Coenzyme q10 liquid supplementation in dyslipidemic subjects with statin-related clinical symptoms: a double-blind, randomized, placebo-controlled study.
Drug design, development and therapy
INTRODUCTION:Statin-associated myalgia occurs in about 1-3% of patients in the medical literature. Plasma CoQ10 levels are reduced in patients undergoing statin. OBJECTIVE:The primary outcome was the detection of clinical symptoms and the perception of pain evaluated throughout specific questionnaires. The secondary outcome was the variation in lipid profile and the variation in safety parameters. METHODS:We enrolled 60 Caucasian patients, intolerant to statins. During the run-in period, patients underwent a 1-month wash-out period during which statins were stopped. At the end of the wash-out period, if CPK and/or transaminases returned within an acceptable range, statins were re-introduced at half of the previously taken dose. After one month, patients were randomized to take either a liquid CoQ10 supplement or a placebo for three months at 100 mg/day. RESULTS:The Clinical Index Score for myalgia assessment was lower after 3 months with CoQ10, while it did not change with the placebo. The VAS score was lower after 3 months of CoQ10 supplementation, while no variation was recorded with the placebo. In the group treated with the dietary supplement, CoQ10 plasma concentrations were inversely correlated with CPK levels, Clinical Index Score absolute values, and VAS. CONCLUSION:The addition of CoQ10 with half dosage statin in patients with previous intolerance to statins improves the perception of clinical symptoms such as asthenia, myalgia or pain.
The Effect of Coenzyme Q10 Supplementation on Vascular Endothelial Growth Factor and Serum Levels of Interleukin 6 and 8 in Women with Breast Cancer: A Double-Blind, Placebo-Controlled, Randomized Clinical Trial.
Therapeutics and clinical risk management
BACKGROUND:To better evaluate the efficacy of CoQ10 on the inflammatory markers in breast cancer patients, we conducted a clinical study of patients with breast cancer undergoing tamoxifen therapy. CoQ10 serves as an antioxidant and inhibits oxidation caused by reactive oxygen species. The aim of the current study was to assess the effect of coenzyme Q10 supplementation on serum levels of interleukin 6, 8, and vascular endothelial growth factor (VEGF) in patients with breast cancer undergoing tamoxifen therapy by a double-blind, placebo-controlled, randomized clinical trial. METHODS:In the study, 30 breast cancer patients and 29 healthy subjects were randomized into four groups. Two groups of intervention received 100 mg CoQ10, and two control groups took placebo once a day for 2 months. Blood draws were obtained at baseline and at the end of the study. Serum levels of IL-6, IL-8 and VEGF were analyzed using ELISA kits. RESULTS:The data of the 59 participants were analyzed. Supplementation with CoQ10 demonstrated a significant decrease in IL-8 and IL-6 serum levels compared to placebo (P< 0.05). Although the downward trend was evident, CoQ10 supplementation did not reveal any significant effect on serum VEGF concentration. The group of patients who received supplements showed the most reduction in serum levels of cytokines among other groups. CONCLUSION:CoQ10 supplementation could be effective in ameliorating inflammatory cytokine levels, thereby reducing the consequences of inflammation caused by breast cancer. To generalize the results, larger and longer intervention studies with higher safe doses are needed and should take account of possible costs and harms as well as benefits (registration number: IRCT2015042021874N1).
One-year outcome of coenzyme Q10 supplementation in ataxia (ARCA2).
Cerebellum & ataxias
BACKGROUND:The recessive ataxia ARCA2 is a rare disorder characterized by Coenzyme Q10 (CoQ10) deficiency due to biallelic mutations in gene. Despite the pathophysiological role, available data are not univocal on clinical efficacy of CoQ10 supplementation in ARCA2. Here we described the long-term motor outcome of 4 untreated ARCA2 patients prospectively followed-up for one year after starting CoQ10 oral supplementation (15 mg/kg/day). METHODS:Clinical rating scales (SARA; 9 holes peg test; 6 min walking test; Timed 25-Foot Walk) and videoelectronic gait analysis were performed at baseline and every 6 months (T0, T1, T2) to evaluate the motor performances. Since two patients discontinued the treatment at the 7th month, we could provide comparative analysis between longer and shorter supplementation. RESULTS:At T2, the gait speed (Timed 25-Foot Walk test) significantly differed between patients with long and short treatment; overall, the clinical condition tended to be better in patients continuing CoQ10. CONCLUSIONS:Although preliminarily, this observation suggests that only prolonged and continuous CoQ10 supplementation may induce mild clinical effects on general motor features of ARCA2. Dedicated trials are now necessary to extend and validate such observation.
Evaluating the protective effect of resveratrol, Q10, and alpha-lipoic acid on radiation-induced mice spermatogenesis injury: A histopathological study.
International journal of reproductive biomedicine
BACKGROUND:Testis is one of the most sensitive organs against the toxic effect of ionizing radiation. Exposure to even a low dose of radiation during radiotherapy, diagnostic radiology, or a radiological event could pose a threat to spermatogenesis. This may lead to temporary or permanent infertility or even transfer of genomic instability to the next generations. OBJECTIVE:In this study, we evaluated the protective effect of treatment with three natural antioxidants; resveratrol, alpha lipoic acid, and coenzyme Q10 on radiation-induced spermatogenesis injury. MATERIALS AND METHODS:30 NMRI mice (6-8 wk, 30 5 gr) were randomly divided into six groups (n = 5/each) as 1) control; 2) radiation; 3) radiation + resveratrol; 4) radiation + alpha lipoic acid; 5) radiation + resveratrol + alpha lipoic acid; and 6) radiation+ Q10. Mice were treated with 100 mg/kg resveratrol or 200 mg/kg alpha lipoic acid or a combination of these drugs. Also, Q10 was administered at 200 mg/kg. All treatments were performed daily from two days before to 30 min before irradiation. Afterward, mice were exposed to 2 Gy Co gamma rays; 37 days after irradiation, the testicular samples were collected and evaluated for histopathological parameters. RESULTS:Results showed that these agents are able to alleviate some toxicological parameters such as basal lamina and epididymis decreased sperm density. Also, all agents were able to increase Johnsen score. However, they could not protect against radiation-induced edema, atrophy of seminiferous tubules, and hyperplasia in Leydig cells. CONCLUSION:This study indicates that resveratrol, alpha-lipoic acid, and Q10 have the potential to reduce some of the side effects of radiation on mice spermatogenesis. However, they cannot protect Leydig cells as a source of testosterone and seminiferous tubules as the location of sperm maturation.
Microarray expression studies on bone marrow of patients with Shwachman-Diamond syndrome in relation to deletion of the long arm of chromosome 20, other chromosome anomalies or normal karyotype.
BACKGROUND:Clonal chromosome changes are often found in the bone marrow (BM) of patients with Shwachman-Diamond syndrome (SDS). The most frequent ones include an isochromosome of the long arm of chromosome 7, i (7)(q10), and an interstitial deletion of the long arm of chromosome 20, del (20)(q). These two imbalances are mechanisms of somatic genetic rescue. The literature offers few expression studies on SDS. RESULTS:We report the expression analysis of bone marrow (BM) cells of patients with SDS in relation to normal karyotype or to the presence of clonal chromosome anomalies: del (20)(q) (five cases), i (7)(q10) (one case), and other anomalies (two cases). The study was performed using the microarray technique considering the whole transcriptome (WT) and three gene subsets selected as relevant in BM functions. The expression patterns of nine healthy controls and SDS patients with or without chromosome anomalies in the bone marrow showed clear differences. CONCLUSIONS:There is a significant difference between gene expression in the BM of SDS patients and healthy subjects, both at the WT level and in the selected gene sets. The deletion del (20)(q), with the gene consistently lost, even in patients with the smallest losses of material, changes the transcription pattern: a low proportion of abnormal cells led to a pattern similar to SDS patients without acquired anomalies, whereas a high proportion yields a pattern similar to healthy subjects. Hence, the benign prognostic value of del (20)(q). The case of i (7)(q10) showed a transcription pattern similar to healthy subjects, paralleling the positive prognostic role of this anomaly as well.
