = 0.001). A sensitivity of 40% and a specificity of 97.5% was calculated with the receiver operating characteristic curve. However, COQ 10 levels did not discriminate between the MSA and PD groups (P = 0.07). Plasma COQ10 levels were correlated with the severity of motor symptoms only in MSA-C patients (b = −0.025, P = 0.009). ConclusionThe association between decreased COQ10 levels and the severity of motor symptoms in MSA-C patients promotes further research. Plasma COQ10 levels alone may not be a reliable MSA diagnostic biomarker, and cannot be considered a useful biomarker in the differential diagnosis of MSA vs PD.

Effect of Metabolic Stress on Lysosomal Proteolysis in the Liver and Brain of Rats Receiving Q10-Enriched Ration.

Activation of lysosomal proteolysis and increased coenzyme Q10 level were revealed in the liver and brain of rats with individual typological features under conditions of food deprivation. Changes in cathepsin B activity in these tissues were different in behaviorally active and passive animals. We observed indirect modulating effect of coenzyme Q10 in the regulation of activity of lysosomal endopeptidases in the brain of animals with different behavior during adaptation to metabolic stress.

MARKERS OF ANTIOXIDANT PROTECTION SYSTEM IN DIAGNOSTICS OF EXTERNAL GENITAL ENDOMETRIOSIS IN INFERTILITY FEMALE PATIENTS

To identify markers of the antioxidant defense, 43 female patients with the infertility associated with external genital endometriosis were examined. The control group consisted of 19 healthy fertile women. In endometriosis patients, a statistically significant (p < 0.01) plasma level of coenzyme Q10 and α-tocopherol, determined by means of high-performance liquid chromatography with electrochemical detection, were noted to be lower in the comparison with the control group. On the basis of the data obtained, there was developed a prognostic scale that allows verifying the presence and severity of external genital endometriosis in infertility female patients.

Effect of Coenzyme Q10 Alone and in Combination with Exercise Training on Oxidative Stress Biomarkers in Rats.

Aim: This study aimed to determine the effect of exercise training alone and in combination with coenzyme Q10 (Q10) supplementation on the Q10 level, oxidative damage, and antioxidant defense markers in blood and skeletal muscle tissue in young and aged rats. Methods: The study included 4-month old (young) and 20-month old (aged) rats. Each group was further divided into control, exercise training, Q10 supplementation, and Q10 supplementation plus exercise training groups. The exercise training program consisted of swimming for 8 weeks, and Q10 or vehicle during the same period. Results: The Q10 concentration in plasma (P<0.05), but not in skeletal muscle (P>0.05) increased significantly following Q10 supplementation in both the young and aged rats. Plasma SOD and CAT activity were significantly higher in the aged rats in the Q10 and Q10 plus exercise training groups than in the other groups (P<0.05); however, there was no significant difference between the groups in skeletal muscle (P>0.05). Additionally, plasma and skeletal GSH levels did not differ between the groups (P>0.05). Conclusion: The present findings indicate that Q10 supplementation increased the Q10 concentration in blood but not in skeletal muscle tissue. On the other hand, Q10 administration alone and in combination with exercise challenge improved antioxidant enzyme capacity especially in the aged rats.

Increased oxidative stress and coenzyme Q10 deficiency in centenarians.

Aging populations are expanding worldwide, and the increasing requirement for nursing care has become a serious problem. Furthermore, successful aging is one of the highest priorities for individuals and societies. Centenarians are an informative cohort to study and inflammation has been found to be a key factor in predicting cognition and physical capabilities. Inflammation scores have been determined based on the levels of cytokines and C-reactive protein, however, serum antioxidants and lipid profiles have not been carefully examined. We found that the redox balance of coenzyme Q10 significantly shifted to the oxidized form and levels of strong antioxidants, such as ascorbic acid and unconjugated bilirubin, decreased significantly compared to 76-year-old controls, indicating an increased oxidative stress in centenarians. Levels of uric acid, an endogenous peroxynitrite scavenger, remained unchanged, suggesting that centenarians were experiencing moderate, chronic inflammatory conditions. Centenarians exhibited a hypocholesterolemic condition, while an increase in the ratio of free cholesterol to cholesterol esters suggests some impairment of liver function. Serum free fatty acids and monoenoic acid composition, markers of tissue oxidative damage, were significantly decreased in centenarians, indicating an impairment in the tissue repair system. Despite an elevation of the coenzyme Q10 binding protein Psap, serum total coenzyme Q10 levels decreased in centenarians. This suggests a serious deficiency of coenzyme Q10 in tissues, since tissue levels of coenzyme Q10 significantly decrease with age. Therefore, coenzyme Q10 supplementation could be beneficial for centenarians.

