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Coenzyme Q10 plays a critical role in cellular energy production and antioxidative processes within mitochondria. This study aimed to evaluate the impact of coenzyme Q10 supplementation on in vitro fertilization outcomes, focusing on antral follicle count, retrieved oocytes, quality of oocytes, fertilization rate, and implantation rate. The study included 270 women undergoing in vitro fertilization treatment, each receiving 200 mg of coenzyme Q10 daily for 60 days before and throughout the in vitro fertilization cycle. Other key nutritional supplements taken by participants included folic acid, vitamin D, omega-3, multivitamins, and probiotics. Coenzyme Q10 supplementation was positively correlated with several in vitro fertilization outcomes. The mean antral follicle count was 12.8, with a positive correlation of 0.35 with the use of coenzyme Q10. The mean number of retrieved oocytes was 9.7, showing a positive correlation of 0.30 with coenzyme Q10. The quality of oocytes had a weaker correlation of 0.20 with coenzyme Q10. Fertilization rate and implantation rate had positive correlations of 0.15 and 0.10, respectively. Additional supplements, such as folic acid and multivitamins, were used by a high percentage of participants, indicating the broader role of nutritional support in in vitro fertilization treatment. Coenzyme Q10 supplementation appears to positively impact several in vitro fertilization outcomes, suggesting its potential as a beneficial adjunct to standard in vitro fertilization protocols. [ABSTRACT FROM AUTHOR]

Coenzyme Q10 (Q10) and cholesterol are end-products of the mevalonate pathway, which is an essential metabolic network in the cell. Q10 has an established role as an electron transporter in the mitochondrial electron transport system and antioxidant protection. Here we investigated the hypothesis that chronic supplementation of Q10 could lower the cholesterol blood level in patients suffering from lipid disorders and ischemic heart disease (IHD). We also determined whether Q10 could influence the course of IHD assessed with the Rose questionnaire for the intensity of stenocardia symptoms. The study was conducted on 13 patients with mixed hyperlipidemia consisting of total cholesterol (TC) >300 mg/dL and triglycerides >200 mg/dL who were divided into those receiving orally either 50 mg Q10 t.i.d. (7 patients) or matching placebo pills (6 patients) over three months. We assessed TC and its fractions at monthly intervals. The findings were that Q10 significantly decreased the level of TC and low-density lipoprotein cholesterol by about 20% either, with inappreciable changes in other lipid fractions. Q10 also had a beneficial effect on stenocardia symptoms, lowering the incidence of chest pain attacks and the number of nitrate pills ingested. We conclude that Q10 exerts anticholesterolemic effects and is a viable candidate for adjunct hypercholesterolemia prophylaxis. [ABSTRACT FROM AUTHOR]

Purpose of Review: Currently, the preventive and treatment strategies for metabolic disorders are not fully effective, and many limitations remain with these tools. Coenzyme Q10 (CoQ10) is a new promising antioxidant and anti-inflammatory option that can target the mechanisms involved in the progression of metabolic disorders. The purpose of this study was to assess and summarize the implication of CoQ10 in diabetes, hyperlipidemia, and kidney disease. Recent Findings: Emerging evidence indicated that CoQ10 is effective for familial hypercholesterolemia, familial combined hyperlipidemia, hypercholesterolemia-induced atherosclerosis and cardiac damage, hypercholesterolemia-induced Alzheimer's-like disease, Type 2 diabetes mellitus, diabetic nephropathy, and metabolic-associated liver disease. Summary: CoQ10 could be a novel agent for the treatment of metabolic disorders including diabetes and its complications, several forms of hyperlipidemia, and metabolic-associated liver disease. [ABSTRACT FROM AUTHOR]