Efficacy of eye drops containing crosslinked hyaluronic acid and CoQ10 in restoring ocular health exposed to chlorinated water.
European journal of ophthalmology
PURPOSE:A prospective, open-label study in 20 professional swimmers evaluated the efficacy and safety of an ophthalmic solution containing crosslinked hyaluronic acid, coenzyme Q10, and vitamin E TPGS in releasing eye irritation and restoring ocular surface damages after prolonged exposure to chlorinated water. METHODS:Individually, one eye was instilled with the ophthalmic solution and the other used as a comparator. Eye drops were self-administered three times a day for 2 months. Tear film breakup time (primary endpoint), Schirmer I test, beating of eyelashes/min, tear osmolarity, corneal and conjunctival staining with fluorescein, Ocular Surface Disease Index questionnaire, subject satisfaction, visual acuity (secondary endpoints), and Efron Grading Scale were evaluated at screening/baseline (V1), week 1 (V2), week 2 (V3), week 4 (V4), and week 8 (V5). RESULTS:After 2 months, breakup time test significantly improved in the treated eyes (+1.67 s) compared to control (-3.00 s) ( = 0.0002). Corneal and conjunctival surfaces of treated eyes recovered significantly compared to control eyes when assessed by fluorescein staining ( < 0.0001), Ocular Surface Disease Index ( < 0.05), and visual analog scale ( = 0.0348) scores. Improvements were also observed with Schirmer I test, beating of eyelashes, and tear osmolarity, despite without statistical significance. Efron Grading Scale was consistent with the other tests. The ocular tolerability was excellent. CONCLUSION:The adequate combination of crosslinked hyaluronic acid, coenzyme Q10, and vitamin E TPGS, contained in the ophthalmic solution VisuXL, has been shown to protect ocular surface from potential damages originating from prolonged exposure to chlorinated water. VisuXL may represent a compelling treatment in other situations beyond dry eye syndrome.
Therapeutic Effects of the Combination of Alpha-Lipoic Acid (ALA) and Coenzyme Q10 (CoQ10) on Cisplatin-Induced Nephrotoxicity.
International journal of inflammation
BACKGROUND:Nephrotoxicity of cisplatin has been recognized since its introduction more than 25 years ago. However, despite intense efforts to develop less toxic and equally effective alternatives, cisplatin continues to be widely prescribed. . The study is aimed at assessing the possible prophylactic effect of coenzyme Q10 (CoQ10) and alpha-lipoic acid (ALA) (separately or in combination) on experimentally cisplatin-induced nephrotoxicity. . An experimental study was performed on adult male albino rats ( = 40), weighing 200-250 g. Rats were randomly divided into 5 groups: group I (normal saline control), group II (cisplatin control), group III (CoQ10 and cisplatin), group IV (ALA and cisplatin), and group V (CoQ10, ALA, and cisplatin). CoQ10 and/or ALA were given as pretreatment for 9 days, followed by cisplatin injection in the 10th day of the study, followed by a short posttreatment course for 3 days. Renal functions, tissue antioxidant activity, and inflammatory markers (tumor necrosis factor, TNF) were estimated along with histopathological study. RESULTS:Renal function tests and urinary proteins were significantly higher within group II compared with other groups ( value <0.001). Creatinine clearance was significantly higher with combination therapy (group V compared to other groups). Both TNF and malondialdehyde (MDA) were significantly higher within group II whereas GSH content, catalase, and superoxide dismutase (SOD) were significantly lower in group II. MDA level was significantly lower when combination therapy was used. Marked renal damage was histologically detected in the cisplatin group, whereas the least renal damage was noticed in the combination group. CONCLUSION:The study confirmed the role of antioxidants in preventing nephrotoxicity caused by cisplatin; the prophylactic effect of combined therapy with CoQ10 and ALA is superior to that of monotherapy.
Coenzyme Q10 coadministration with diclofenac augmented impaired renal function in broiler chickens (.
AIM:This study aimed to investigate the effects of coenzyme Q10 (COQ10) and diclofenac coadministration on the hepatorenal function in broiler chickens (). MATERIALS AND METHODS:Birds (21 days old) were divided into six groups of eight birds each. The 1 group was the control, the 2 group was treated orally with COQ10(30mg/kg b.wt), the 3and 4groups were treated intraperitoneally with diclofenac sodium at doses 1 and 2mg/kg b.wt, respectively, and the 5and 6groups were treated with COQ10 (dose 30mg/kg b.wt, P.O.) and diclofenac sodium (dose 1mg/kg b.wt, I.P.) and COQ10 (dose 30mg/kg b.wt, P.O.) and diclofenac sodium (dose 2mg/kg b.wt, I.P.), respectively. The experiment lasted 5days. Twenty-four hours after the last administration, all the birds were sacrificed through cervical dislocation; blood samples were collected for serum biochemical analysis. RESULTS:COQ10 induced a significant increase in aspartate aminotransferase (AST), urea, creatinine, sodium, potassium, and chloride, while diclofenac induced a significant increase in alanine aminotransferase (ALT), AST, total cholesterol, triglyceride, high-density lipoprotein, urea, creatinine, sodium, potassium, and chloride. However, when COQ10 and diclofenac were coadministered, we observed that COQ10 decreased the liver injury caused by diclofenac. However, COQ10 could not relieve the kidney injury caused by diclofenac, but worsened the impaired renal function. CONCLUSION:COQ10 protects the liver against diclofenac-induced liver injury while augmenting diclofenac-induced kidney injury.
mutation in patients with nephrotic syndrome, sensorineural deafness, and optic atrophy.
INTRODUCTION:Primary coenzyme Q10 (CoQ10) deficiencies are a group of mitochondrial disorders that has proven responsiveness to replacement therapy. Mutations in enzymes involved in the biosynthesis of CoQ10 genes are associated with these deficits. The clinical presentation of this rare autosomal recessive disorder is heterogeneous and depends on the gene involved. Mutations in the , and genes are responsible for steroid-resistant nephrotic syndrome (SRNS), which is associated with extra-renal symptoms. Previous studies have reported mutations in 11 patients from five different families presenting with SRNS and sensorineural deafness. CASE REPORTS:Our study reports the cases of two brothers of Turkish origin with renal failure and sensorineural deafness associated with mutations responsible of CoQ10 deficiency. Optical symptoms were present in the eldest, that improved with Idebenone. CONCLUSION/DISCUSSION:For the first time, mutation with optical involvement is associated with renal and hearing impairment. Although the response to replacement CoQ10 therapy was difficult to evaluate, we think that this treatment was able to stop the disease progression in both patients, and even to prevent the occurrence/development of optical and neurological impairment in the younger brother. Mitochondrial dysfunction secondary to CoQ10 deficiency should always be suspected in patients with SRNS and extra-renal symptoms. Early recognition of this genetic SRNS is mandatory since SRNS can be avoided by adequate treatment based on CoQ10 supplement or an analogue. All cases of primary CoQ10 deficiency should be treated at an early stage to limit the progression of lesions and prevent the emergence of new symptoms.
Nano-Encapsulation of Coenzyme Q10 in Secondary and Tertiary Nano-Emulsions for Enhanced Cardioprotection and Hepatoprotection in Human Cardiomyocytes and Hepatocytes During Exposure to Anthracyclines and Trastuzumab.