The antioxidant status of coenzyme Q10 and vitamin E in children with type 1 diabetes

ObjectiveThe purpose of this study was to evaluate the antioxidant status of plasma vitamin E and plasma and intracellular coenzyme Q10 in children with type 1 diabetes. MethodThis case–control study was conducted on 72 children with type 1 diabetes and compared to 48 healthy children, who were age, sex, and ethnicity-matched. The diabetic children were divided according to their glycosylated hemoglobin (A1c %) into two groups: poor and good glycemic control groups. All children underwent full history taking, clinical examination, and laboratory measurement of complete blood count, A1c %, plasma cholesterol, triglycerides, and vitamin E levels and coenzyme Q10 levels in plasma, erythrocytes, and platelets. ResultsChildren with poor glycemic control showed significantly higher plasma vitamin E, coenzyme Q10, triglycerides, low-density lipoproteins, waist circumference/height ratio, cholesterol levels, and lower high-density lipoproteins and platelet coenzyme Q10 redox status in comparison to those with good glycemic control and the control group (p<0.05). Plasma coenzyme Q10 showed a positive correlation with the duration of type 1 diabetes, triglycerides, cholesterol, vitamin E, and A1c %, and negative correlation with the age of the diabetic group (p<0.05). The platelet redox status showed a negative correlation with the A1c % levels (r=−0.31; p=0.022) and the duration of type 1 diabetes (r=−0.35, p=0.012). ConclusionPatients with type 1 diabetes, especially poorly controlled, had elevation of plasma vitamin E and coenzyme Q10 levels and decreased platelet redox status of coenzyme Q10, which may be an indicator of increased oxidative stress.

Simultaneous detection of reduced and oxidized forms of coenzyme Q10 in human cerebral spinal fluid as a potential marker of oxidative stress.

The redox balance of coenzyme Q10 in human plasma is a good marker of oxidative stress because the reduced form of coenzyme Q10 (ubiquinol-10) is very sensitive to oxidation and is quantitatively converted to its oxidized form (ubiquinone-10). Here we describe an HPLC method for simultaneous detection of ubiquinol-10 and ubiquinone-10 in human cerebral spinal fluid to meet a recent demand for measuring local oxidative stress. Since the levels of coenzyme Q10 in human cerebral spinal fluid are less than 1/500 of those in human plasma, cerebral spinal fluid extracted with 2-propanol requires concentration for electrochemical detection. Using human plasma diluted 500-fold with physiological saline as a pseudo-cerebral spinal fluid, we found that addition of tert-butylhydroquinone was effective in preventing the oxidation of ubiquinol-10. The optimized tert-butylhydroquinone concentration in the extraction solvent was 20 µM. The addition of 20 µM ascorbic acid or co-addition of tert-butylhydroquinone and ascorbic acid (20 µM each) were also effective in preventing the oxidation of ubiquinol-10, but ascorbic acid alone gave poor reproducibility. Good within day reproducibility was observed, and day-to-day analytical variance was excellent.

The relationship between coenzyme Q10 level and diastolic dysfunction in coronary artery disease patients with preserved left ventricular systolic function

The relationship between coenzyme Q10 level and diastolic dysfunction in coronary artery disease patients with preserved left ventricular systolic function

Oxidative stress in adult growth hormone deficiency: different plasma antioxidant patterns in comparison with metabolic syndrome.