The most common mutation in southern Chinese individuals with late-onset multiple acyl-coenzyme A dehydrogenase deficiency (MADD; a fatty acid metabolism disorder) is c.250G > A (p.Ala84Thr) in the electron transfer flavoprotein dehydrogenase gene (ETFDH). Various phenotypes, including episodic weakness or rhabdomyolysis, exercise intolerance, and peripheral neuropathy, have been reported in both muscular and neuronal contexts. Our cellular models of MADD exhibit neurite growth defects and excessive apoptosis. Given that axonal degeneration and neuronal apoptosis may be regulated by B-cell lymphoma (BCL)-2 family proteins and mitochondrial outer membrane permeabilization through the activation of proapoptotic molecules, we measured the expression levels of proapoptotic BCL-2 family proteins (e.g., BCL-2-associated X protein and p53-upregulated modulator of apoptosis), cytochrome c, caspase-3, and caspase-9 in NSC-34 cells carrying the most common ETFDH mutation. The levels of these proteins were higher in the mutant cells than in the wide-type cells. Subsequent treatment of the mutant cells with coenzyme Q10 downregulated activated protein expression and mitigated neurite growth defects. These results suggest that the activation of the BCL-2/mitochondrial outer membrane permeabilization/apoptosis pathway promotes apoptosis in cellular models of MADD and that coenzyme Q10 can reverse this effect. Our findings aid the development of novel therapeutic strategies for reducing axonal degeneration and neuronal apoptosis in MADD. [ABSTRACT FROM AUTHOR]

Background: The effectiveness and adverse effects of coenzyme Q10 for heart failure remain unclear owing to small sample sizes and variations in the quality of existing studies in literature. Methods: The databases of EMBASE, PubMed, Web of Science, CINAHL databases, Scopus, Cochrane Central Register of Controlled Trials, VIP, Wanfang, and CNKI were searched for randomized controlled trials on the coenzyme Q10-assisted treatment of heart failure. Relevant literature was retrieved, data were extracted, and the risk of bias of the included studies was evaluated by two investigators independently using the Review Manager 5.4 software and the STATA 15 software. Results: In total, 33 studies were included in this meta-analysis, which showed that all-cause mortality [RR = 0.64, 95% CI (0.48, 0.85), P = 0.002; GRADE: moderate quality], hospitalization for heart failure [RR = 0.50, 95% CI (0.37, 0.67), P < 0.00001; GRADE: moderate quality], New York Heart Association classification [MD = − 0.29, 95% CI (− 0.39, − 0.19), P < 0.00001; GRADE: low quality], and brain natriuretic peptide level [MD = − 91.97, 95% CI (− 103.11, − 80.83), P < 0.00001; GRADE: low quality] were lower in the coenzyme Q10 group than in the control group. Meanwhile, left ventricular ejection fraction [MD = 0.51, 95% CI (0.31, 0.71), P < 0.00001; GRADE: low quality] and 6-min walk test result [MD = 31.70, 95% CI (19.96, 43.43), P < 0.00001; GRADE: moderate quality] were better than those in the control group. Conclusions: According to the existing evidence, coenzyme Q10 reduces all-cause mortality, hospitalization for heart failure, New York Heart Association classification, and brain natriuretic peptide level and improves left ventricular ejection fraction and 6-min walk test result in those with heart failure without major adverse effects. Trial registration: This study protocol was registered in the International Prospective Register of Systematic Reviews (PROSPERO, http://www.crd.york.ac.uk/prospero), with the registration number CRD42023493184. [ABSTRACT FROM AUTHOR]