International journal of nanomedicine
INTRODUCTION:CoenzymeQ (CoQ) is a well-known antioxidant and anti-inflammatory agent with cardioprotective properties. However, clinical trials based on its oral administration have failed to provide significant effect on cardiac functionality. The main limitation of CoQ is based on its very low oral bioavailability and instability that limit dramatically its effects as a cardioprotective agent. Herein, we loaded CoQ in high bioavailable nano-emulsions (NEs) coated with chitosan or chitosan and hyaluronic acid in order to improve its performance. METHODS:We tested cardioprotective and hepatoprotective effects of CoQ-loaded nano-carriers against Doxorubicin and Trastuzumab toxicities in cardiomyocytes and liver cells through analysis of cell viability, lipid peroxidation, expression of leukotrienes, p65/NF-kB and pro-inflammatory cytokines involved in anticancer-induced cardio and hepatotoxicity. RESULTS:Nano-carriers showed high stability and loading ability and increased cell viability both in hepatocytes and cardiomyocytes during anticancer treatments. We observed that these effects are mediated by the inhibition of lipid peroxidation and reduction of the inflammation. CoQ-loaded nano-emulsions showed also strong anti-inflammatory effects reducing leukotriene B4 and p65/NF-κB expression and Interleukin 1β and 6 production during anticancer treatments. DISCUSSION:Anthracyclines and Human epidermal growth factor receptor (HER2) inhibitors have shown significant anticancer effects in clinical practice but their use is characterized by cardiotoxicity and hepatotoxicity. Nano-carriers loaded with CoQ showed cardio and hepatoprotective properties mediated by reduction of oxidative damages and pro-inflammatory mediators. These results set the stage for preclinical studies of cardio and hepatoprotection in HER2+ breast cancer-bearing mice treated with Doxorubicin and Trastuzumab.
Coenzyme Q10 and Silymarin Reduce CCl-Induced Oxidative Stress and Liver and Kidney Injury in Ovariectomized Rats-Implications for Protective Therapy in Chronic Liver and Kidney Diseases.
Lamia Samanta Sifat,Emran Tushar,Rikta Jubaida Khatun,Chowdhury Nowreen Islam,Sarker Manoneeta,Jain Preeti,Islam Tabinda,Gias Zarin Tasnim,Shill Manik Chandra,Reza Hasan Mahmud
Pathophysiology : the official journal of the International Society for Pathophysiology
Oxidative stress is one of the key factors in the pathophysiology of liver disease. The present study aimed to evaluate the potential impact of two antioxidants, namely coenzyme Q10 (CoQ10) and silymarin, on carbon tetrachloride (CCl)-induced oxidative stress and hepatic damage in ovariectomized rats. Female Long Evans rats were divided into six groups (n = 6): control, CCl, CCl + CoQ10 (200 mg/kg), CCl + silymarin (140 mg/kg), Control + CoQ10, and Control + silymarin. Plasma and tissues from liver and kidney were analyzed for oxidative stress parameters and antioxidant enzyme activities using biochemical assays. Infiltration of inflammatory cells and fibrosis were assessed by histological staining of tissue sections. Both CoQ10 and silymarin significantly lowered serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) levels that were detected to be higher in CCl rats compared to controls. Significant reduction in CCl-induced elevated levels of oxidative stress markers malondialdehyde (MDA), nitric oxide (NO), and advanced protein oxidation product (APOP) was observed with both antioxidants. However, in control rats, CoQ10 and silymarin did not produce a significant effect. Histological analysis revealed that CCl markedly increased the level of inflammatory cells infiltration and fibrosis in liver and kidney tissues, but this was significantly reduced in CCl + CoQ10 and CCl + silymarin groups. Taken together, our results suggest that CoQ10 and silymarin can protect the liver against oxidative damage through improved antioxidant enzyme activities and reduced lipid peroxidation. Thus, supplementation of the aforementioned antioxidants may be useful as a therapeutic intervention to protect liver health in chronic liver diseases.
Efficacy of coenzyme Q10 in supportive therapy of the cardiovascular diseases and in the prevention of cardiotoxicity caused by chemotherapy.
Miedziaszczyk Miłosz,Cieślewicz Artur,Jabłecka Anna
Polski merkuriusz lekarski : organ Polskiego Towarzystwa Lekarskiego
Cardiovascular diseases are the most common cause of death in Poland and in the world. People with cardiovascular disease or high cardiovascular risk require early detection and pharmacotherapy. New methods of prevention and treatment are needed. Coenzyme Q10 (CoQ10) is an essential component of the human body. CoQ10 plays an important role in the biosynthesis of adenosine-5'-triphosphate (ATP) and has antioxidant activity. More and more evidence indicates that CoQ10 is closely related to cardiovascular disorders. Its supplementation may be beneficial in various chronic and acute disorders. Coenzyme Q10 used in heart failure reduces mortality and improves exercise capacity. CoQ10 can reduce the values of systolic blood pressure (SBP) and diastolic blood pressure (DBP) in hypertensive patients. CoQ10 supplementation prevents electrocardiographic (ECG) changes in patients taking doxorubicin and has a positive effect on heart function during anthracycline chemotherapy. The review article was based on available literature found in the Medline database and includes preclinical and clinical research. Further research related to CoQ10 can contribute to significant progress in the prevention and treatment of cardiovascular diseases but may also be the basis for increasing the range of indications for this drug.
Effects of coenzyme Q10 supplementation on statin-induced myopathy: a meta-analysis of randomized controlled trials.
Wei Han,Xin Xiaojun,Zhang Jing,Xie Qingya,Naveed Muhammad,Kaiyan Chen,Xiao Pingxi
Irish journal of medical science
BACKGROUND:Statins can trigger a series of muscle-related adverse events, commonly referred to collectively as statin-induced myopathy. Although coenzyme Q10 (CoQ10) is widely used as a supplement in statin therapy, there is little clinical evidence for this practice. AIM:This study aims to assess the effect of adding CoQ10 on statin-induced myopathy. METHODS:Searching the PubMed, EMBASE, and the Cochrane Library databases to identify randomized controlled trials investigating the effect of adding CoQ10 on creatine kinase (CK) activity and degree of muscle pain as two indicators of statin-induced myopathy. Two reviewers will independently extract data from the included articles. RESULTS:Study screening included a randomized controlled trial of oral CoQ10 versus placebo in patients with statin-induced myopathy. We had a total of 8 studies in which 472 patients were treated with statins: 6 studies with 281 participants assessed the impact of adding CoQ10 on CK activity, and 4 studies with 220 participants were included to evaluate the impacts of CoQ10 addition on muscle pain. Compared with the controls, CK activity increased after adding CoQ10, but the change was not significant (mean difference, 3.29 U/L; 95% CI, - 29.58 to 36.17 U/L; P = 0.84). Similarly, the meta-analysis did not benefit CoQ10 over placebo in improving muscle pain (standardized mean difference, - 0.59; 95% CI, - 1.54 to 0.36; P = 0.22). CONCLUSION:The outcomes of this meta-analysis of existing randomized controlled trials showed that supplementation with CoQ10 did not have any significant benefit in improving statin-induced myopathy.
Neuroprotective effects of coenzyme Q10 in Parkinson's model via a novel Q10/miR-149-5p/MMPs pathway.