Growth hormone deficiency (GHD) is a condition associated with increased cardiovascular risk and insulin-resistance. Oxidative stress (OS) could be a mechanism underlying both these phenomena. In order to investigate plasma antioxidant defenses in such condition, we evaluated adults with GHD, compared with controls and metabolic syndrome patients (MetS), studying plasma total antioxidant capacity (TAC) and coenzyme Q10 (CoQ10, lipophilic antioxidant) levels, both in its oxidized and reduced forms, correlating this data with metabolic and hormonal pattern. In this case-control study, 51 GHD, 36 controls, and 35 MetS were enrolled. An evaluation of hormonal and metabolic parameters was performed. TAC was measured using the system metmyoglobin -H202 and the chromogen ABTS, whose radical form is spectroscopically revealed; latency time (LAG) in the appearance of ABTS● is proportional to antioxidant in sample. CoQ10 was assayed by electrochemical method. Despite HOMA index was higher in both GHD and MetS (2.2 ± 0.3 and 3.1 ± 0.3 vs. 1.2 ± 0.2 in controls), only in MetS we observed lower LAG levels (64.5 ± 3.1 s vs. 82.8 ± 5.8 in GHD and 80.6 ± 6.6 in controls), suggesting an increased consumption of antioxidants. LAG significantly correlated with uric acid only in MetS (r 2 = 0.65, p < 0.001), suggesting a different pattern of antioxidants. CoQ10 exhibited a trend toward lower levels in GHD, although not significant. Our data indicate that GHD, although sharing with MetS various metabolic features, including increased HOMA levels, showed a different pattern of plasma antioxidants, suggesting inadequate reactivity toward radical production rather than an antioxidants consumption as in MetS.

Cerebrospinal fluid levels of coenzyme Q10 are reduced in multiple system atrophy

IntroductionThe finding of mutations of the COQ2 gene and reduced coenzyme Q10 levels in the cerebellum in multiple system atrophy (MSA) suggest that coenzyme Q10 is relevant to MSA pathophysiology. Two recent studies have reported reduced coenzyme Q10 levels in plasma and serum (respectively) of MSA patients compared to Parkinson's disease and/or control subjects, but with largely overlapping values, limited comparison with other parkinsonisms, or dependence on cholesterol levels. We hypothesized that cerebrospinal fluid (CSF) is reliable to assess reductions in coenzyme Q10 as a candidate biomarker of MSA. MethodsIn this preliminary cross-sectional study we assessed CSF coenzyme Q10 levels in 20 patients with MSA from the multicenter Catalan MSA Registry and of 15 PD patients, 10 patients with progressive supranuclear palsy (PSP), and 15 control subjects from the Movement Disorders Unit Biosample Collection of Hospital Clinic de Barcelona. A specific ELISA kit was used to determine CSF coenzyme Q10 levels. CSF coenzyme Q10 levels were compared in MSA vs. the other groups globally, pair-wise, and by binary logistic regression models adjusted for age, sex, disease severity, disease duration, and dopaminergic treatment. ResultsCSF coenzyme Q10 levels were significantly lower in MSA than in other groups in global and pair-wise comparisons, as well as in multivariate regression models. Receiver operating characteristic curve analyses yielded significant areas under the curve for MSA vs. PD, PSP and controls. ConclusionsThese findings support coenzyme Q10 relevance in MSA. Low CSF coenzyme Q10 levels deserve further consideration as a biomarker of MSA.

P 174 - Placental and mitochondrial Q10 content after CoQ10 supplementation during pregnancy