Background: Hyperglycemia-induced oxidative stress can damage the liver and lead to diabetes complications. Coenzyme Q10 (CoQ-10) reduces diabetes-related oxidative stress. However, its molecular mechanisms are still unclear. This study aimed to examine CoQ-10's antioxidant capabilities against hyperglycemia-induced oxidative stress in the livers of diabetic rats, specifically targeting the Nrf2/Keap1/ARE signaling pathway. Methods: This study was conducted between 2020-2021 at Arak University of Medical Sciences. A total of 30 male adult Wistar rats (8 weeks old) weighing 220-250 g were randomly assigned to five groups (n=6 in each group): control healthy, sesame oil (CoQ-10 solvent), CoQ-10 (10 mg/Kg), diabetic, and diabetic+CoQ-10. Liver oxidative stress indicators, including malondialdehyde, catalase, glutathione peroxidase, and glutathione, were estimated using the spectrophotometry method. Nrf2, Keap1, HO-1, and NQO1 gene expressions were measured using real-time PCR tests in the liver tissue. All treatments were conducted for 6 weeks. Statistical analysis was performed using SPSS software. One-way ANOVA followed by LSD's or Tukey's post hoc tests were used to compare the results of different groups. P<0.05 was considered statistically significant. Results: The findings showed that induction of diabetes significantly increased Keap1 expression (2.1±0.9 folds, P=0.01), and significantly inhibited the mRNA expression of Nrf2 (0.38±0.2 folds, P=0.009), HO-1 (0.27±0.1 folds, P=0.02), and NQO1 (0.26±0.1 folds P=0.01), compared with the healthy group. In the diabetic group, the activity of glutathione peroxidase, catalase enzymes, and glutathione levels was decreased with an increase in malondialdehyde level. CoQ-10 supplementation significantly up-regulated the expressions of Nrf2 (0.85±0.3, P=0.04), HO-1 (0.94±0.2, P=0.04), NQO1 (0.88±0.5, P=0.03) genes, and inhibited Keap1 expression (1.1±0.6, P=0.02). Furthermore, as compared to control diabetic rats, CoQ-10 ameliorated oxidative stress by decreasing malondialdehyde levels and increasing catalase, glutathione peroxidase activities, and glutathione levels in the liver tissues of the treated rats in the treatment group. Conclusion: The findings of this study revealed that CoQ-10 could increase the antioxidant capacity of the liver tissue in diabetic rats by modulating the Nrf2/Keap1/HO-1/NQO1 signaling pathway. [ABSTRACT FROM AUTHOR]

• CoQ10 promotes nerve regeneration by enhancing mitochondrial biogenesis. • CoQ10 improves antioxidative mechanisms led to accelerating neural tissue healing. • CoQ10 can protect against neuroinflammation in neurosensory disturbances. • Early CoQ10 supplementation enhances neuroprotection. • CoQ10 supplementation may serve as adjunctive treatment for peripheral nerve injury. Peripheral nerve injuries (PNIs) are prevalent conditions mainly resulting from systemic causes, including autoimmune diseases and diabetes mellitus, or local causes, for example, chemical injury and perioperative nerve injury, which can cause a varying level of neurosensory disturbances (NSDs). Coenzyme Q10 (CoQ10) is an essential regulator of mitochondrial respiration and oxidative metabolism. Here, we review the pathophysiology of NSDs caused by PNIs, the current understanding of CoQ10's bioactivities, and its potential therapeutic roles in nerve regeneration, based on evidence from experimental and clinical studies involving CoQ10 supplementation. In summary, CoQ10 supplementation shows promise as a neuroprotective agent, potentially enhancing treatment efficacy for NSDs by reducing oxidative stress and inflammation. Future studies should focus on well-designed clinical trials with large sample sizes, using CoQ10 formulations with proven bioavailability and varying treatment duration, to further elucidate its neuroprotective effects and to optimize nerve regeneration in PNIs-induced NSDs. [Display omitted] Graphical abstract legend Coenzyme Q10 may serve as a potential therapeutic agent in preventing and mitigating neurosensory disturbances induced by peripheral nerve injury, primarily through enhancing mitochondrial biogenesis and bolstering antioxidant mechanisms. Additionally, its anti-inflammatory properties offer an appealing avenue for shielding against neuroinflammation, thereby augmenting its efficacy in treating neurosensory disorders. [ABSTRACT FROM AUTHOR]