Ghasemloo Elham,Mostafavi Hossein,Hosseini Masoumeh,Forouzandeh Meysam,Eskandari Mehdi,Mousavi Seyyed Saeid
Metabolic brain disease
Parkinson's disease (PD) is a complex neurodegenerative disease in which the understanding of the underlying molecular mechanisms can be constructive in the diagnosis and treatment. Matrix metalloproteinase (MMPs) elevation and damage to the blood-brain barrier (BBB) are critical mechanisms involved in the PD separation. Studies have revealed that changes in miR-149-5p and CoQ10 are associated with BBB damage, and CoQ10 can affect the levels of some miRs. Hence, in the present study, we aimed to evaluate CoQ10 and miR-149-5p mimic on miR-149-5p, MMPs and TH expression, and behavioral functions of the PD models. PD was induced by injection of 6-OHDA into the rats' Medial Forbrain Bundle (MFB). The behavioral tests, including the Rotation test, Rotarod test, and Open field test, have been directed two weeks after PD induction. Next, the MiR-149-5p mimic (miR-mimic) and CoQ10 have been administered to rats. The same behavioral tests have been evaluated two weeks after administration to investigate the effect of miR-149-5p mimic and CoQ10. The rats were followed extra four weeks, and the behavioral tests have performed again. Finally, the expression of MMPs and miR-149-5p genes was measured using RT-qPCR, and tyrosine hydroxylase (TH) was assessed through immunohistochemistry analysis. According to the obtained results, the level of miR-149-5p has decreased, followed by PD induction in rats. RT-qPCR analysis has represented upregulation and downregulation of miR-149-5p and MMP-2,9, respectively, after miR-mimic and CoQ10 treatment. The treated rats have also represented improved motor function and increased TH + cells in the striatum according to the behavioral tests and immunohistochemistry assay. Taking together miR-149 and CoQ10 has shown to have an impressive potential to prevent damage to dopaminergic neurons caused by 6-OHDA injection through reducing MMP-2,9, increased TH expression, and improved motor function.
Coenzyme Q10 ameliorates the quality of mouse oocytes during culture.
Lee Chan Hee,Kang Min Kook,Sohn Dong Hyun,Kim Hye Min,Yang Juri,Han Seung Jin
Zygote (Cambridge, England)
Oxidative stress causes several diseases and dysfunctions in cells, including oocytes. Clearly, oxidative stress influences oocyte quality during in vitro maturation and fertilization. Here we tested the ability of coenzyme Q10 (CoQ10) to reduce reactive oxygen species (ROS) and improve mouse oocyte quality during in vitro culture. Treatment with 50 μM CoQ10 efficiently reduced ROS levels in oocytes cultured in vitro. The fertilizable form of an oocyte usually contains a cortical granule-free domain (CGFD). CoQ10 enhanced the ratio of CGFD-oocytes from 35% to 45%. However, the hardening of the zona pellucida in oocytes was not affected by CoQ10 treatment. The in vitro maturation capacity of oocytes, which was determined by the first polar body extrusion, was enhanced from 48.9% to 75.7% by the addition of CoQ10 to the culture medium. During the parthenogenesis process, the number of two-cell embryos was increased by CoQ10 from 43.5% to 67.3%. Additionally, treatment with CoQ10 increased the expression of Bcl2 and Sirt1 in cumulus cells. These results suggested that CoQ10 had a positive effect on ROS reduction, maturation rate and two-cell embryo formation in mouse oocyte culture.
Systematic Review and Meta-analysis on Effect of Carnitine, Coenzyme Q10 and Selenium on Pregnancy and Semen Parameters in Couples With Idiopathic Male Infertility.
OBJECTIVE:To study the effect of 3 antioxidants viz. selenium, carnitine and coenzyme Q10, alone or in combination, on both semen parameters and pregnancy rates in couples with male factor infertility. METHODS:Using PRISMA guidelines, a systematic search was performed of the PubMed, Scopus, EMBASE, and Web of Science databases for randomized studies comparing selenium, carnitine or coenzyme Q10 with placebo in the treatment of male infertility and reporting semen and pregnancy outcomes. RESULTS:A total of 3304 studies were screened of which 20 were included. The study protocol was registered with PROSPERO (CRD42020210284). Pregnancy rate in the treatment group (69/426, 16.2%) was not different from the placebo (45/401, 11.2%) (P = .05). Treatment group showed higher motility [mean difference 5.05, 95% CI (2.77, 7.34), P =<.0001], progressive motility [mean difference 5.72, 95% CI (2.77, 8.66), P = .0001], sperm concentration [mean difference 6.58, 95% CI (3.22, 9.93), P = .0001] than placebo. CONCLUSION:Although antioxidants and their combinations are associated with improvement in sperm concentration, motility, and semen volume, the differences are small. There is no difference in pregnancy rates between patients receiving selenium, carnitine, and coenzyme Q10, or placebo. The quality of studies is poor, limiting the level of evidence.
Possible protective effects of CO Q10 against vincristine-induced peripheral neuropathy: Targeting oxidative stress, inflammation, and sarmoptosis.
Elshamy Amira M,Salem Ola M,Safa Mohamed A E,Barhoma Ramez A E,Eltabaa Eman F,Shalaby Amany M,Alabiad Mohamed A,Arakeeb Heba M,Mohamed Hoda A
Journal of biochemical and molecular toxicology
Vincristine is a chemotherapy drug that belongs to the vinca alkaloids group. It is used for treatment of hematologic malignancies and several solid tumors. Vincristine-induced peripheral neuropathy is a major dose-limiting side effect. Coenzyme Q10 (Co Q10), an essential component of the mitochondrial electron transport chain, participates in energy production. It is a powerful fat-soluble antioxidant and also exerts anti-inflammatory effects. Therefore, this study was aimed to focus on the mechanistic insights of vincristine-induced peripheral neuropathy in addition to shedding the light on the modulatory effect of Co Q10. Twenty-eight rats were randomly divided into four groups. Peripheral neuropathy was induced by intraperitoneal injection of vincristine (0.1 mg/kg body weight). Co Q10 was injected intraperitoneally (10 mg/kg body weight) for 24 days. Sciatic nerve MDA, TAC, GSH, 8-OHdG, TNF-α, IL-1β, and NF-κB levels were assessed. Gene expression of SARM1 and Nrf2 was also assessed. Serum neurofilament light chain was immunoassayed, in addition to the behavioral assessment. Co Q10 significantly improved oxidative stress and inflammatory biomarkers. It also decreased serum NFL levels. It enhanced Nrf2 and decreased SARM1 gene expression. Histopathological findings proved the biochemical and molecular findings. Our results support Co Q10 as a potential protective agent against vincristine-induced peripheral neuropathy.
CoQ10 Promotes Resolution of Necrosis and Liver Regeneration After Acetaminophen-Induced Liver Injury.
Chen Shen,Tang Yi,Fang Wanjun,He Taiping,Chen Xu,Zhang Peiwen
Toxicological sciences : an official journal of the Society of Toxicology
Coenzyme Q10 (CoQ10) which acts as an electron transporter in the mitochondrial respiratory chain has many beneficial effects on liver diseases. In our previous research, CoQ10 has been found to attenuate acetaminophen (APAP)-induced acute liver injury (ALI). However, whether CoQ10 administration is still effective at the late stage of APAP overdose is still unknown. In this study, we aimed to test CoQ10 efficacy at the late stage of APAP overdose. C57BL/6J mice were intraperitoneally treated with APAP to induce liver injury. CoQ10 (5 mg/kg) was given to mice at 16 h after APAP treatment. The results showed that while CoQ10 treatment at 16 h post-APAP overdose had no effects on the expression of ROS generated genes or scavenged genes, it still significantly decreased necrosis of hepatocytes following APAP-induced ALI. Moreover, CoQ10 increased MerTK+ macrophages accumulation in the APAP-overdose liver and inhibition of MerTK signaling partly abrogated the protective role of CoQ10 treatment on the hepatic necrosis. CoQ10 treatment also significantly enhanced hepatocytes proliferation as shown in the increased 5-bromodeoxyuridine incorporation in the APAP-intoxicated mice liver section. In addition, CoQ10 treatment increased hepatic Proliferating Cell Nuclear Antigen (PCNA) and Cyclin D1 expression and promoted activation of the β-catenin signaling in APAP-overdose mice. To conclude, these data provide evidence that CoQ10 treatment is still effective at the late stage of APAP-induced ALI and promotes resolution of necrosis and liver regeneration following ALI.