Pre-eclampsia is a common disorder of human pregnancy (about 7% of all pregnancies) in which the normal hemodynamic response to pregnancy is compromised. In 2009, we demonstrated that supplementation with CoQ10 reduces significantly the risk of developing pre-eclampsia in women at risk for the condition. From these women, placental and mitochondrial Q10 levels, in women receiving either placebo or 200 mg CoQ10 daily were measured. Results showed that before supplementation, at week 20 of pregnancy, plasma CoQ10 levels showed no difference between the control (0.134±0.05 umol/l) and supplemented (0.139±0.06 umol/l) groups. Interestingly, at delivery, placental tissue showed no differences in the placebo group between women with normal pregnancy and those with preeclampsia; while in the Q10 group, women with preeclampsia showed significantly higher placental levels (0.31±0.20 ug/mg of protein) compared to normal pregnant women (0.18±0.08 ug/mg of protein; p=0.005). However, mitochondrial levels of Q10 in placenta from pregnant women with preeclampsia receiving placebo did not show differences compared to those receiving CoQ supplementation (0.82±0.41 vs. 0.77±0.42 ug/mg of protein). These results suggest that in women with preeclampsia, although CoQ10 reduced preeclampsia and increased its content in placental tissue, it is not able to increase the mitocondrial levels of CoQ10.

May supplementation of coenzyme Q10 help prevent development of hydatidiform mole?

The pathological mechanisms of gestational trophoblastic disease have not yet been clearly determined. It is thought that oxidative damage contributes to the process. The aim of this study was to determine the levels of coenzyme Q10 (CoQ 10), DNA damage, and lipid peroxidation in patients with hydatidiform mole. The authors studied the levels of CoQ10, 8-hydroxydeoxyguanosine (8-OHdG), malondialdehyde (MDA) by high-performance liquid chromatography (HPLC), and the activity of glutathione peroxidase (GPX) by spectrophotometric method in blood obtained from patients with a complete hydatidiform mole (n=29), healthy pregnant women (n=29), and healthy non-pregnant women (n=29). The 8-OHdG/dG ratio (2.8148 ± 0.81592) and MDA (10.8341 ± 4.64875 μmol) were significantly higher in patients with complete hydatidiform mole, while the ubiquinol-10/ubiquinone-10 ratio (0.2107 ± 0.15675) and GPX activity (43.4606 ± 18.31694 mU/mI) were lower (p < 0.001). The authors suggest that both mitochondrial oxidative and oxidative DNA damage play important roles in the pathogenesis of complete hydatidiform mole. Therefore supplementation of CoQ10 prevents recurrent gestational trophoblastic disease.

Depletion of ubiA prenyltransferase domain containing 1 expression promotes angiotensin II‑induced hypertrophic response in AC16 human myocardial cells via modulating the expression levels of coenzyme Q10 and endothelial nitric oxide synthase.

UbiA prenyltransferase domain containing1 (UBIAD1) is closely associated with cardiovascular diseases. However, at the cellular level, little is known about how UBIAD1 is expressed and functions in cardiomyocyte hypertrophy. The aim of the present study was to investigate the expression and role of UBIAD1 in angiotensin II (Ang II)‑induced hypertrophy in AC16 cardiomyoblast cells. The loss‑of‑function approach was used to knock down UBIAD1 in vehicle‑ and Ang II‑stimulated AC16 cells. The levels of atrial natriuretic factor (ANF) and caspase-3 were measured and compared between vehicle‑ and Ang II‑treated AC16 cells pretreated with control siRNA or siRNA against UBIAD1. In addition, the levels of coenzyme Q10 (CoQ10) and endothelial nitric oxide synthase (eNOS) were evaluated and compared between these groups. Ang II induced hypertrophy and apoptosis in AC16 cells, accompanied by increased expression of ANF and caspase-3, and decreased expression of UBIAD1. These effects were potentiated by UBIAD1 knockdown. In addition, Ang II treatment suppressed the expression of CoQ10 and eNOS, as well as the production of NO, and these inhibitory effects were also enhanced by UBIAD1 knockdown. Thus, silencing of UBIAD1 expression promotes a myocardial hypertrophic response to Ang II stimulation, in part, by suppressing the expression of CoQ10 and eNOS.

Erratum to: The association between coenzyme Q10 concentrations in follicular fluid with embryo morphokinetics and pregnancy rate in assisted reproductive techniques.

Purpose This study seeks to evaluate the association between follicular fluid (FF) coenzyme Q10 (CoQ10) levels, embryo morphokinetics, and pregnancy rate.