Selenoprotein P (SELENOP) transports selenium to extrahepatic tissues and is a biomarker of selenium status. Low soil selenium leads to low dietary selenium intake. A consequence is an increased risk of cardiovascular disease. To investigate clinical aspects associated with SELENOP deficiency, including biomarkers of inflammation, quality of life, and mortality within 12 years, and the effect of dietary selenium and coenzyme Q 10 supplementation on SELENOP. SELENOP was determined at inclusion and after four years of supplementation in 403 elderly community-living participants low in selenium receiving selenium yeast (200 μg/day) and coenzyme Q 10 (200 mg/day), or placebo. Pre-intervention, the average serum selenium level was 67 μg/L. T-tests, repeated measures of variance, Cox proportional regressions analyses, Kaplan-Meier graphs and ANCOVA analyses were applied. Associations with biomarkers of inflammation, telomere length, quality of life and mortality were investigated. Benchmark modelling was used to determine the serum selenium concentration at which the saturation levels of SELENOP and GPx3 was achieved. Comparison with GPx3 and serum selenium to identify increased mortality risk was performed, and the effect of supplementation on SELENOP levels were evaluated. Inverse associations were observed between the level of SELENOP at inclusion and biomarkers for inflammation. At follow-up, shorter telomere lengths were seen in those with low levels of SELENOP at inclusion, whereas high levels of SELENOP were associated with better quality of life and decreased mortality. SELENOP had increased prognostic power compared to GPx3 and selenium. Saturation of SELENOP was achieved at a serum selenium level of 146 μg/L, and for GPx3 at 99 μg/L. Supplementation induced higher levels of SELENOP. Significant associations between SELENOP and inflammation, length of telomeres, quality of life, and mortality were observed. Thus, selenium supplementation improved SELENOP expression, thereby facilitating systemic selenium bioavailability and resulting in the observed positive health effects. [Display omitted] • Low and decreasing selenoprotein P (SELENOP) status in elderly subjects associated with all-cause and cardiovascular mortality. • Low SELENOP was associated with increased telomere attrition and impaired quality of life. • Randomized controlled intervention with selenium and coenzymeQ10 raised serum SELENOP. • Increased SELENOP associated with reduced telomere attrition, mortality, and improved quality of life. • SELENOP may translate the applied supplements into improved selenium transport, status and health benefits. [ABSTRACT FROM AUTHOR]

Objectives: To evaluate the effects of coenzyme Q10 (CoQ10) on alveolar bone remodeling and orthodontic tooth movement (OTM). Materials and methods: An orthodontic appliance was placed in 42 female Sprague‒Dawley rats were divided into two groups: the orthodontic force (OF) group (n = 21) and the OF + CoQ10 (CoQ10) treatment group (n = 21). Each group was divided into 3 subgroups, and the rats were sacrificed on days 3, 7 and 14. The rats in CoQ10 and OF groups were administered 100 mg/kg b.w./day CoQ10 (in 1 mL/b.w. soybean oil) and 1 mL b.w./day soybean oil, respectively, by orogastric gavage. The OTM was measured at the end of the experiment. The osteoclast, osteoblast and capillary numbers; vascular endothelial growth factor (VEGF), receptor activator nuclear kappa B ligand (RANKL) and osteoprotegrin (OPG) levels in tissue; and total antioxidant status (TAS) and total oxidant status (TOS) in blood were determined. Results: Compared with the OF group, the CoQ10 treatment group exhibited decreased orthodontic tooth movement and osteoclast and capillary numbers. Indeed, the levels of VEGF and RANKL decreased, while the levels of OPG increased except on day 7. Additionally, the CoQ10 treatment group exhibited lower TOS and higher TAS on days 7 and 14 (p < 0.05). Histological findings showed that the morphology of osteoblasts changed in the CoQ10 group; however, there was no significant difference in the number of osteoblasts between the groups (p > 0.05). Conclusion: Due to its effect on oxidative stress and inflammation, CoQ10 regulates bone remodeling by inhibiting osteoclast differentiation, promoting osteoblast differentiation and reducing the amount of OTM. Clinical relevance: Considering that OTM may be slowed with the use of CoQ10, topics such as orthodontic treatment duration, orthodontic force activation and appointment frequency should be considered in treatment planning. It is predicted that the use of CoQ10 will support the effectiveness of treatment in clinical applications such as preventing relapse in orthodontic treatment by regulating bone modulation and anchorage methods that suppress/optimize unwanted tooth movement. [ABSTRACT FROM AUTHOR]

In recent years, Sunset Yellow (SY) has been widely used as a food additive, sparking debates about its potential toxicity. This research aims to investigate SY's effects at both the molecular and histopathological levels, along with the protective benefits of Coenzyme Q10 (CoQ10) supplementation in male rat testes. Forty-two male Sprague-Dawley rats were randomly divided into six groups (n = 7) and given daily oral gavages for six weeks. The groups included: a low dose of Sunset Yellow (2.5 mg/kg/day), a high dose of Sunset Yellow (70 mg/kg/day), CoQ10 (10 mg/kg/day), CoQ10 with the low dose of Sunset Yellow, CoQ10 with the high dose of Sunset Yellow, and deionized water as a control. After anesthesia, the rats' testes were removed for molecular and histological analysis. The findings showed a dose-dependent rise in the expression of oxidative stress genes (Sod, Gpx, and Cata) and a notable decrease in the expression of the steroidogenic acute regulatory (Star) gene (P value < 0.05) with increasing SY doses. Histological results supported these outcomes. Additionally, there was no significant distinction between rats treated with CoQ10 along with low doses of Sunset Yellow (CoQ10+LD) and control rats given low doses of Sunset Yellow (SY-LD). Conclusions: This study illustrates that SY, as an artificial food dye, has harmful effects on the male reproductive system, while the utilization of CoQ10 can alleviate the negative impacts of SY exposure. [ABSTRACT FROM AUTHOR]