Coenzyme Q10 effects in neurological diseases.
Coenzyme Q10 (CoQ10), a lipophilic substituted benzoquinone, is present in animal and plant cells. It is endogenously synthetized in every cell and involved in a variety of cellular processes. CoQ10 is an obligatory component of the respiratory chain in inner mitochondrial membrane. In addition, the presence of CoQ10 in all cellular membranes and in blood. It is the only endogenous lipid antioxidant. Moreover, it is an essential factor for uncoupling protein and controls the permeability transition pore in mitochondria. It also participates in extramitochondrial electron transport and controls membrane physicochemical properties. CoQ10 effects on gene expression might affect the overall metabolism. Primary changes in the energetic and antioxidant functions can explain its remedial effects. CoQ10 supplementation is safe and well-tolerated, even at high doses. CoQ10 does not cause any serious adverse effects in humans or experimental animals. New preparations of CoQ10 that are less hydrophobic and structural derivatives, like idebenone and MitoQ, are being developed to increase absorption and tissue distribution. The review aims to summarize clinical and experimental effects of CoQ10 supplementations in some neurological diseases such as migraine, Parkinson´s disease, Huntington´s disease, Alzheimer´s disease, amyotrophic lateral sclerosis, Friedreich´s ataxia or multiple sclerosis. Cardiovascular hypertension was included because of its central mechanisms controlling blood pressure in the brainstem rostral ventrolateral medulla and hypothalamic paraventricular nucleus. In conclusion, it seems reasonable to recommend CoQ10 as adjunct to conventional therapy in some cases. However, sometimes CoQ10 supplementations are more efficient in animal models of diseases than in human patients (e.g. Parkinson´s disease) or rather vague (e.g. Friedreich´s ataxia or amyotrophic lateral sclerosis).
Coenzyme Q10 Supplement Rescues Postovulatory Oocyte Aging by Regulating SIRT4 Expression.
Xing Xupeng,Zhang Jinjing,Zhang Jingcheng,Wang Yongsheng,Wang Jingyi,Kang Jian,Quan Fusheng,Su Jianmin,Zhang Yong
Current molecular pharmacology
BACKGROUND:High-quality of the oocyte is crucial for embryo development and the success of human-assisted reproduction. The postovulatory aged oocytes lose developmental competence with mitochondrial dysfunction and oxidative stress. Coenzyme Q10 (CoQ10) is widely distributed in the membranes of cells and has an important role in the mitochondrial respiration chain against oxidative stress and modulation of gene expression. OBJECTIVE:The objective of this study is to investigate the functions and mechanisms of CoQ10 on delaying postovulatory oocyte aging. METHODS:Quantitative real-time PCR and Immunofluorescence staining were used to determine the expression patterns of the biogenesis genes of CoQ10 in postovulatory aged oocytes compared with fresh oocytes. The mitochondrial function, apoptosis, reactive oxygen species (ROS) accumulation and spindle abnormalities were investigated after treatment with 10 μM CoQ10 in aged groups. SIRT4 siRNA or capped RNA was injected into oocytes to investigate the function of SIRT4 on postovulatory oocyte aging and the relationship between CoQ10 and SIRT4. RESULTS:Multiple CoQ10 biosynthesis enzymes are insufficient, and a supplement of CoQ10 can improve oocyte quality and elevate the development competency of postovulatory aged oocytes. CoQ10 can attenuate the aging-induced abnormalities, including mitochondrial dysfunction, ROS accumulation, spindle abnormalities, and apoptosis in postovulatory aged oocytes. Furthermore, SIRT4, which was first found to be up-regulated in postovulatory aged oocytes, decreased following CoQ10 treatment. Finally, knockdown of SIRT4 can rescue aging-induced dysfunction of mitochondria, and the efficiency of CoQ10 rescuing dysfunction of mitochondria can be weakened by SIRT4 overexpression. CONCLUSION:Supplement of CoQ10 protects oocytes from postovulatory aging by inhibiting SIRT4 increase.
Effects of Quercetin and Coenzyme Q10 on Biochemical, Molecular, and Morphological Parameters of Skeletal Muscle in Trained Diabetic Rats.
Youssef Amal M,Mohamed Dalia A,Hussein Samia,Abdullah Doaa M,Abdelrahman Shaimaa A
Current molecular pharmacology
BACKGROUND:Diabetes mellitus (DM) affects the musculoskeletal system through its metabolic perturbations. Exercise modulates blood sugar levels and increases the body's sensitivity to insulin in patients with DM. OBJECTIVE:This study aimed to investigate the potential effects of combined quercetin and coenzyme Q10 (CoQ10) supplements with or without exercise on the histological, biochemical and molecular structures of diabetic rat's skeletal muscle Methods: A total of 64 adult male albino rats were divided into six groups: control, trained nondiabetic, non-trained diabetic, diabetic rats treated with combined CoQ10 and quercetin, diabetic rats with treadmill training, and diabetic rats treated with treadmill training and CoQ10 and quercetin. Blood and skeletal muscle samples were obtained from all groups for routine histological examination and biochemical determination of cytokine levels and protein activities. Quantitative real-time polymerase chain reaction (qRT-PCR) and morphometric analysis of PAS and Bax expressions were also performed. RESULTS:Biochemical analysis revealed improvement in all studied parameters with combined Co- Q10 and quercetin than exercise training alone. Combined treatment and exercise showed significant improvement in all parameters especially interleukin 6 and malondialdehyde. Fibronectin type III domain-containing protein 5 (FNDC5) expression and irisin levels increased in all trained groups but combined treatment with exercise significantly increased their levels than exercise alone. Histological analysis revealed improvement after exercise or combined treatment; however, when exercise was combined with CoQ10 and quercetin, marked improvement was observed. CONCLUSION:the combination of CoQ10 and quercetin could be promising in preserving musculoskeletal function in patients with DM concomitantly with physical exercise.
Potential Protective Effect of Coenzyme Q10 on Doxorubicin-Induced Neurotoxicity and Behavioral Disturbances in Rats.
Okudan Nilsel,Belviranlı Muaz,Sezer Tuğba
The aim of this study was to investigate the potential neuroprotective efficacy of coenzyme Q10 (CoQ10) against doxorubicin (DOX) -induced behavioral disturbances in rats. Female rats were randomly assigned into 4 groups as control, CoQ10, DOX, and DOX plus CoQ10. The CoQ10 groups received CoQ10 (200 mg kg) for 21 days, and the DOX groups received DOX (4 mg kg) on days 7 and 14 of the study. The open field (OF) and elevated plus maze (EPM) tests were performed to assess locomotor activity and anxiety levels. Additionally, malondialdehyde (MDA), and protein carbonyl (PC) levels and acetylcholinesterase (AChE), and glutathione peroxidase (GPx) activities and total antioxidant capacity (TAC) were quantified in brain tissue. DOX administration caused alterations in locomotor activity, and anxiety-like behaviors. Moreover, DOX produced significant elevation in AChE activity . PC level and GPx activity tended to alter with DOX administration. Co-treatment with CoQ10 significantly attenuated DOX-induced behavioral alterations via improving AChE activity in the brain tissue of rats. CoQ10 treatment may be potential for the alleviation of DOX-induced behavioral disturbances. This improvement might be due to the inhibition of AChE activity.
Coenzyme Q10 reduces expression of apoptotic markers in adult rat nucleus accumbens dopaminergic neurons treated with methamphetamine.
Jameie S B,Kazemian A,Sanadgol Z,Asadzadeh Bayqara S,Jameie Mana Sadat,Farhadi M
Molecular biology reports
BACKGROUND:Abuse of addictive drugs such as methamphetamine (METH) has become a global problem, leading to many social, economic, and health disturbances, including neurological and cognitive disorders. Neuronal damage is reported in chronic METH abusers. The neuroprotective role of CoQ10 has been shown in many studies. In the present study, we aimed to assess the pre and post-efficacy of CoQ10 on the dopaminergic neurons of the Nucleus Accumbens (de Miranda et al. in Food Res Int 121:641-647, 2019) in the male adult rats treated with METH. METHODS:80 rats were randomly divided into eight groups (n = 10), including: negative control (intact), positive control (received 5 mg/kg/day METH/IP), three post-treatment groups (METH + 5, 10, 20 mg/kg CoQ10) and three pre-treatment groups (received 5, 10, 20 mg/kg CoQ10 as pre-treatment for 14 days before METH injection). The expression of Bax, Bcl-2, Bax/Bcl-2 ratio, P53, Caspase-3 and tyrosine hydroxylase in NAc studied using western blotting. Nissl staining was used to study the neuronal density of NAc. RESULTS:Our results showed that the different doses of CoQ10 in METH-treated animals significantly changed pro-apoptotic proteins' expression in the benefit of neuronal survival of NAc (P < 0.05). Neuronal density in NAc were significantly lower in the METH group compared to the control and CoQ10 treated groups. Pre- and post-treatment with different doses of CoQ10 restored the neuronal damage in NAc. CONCLUSIONS:CoQ10 could decrease the activation of pro-apoptotic proteins and reduce the neurodegenerative effects induced by METH. From a clinical point of view, it seems that certain antioxidants such as CoQ10 should receive more attention in clinical trial research. We believe that antioxidants could be the promising for drug abuse treatment in the future.
Targeting coenzyme Q10 synthesis overcomes bortezomib resistance in multiple myeloma.
Zaal Esther A,de Grooth Harm-Jan,Oudaert Inge,Langerhorst Pieter,Levantovsky Sophie,van Slobbe Gijs J J,Jansen Jeroen W A,Menu Eline,Wu Wei,Berkers Celia R
During the development of drug resistance, multiple myeloma (MM) cells undergo changes to their metabolism. However, how these metabolic changes can be exploited to improve treatment efficacy is not known. Here we demonstrate that targeting coenzyme Q10 (CoQ) biosynthesis through the mevalonate pathway works in synergy with the proteasome inhibitor bortezomib (BTZ) in MM. We show that gene expression signatures relating to the mitochondrial tricarboxylic acid (TCA) cycle and electron transport chain (ETC) predispose to clinical BTZ resistance and poor prognosis in MM patients. Mechanistically, BTZ-resistant cells show increased activity of glutamine-driven TCA cycle and oxidative phosphorylation, together with an increased vulnerability towards ETC inhibition. Moreover, BTZ resistance is accompanied by high levels of the mitochondrial electron carrier CoQ, while the mevalonate pathway inhibitor simvastatin increases cell death and decreases CoQ levels, specifically in BTZ-resistant cells. Both and , simvastatin enhances the effect of bortezomib treatment. Our study links CoQ synthesis to drug resistance in MM and provides a novel avenue for improving BTZ responses through statin-induced inhibition of mitochondrial metabolism.
Systematic Understanding of Anti-Aging Effect of Coenzyme Q10 on Oocyte Through a Network Pharmacology Approach.
Yang Liuqing,Wang Heng,Song SuJie,Xu Hongbin,Chen Yun,Tian Saisai,Zhang Yiqun,Zhang Qin
Frontiers in endocrinology
Background:Maternal oocyte aging is strongly contributing to age-related decline in female fertility. Coenzyme Q10 (CoQ10) exerts positive effects in improving aging-related deterioration of oocyte quality, but the exact mechanism is unclear. Objective:To reveal the system-level mechanism of CoQ10's anti-aging effect on oocytes based on network pharmacology. Methods:This study adopted a systems network pharmacology approach, including target identification, data integration, network and module construction, bioinformatics analysis, molecular docking, and molecular dynamics simulation. Result:A total of 27 potential therapeutic targets were screened out. Seven hub targets (PPARA, CAT, MAPK14, SQSTM1, HMOX1, GRB2, and GSR) were identified. Functional and pathway enrichment analysis indicated that these 27 putative targets exerted therapeutic effects on oocyte aging by regulating signaling pathways (e.g., PPAR, TNF, apoptosis, necroptosisn, prolactin, and MAPK signaling pathway), and are involved oxidation-reduction process, mitochondrion, enzyme binding, reactive oxygen species metabolic process, ATP binding, among others. In addition, five densely linked functional modules revealed the potential mechanisms of CoQ10 in improving aging-related deterioration of oocyte quality are closely related to antioxidant, mitochondrial function enhancement, autophagy, anti-apoptosis, and immune and endocrine system regulation. The molecular docking study reveals that seven hub targets have a good binding affinity towards CoQ10, and molecular dynamics simulation confirms the stability of the interaction between the hub targets and the CoQ10 ligand. Conclusion:This network pharmacology study revealed the multiple mechanisms involved in the anti-aging effect of CoQ10 on oocytes. The molecular docking and molecular dynamics simulation provide evidence that CoQ10 may act on these hub targets to fight against oocytes aging.
Comparison of the effects of coenzyme Q10 and Centrum multivitamins on semen parameters, oxidative stress markers, and sperm DNA fragmentation in infertile men with idiopathic oligoasthenospermia.
Alahmar Ahmed T,Singh Rajender
Clinical and experimental reproductive medicine
OBJECTIVE:Oxidative stress and sperm DNA fragmentation (SDF) have been linked to idiopathic male infertility (IMI). Various antioxidants have been tried to improve semen parameters and fertility potential in IMI patients, but with inconsistent results. The study aimed to compare the effects of coenzyme Q10 (CoQ10) and Centrum multivitamins on semen parameters, seminal antioxidant capacity, and SDF in infertile men with idiopathic oligoasthenospermia (OA). METHODS:This prospective controlled clinical study involved 130 patients with idiopathic OA and 58 fertile controls. The patients were divided randomly into two groups: the first group received CoQ10 (200 mg/day orally) and the second group received Centrum multivitamins (1 tablet/day) for 3 months. Semen parameters, CoQ10 levels, reactive oxygen species (ROS), total antioxidant capacity (TAC), catalase, SDF, and serum hormone levels (follicle-stimulating hormone, luteinizing hormone, testosterone, and prolactin) were compared at baseline and after 3 months. RESULTS:Both CoQ10 and Centrum improved sperm concentration and motility, but the improvement was greater with Centrum therapy (p<0.05). Similarly, both therapies improved antioxidant capacity, but TAC and catalase improvement was greater (p<0.01 and p<0.001 respectively) with CoQ10, whereas ROS (p<0.01) and SDF (p<0.001) improvements were greater with Centrum administration. Centrum therapy was associated with reduced serum testosterone (p<0.05). CONCLUSION:In conclusion, both CoQ10 and Centrum were effective in improving semen parameters, antioxidant capacity, and SDF, but the improvement was greater with Centrum than with CoQ10. Therefore, Centrum-as a source of combined antioxidants-may provide more effective results than individual antioxidants such as CoQ10 in the treatment of infertile men with idiopathic OA.
Effects of antioxidant co-supplementation therapy on spermatogenesis dysfunction in relation to the basal oxidation-reduction potential levels in spermatozoa: A pilot study.
Yamasaki Kazumitsu,Uchida Masahiro,Watanabe Noriko,Ihana Tatsuji,Ishiguro Yukari,Kuroda Shinnosuke,Takeshima Teppei,Yumura Yasushi,Mieno Makiko,Yoshida Kaoru,Iwamoto Teruaki,Nishiyama Hiroyuki
Reproductive medicine and biology
Purpose:In this pilot study, the authors compared the effects of antioxidant co-supplementation therapy and methylcobalamin therapy in patients with impaired semen quality. Methods:Eighty-four subjects who visited male infertility clinics and showed abnormal semen test results were randomly subjected to one of the two therapies: antioxidant co-supplementation therapy with vitamin C, vitamin E, coenzyme Q10, and flaxseed oil or methylcobalamin therapy. The oxidation-reduction potential (ORP) and 8-hydroxy-2'-deoxyguanosine levels were used as indicators of oxidative stress levels in semen. Semen analysis was also performed. Results:The authors obtained results from 67 patients who had completed 3 months of treatment. Neither antioxidant co-supplementation therapy nor methylcobalamin therapy changed the semen parameters significantly (except for the sperm concentration, which was increased by the latter therapy). When the pre-treatment ORP value in semen was higher than the cutoff value, both therapies significantly increased the sperm concentration. The 8-hydroxy-2'-deoxyguanosine level did not yield any meaningful predictive value with regard to increased sperm concentrations. Conclusions:Both antioxidant co-supplementation therapy and methylcobalamin therapy increased the sperm concentration in patients with impaired semen quality when the basal ORP levels in their semen were elevated.
Coenzyme Q10 deficiency can be expected to compromise Sirt1 activity.
DiNicolantonio James J,McCarty Mark F,O'Keefe James H
For reasons that remain unclear, endogenous synthesis and tissue levels of coenzyme Q10 (CoQ10) tend to decline with increasing age in at least some tissues. When CoQ10 levels are sufficiently low, this compromises the efficiency of the mitochondrial electron transport chain, such that production of superoxide by site 2 increases and the rate of adenosine triphosphate production declines. Moreover, CoQ10 deficiency can be expected to decrease activities of Sirt1 and Sirt3 deacetylases, believed to be key determinants of health span. Reduction of the cytoplasmic and mitochondrial NAD/NADH ratio consequent to CoQ10 deficit can be expected to decrease the activity of these deacetylases by lessening availability of their obligate substrate NAD The increased oxidant production induced by CoQ10 deficiency can decrease the stability of Sirt1 protein by complementary mechanisms. And CoQ10 deficiency has also been found to lower mRNA expression of Sirt1. An analysis of the roles of Sirt1/Sirt3 in modulation of cellular function helps to rationalise clinical benefits of CoQ10 supplementation reported in heart failure, hypertension, non-alcoholic fatty liver disease, metabolic syndrome and periodontal disease. Hence, correction of CoQ10 deficiency joins a growing list of measures that have potential for amplifying health protective Sirt1/Sirt3 activities.
Efficacy and Safety of Q10 Ubiquinol With Vitamins B and E in Neurodevelopmental Disorders: A Retrospective Chart Review.
Cucinotta Francesca,Ricciardello Arianna,Turriziani Laura,Mancini Arianna,Keller Roberto,Sacco Roberto,Persico Antonio M
Frontiers in psychiatry
Increased oxidative stress and defective mitochondrial functioning are shared features among many brain disorders. The aim of this study was to verify retrospectively the clinical efficacy and safety of a metabolic support therapy with Q10 ubiquinol, vitamin E and complex-B vitamins in various neurodevelopmental disorders. This retrospective chart review study included 59 patients (mean age 10.1 ± 1.2 y.o., range 2.5-39 years; M:F = 2.47:1), diagnosed with Autism Spectrum Disorder ( = 17), Autism Spectrum Disorder with co-morbid Intellectual Disability ( = 19), Intellectual Disability or Global Developmental Delay ( = 15), Attention-Deficit/Hyperactivity Disorder ( = 3) and Intellectual Disability in Phelan-McDermid syndrome due to chr. 22q13.33 deletion ( = 5). After a minimum of 3 months of therapy, a positive outcome was recorded in 45/59 (76.27%) patients, with Clinical Global Impression-Improvement scores ranging between 1 ("very much improved") and 3 ("minimally improved"). The most widespread improvements were recorded in cognition ( = 26, 44.1%), adaptative functioning ( = 26, 44.1%) and social motivation ( = 19, 32.2%). Improvement rates differed by diagnosis, being observed most consistently in Phelan-McDermid Syndrome (5/5, 100%), followed by Intellectual Disability/Global Developmental Delay (13/15, 86.7%), Autism Spectrum Disorder with co-morbid Intellectual Disability (15/19, 78.9%), Autism Spectrum Disorder (11/17, 64.7%) and ADHD (1/3, 33.3%). No significant adverse event or side effect leading to treatment discontinuation were recorded. Mild side effects were reported in 18 (30.5%) patients, with the most frequent being increased hyperactivity (9/59, 15.3%). This retrospective chart review suggests that metabolic support therapy with Q10 ubiquinol, vitamin E and complex-B vitamins is well tolerated and produces some improvement in the majority of patients with neurodevelopmental disorders, especially in the presence of intellectual disability. Randomized controlled trials for each single neurodevelopmental disorder are now warranted to conclusively demonstrate the efficacy of these mitochondrial bioenergetic and antioxidant agents and to estimate their therapeutic effect size.
Antioxidant and Anti-Inflammatory Effects of Coenzyme Q10 Supplementation on Infectious Diseases.
Sifuentes-Franco Sonia,Sánchez-Macías Dellaneira Carolina,Carrillo-Ibarra Sandra,Rivera-Valdés Juan José,Zuñiga Laura Y,Sánchez-López Virginia Aleyda
Healthcare (Basel, Switzerland)
With the appearance of new viruses and infectious diseases (ID) such as COVID-19 in 2019, as well as the lack of specific pharmacological tools for the management of patients with severe complications or comorbidities, it is important to search for adjuvant treatments that help improve the prognosis of infectious disease patients. It is also important that these treatments limit the oxidative and hyperinflammatory damage caused as a response to pathogenic agents, since, in some cases, an inflammatory syndrome may develop that worsens the patient's prognosis. The potential benefits of complementary nutrients and dietary interventions in the treatment of pathological processes in which oxidative stress and inflammation play a fundamental role have been widely evaluated. Coenzyme Q10 (CoQ10) is a supplement that has been shown to protect cells and be effective in cardiovascular diseases and obesity. Additionally, some studies have proposed it as a possible adjuvant treatment in viral infections. Preclinical and clinical studies have shown that CoQ10 has anti-inflammatory and antioxidant effects, and effects on mitochondrial dysfunction, which have been linked to the inflammatory response.
Post-weaning exposure to Sunset Yellow FCF induces behavioral impairment and structural changes in the adult rat medial prefrontal cortex: Protective effects of Coenzyme Q10.
Karimi Fatemeh,Anari Hamideh,Yousefi Nejad Amirhossein,Karbalay-Doust Saied,Naseh Maryam
International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
Sunset Yellow FCF (E110) is a water-soluble synthetic dye that has adverse neurobehavioral effects. Coenzyme Q10 (CoQ10) is known as a neuroprotective agent. The present study aimed to evaluate the effects of post-weaning exposure to Sunset Yellow FCF on behavioral and structural changes in the adult rat medial prefrontal cortex (mPFC) and the protective effects of CoQ10. The weanling rats were randomly divided into six groups: distilled water, CoQ10 (10 mg/kg/day), and low (2.5 mg/kg/day) and high (70 mg/kg/day) doses of Sunset Yellow FCF with or without CoQ10 consumption for 6 weeks. A battery of behavioral tests including open field and Morris water maze tests were done at the end of the sixth week, and then the animals' brains were removed for stereological methods. Our finding indicated that the high dose of Sunset Yellow FCF led to a reduced total volume of mPFC (15.16%), especially in the anterior cingulate cortex (ACC) region (21.96%), along with loss of neurons (32%) and glial cells (37%), which was associated with higher anxiety behavior and loss of spatial memory. However, CoQ10 prevented the neural loss and glial cells, improved anxiety-like behaviors, and memory impairment. On the other hand, the acceptable daily dose (low dose of Sunset Yellow FCF) did not show a discernible effect on the same parameters. This study showed that the CoQ10 can protect the alteration in mPFC structure and behavioral changes of the rats exposed to high dose of Sunset Yellow FCF.
Could nutrient supplements provide additional glycemic control in diabetes management? A systematic review and meta-analysis of randomized controlled trials of as an add-on nutritional supplementation therapy.
Kim Yoonhye,Oh Yun Kyoung,Lee Junhee,Kim Eunyoung
Archives of pharmacal research
This systematic review and meta-analysis assessed the antidiabetic effect of pharmaconutrients as an add-on in type 2 diabetes mellitus patients by pooling data from currently available randomized controlled trials (RCTs). Data sources included the PubMed and EMBASE, Cochrane Central Register of Controlled Trials. RCTs reporting changes in glycosylated hemoglobin (HbA1c), fasting blood glucose (FBG), or homeostasis model assessment of insulin resistance (HOMA-IR) levels following add-on pharmaconutritional therapies for T2DM patients consuming antidiabetic drugs were targeted. Using random-effects meta-analyses, we identified pharmaconutrients with effects on glycemic outcomes. Heterogeneity among studies was presented using I values. Among 9537 articles, 119 RCTs with nine pharmaconutrients (chromium; coenzyme Q10; omega-3 fatty acids; vitamins C, D, and E; alpha-lipoic acid; selenium; and zinc) were included. Chromium (HbA1c, FBG, and HOMA-IR), coenzyme Q10 (HbA1c and FBG), vitamin C (HbA1c and FBG), and vitamin E (HbA1c and HOMA-IR) significantly improved glycemic control. Baseline HbA1c level and study duration influenced the effects of chromium and vitamin E on HbA1c level. Sensitivity analyses did not modify the pooled effects of pharmaconutrients on glycemic control. Administration of chromium, coenzyme Q10, and vitamins C and E for T2DM significantly improved glycemic control. This study has been registered in PROSPERO (CRD42018115229).
Coenzyme Q10 as Adjunctive Therapy for Cardiovascular Disease and Hypertension: A Systematic Review.
Sue-Ling Carolyn B,Abel Willie M,Sue-Ling Keith
The Journal of nutrition
BACKGROUND:Mitochondrial adenosine triphosphate (ATP) production requires a small electron carrier, co-enzyme Q10 (CoQ10), which has been used as adjunctive therapy in patients with cardiovascular disease (CVD) and hypertension because of its bioenergetics and antioxidant properties. Randomized controlled trials (RCTs) beyond the last two decades evaluating CoQ10 added to conventional therapy resulted in mixed results and were underpowered to address major clinical endpoints. OBJECTIVES:The objective of this systematic review was to examine the impact of CoQ10 supplementation on older adults with CVD or hypertension in the last two decades (2000-2020). METHODS:PubMed/MEDLINE, Cochrane Database, CINAHL, and Google Scholar databases were searched systematically, as well as manual review of references from selected studies, to identify RCTs or cross-over studies evaluating the efficacy of CoQ10 supplementation. Data extracted from selected studies include trial design and duration, treatment, dose, participant characteristics, study variables, and important findings. RESULTS:A total of 14 studies (1067 participants) met the inclusion criteria. The effect of CoQ10 supplementation was examined among predominantly older adult males with heart failure (n = 6), hypertension (n = 4), ischemic heart disease (n = 3), and preoperatively in patients scheduled for cardiac surgery (n = 1). CoQ10 supplementation in patients with heart failure improved functional capacity, increased CoQ10 serum levels, and led to fewer major adverse cardiovascular events (MACE). CoQ10 had positive quantifiable effects on inflammatory markers in patients with ischemic heart disease. Myocardial hemodynamics improved in patients who received CoQ10 supplementation prior to cardiac surgery. Effects on hypertension were inconclusive. CONCLUSION:In predominantly older adult males with CVD or hypertension, CoQ10 supplementation added to conventional therapy is safe and offers benefits clinically and at the cellular level. However, results of the trials need to be viewed with caution, and further studies are indicated before wide spread usage of CoQ10 is recommended in all older adults.
UBIAD1 alleviates ferroptotic neuronal death by enhancing antioxidative capacity by cooperatively restoring impaired mitochondria and Golgi apparatus upon cerebral ischemic/reperfusion insult.
Huang Yan,Liu Jianyang,He Jialin,Hu Zhiping,Tan Fengbo,Zhu Xuelin,Yuan Fulai,Jiang Zheng
Cell & bioscience
BACKGROUND:Neuronal death due to over-oxidative stress responses defines the pathology of cerebral ischemic/reperfusion (I/R) insult. Ferroptosis is a form of oxidative cell death that is induced by disruption of the balance between antioxidants and pro-oxidants in cells. However, the potential mechanisms responsible for cerebral I/R-induced ferroptotic neuronal death have not been conclusively determined. UBIAD1, is a newly identified antioxidant enzyme that catalyzes coenzyme Q10 (CoQ10) and vitamin K2 biosynthesis in the Golgi apparatus membrane and mitochondria, respectively. Even though UBIAD1 is a significant mediator of apoptosis in cerebral I/R challenge, its roles in ferroptotic neuronal death remain undefined. Therefore, we investigated whether ferroptotic neuronal death is involved in cerebral I/R injury. Further, we evaluated the functions and possible mechanisms of UBIAD1 in cerebral I/R-induced ferroptotic neuronal death, with a major focus on mitochondrial and Golgi apparatus dysfunctions. RESULTS:Ferroptosis occurred in cerebral I/R. Ferroptotic neuronal death promoted cerebral I/R-induced brain tissue injury and neuronal impairment. UBIAD1 was expressed in cerebral tissues and was localized in neurons, astrocytes, and microglia. Under cerebral I/R conditions overexpressed UBIAD1 significantly suppressed lipid peroxidation and ferroptosis. Moreover, upregulated UBIAD1 protected against brain tissue damage and neuronal death by alleviating I/R-mediated lipid peroxidation and ferroptosis. However, UBIAD1 knockdown reversed these changes. Enhanced UBIAD1-mediated ferroptosis elevated the antioxidative capacity by rescuing mitochondrial and Golgi apparatus dysfunction in cerebral I/R-mediated neuronal injury. They improved the morphology and biofunctions of the mitochondria and Golgi apparatus, thereby elevating the levels of SOD, T-AOC and production of CoQ10, endothelial nitric oxide synthase (eNOS)-regulated nitric oxide (NO) generation as well as suppressed MDA generation. CONCLUSIONS:The neuroprotective agent, UBIAD1, modulates I/R-mediated ferroptosis by restoring mitochondrial and Golgi apparatus dysfunction in damaged brain tissues and neurons, thereby enhancing antioxidative capacities. Moreover, the rescue of impaired mitochondrial and Golgi apparatus as a possible mechanism of regulating ferroptotic neuronal death is a potential treatment strategy for ischemic stroke.