Heavy metal contamination is an alarming concern on a global scale, as drinking tainted water significantly increases human susceptibility to heavy metals. In a realistic scenario, humans are often exposed to a combination of harmful chemicals rather than a single toxicant. Phloretin (PHL), biochanin‐A (BCA), and coenzyme Q10 (CoQ10) are bioactive compounds owning plentiful pharmacological properties. Henceforth, the current research explored the putative energizing effects of selected nutraceuticals in combined chromium (Cr) and arsenic (As) intoxicated Swiss albino mice. Potassium dichromate (75 ppm) and sodium meta‐arsenite (100 ppm) were given in the drinking water to induce hepatotoxicity, conjugated with PHL and BCA (50 mg/kg each), and CoQ10 (10 mg/kg) intraperitoneally for 2 weeks. After the statistical evaluation, it was observed that the hepato‐somatic index, metal load, and antioxidant activity (lipid peroxidation and protein carbonyl content) increased along with the concomitant decrease in the antioxidants (catalase, glutathione‐S‐transferase, superoxide dismutase, reduced glutathione, and total thiol) in the Cr and As intoxicated mice. Additionally, light microscopy observations, DNA breakages, decreased silent information regulator 1 (SIRT1), nuclear factor (erythroid‐derived 2)‐like 2 (Nrf2), heme oxygenase (HO‐1), and NAD(P)H quinone dehydrogenase 1 (NQO1) gene expressions, together with stimulated apoptotic cell death manifested by the increased expressions of caspase 8 and caspase 3, thus, proved consistency with the aforementioned outcomes. Importantly, the treatment with nutraceuticals not only restored the antioxidant activity but also favorably altered the expressions of SIRT1, Nrf2, HO‐1, and NQO1 signaling and apoptosis markers. These findings highlight the crucial role of the PHL, BCA, and CoQ10 combination in reducing Cr and As‐induced hepatotoxicity in mice. By averting the triggered apoptosis in conjunction with oxidative stress, this combination increases the SIRT1, Nrf2, HO‐1, and NQO1 signaling, thereby reassuringly maintaining the cellular equilibrium. Highlights: Chromium and arsenic are the two major heavy metals that pose a significant threat to living beings by altering the biochemical equilibrium.Exposure to combined Cr + As for 2 weeks led to the generation of free radicals resulting in the damage of liver tissue.Treatment with natural bioactive compounds (PHL, BCA, and CoQ10) impeded the Cr + As‐induced hepatic toxicity by scavenging the free radicals and reducing the triggered oxidative stress together with preventing the dysfunctioning of SIRT1/Nrf2/HO‐1/NQO1 and caspase cascade. [ABSTRACT FROM AUTHOR]

Previous studies have shown that post-thaw sperm performance is affected by multiple stressors during cryopreservation, such as those induced by physical, chemical, mechanical and physiological changes. One of these is the balance disturbance between the antioxidant defense system and reactive oxygen species (ROS) production. This study investigated whether this disturbance could be alleviated by the addition of different antioxidants to cryoprotective solution [8% dimethyl sulfoxide (DMSO) in 1 µm filtered seawater] optimized for the sperm in dwarf surf clam Mulinia lateralis, the model bivalve species used in many different types of studies. Results showed that the addition of 20 μM coenzyme Q10 (Q10) to 8% DMSO achieved a D-stage larval rate similar to that of the fresh control at a sperm-to-egg ratio at least 50% less than the 8% DMSO treatment alone. The addition of other antioxidants (glycine, melatonin and polyvinylpyrrolidone) did not have any positive effects. The improvement in post-thaw sperm quality by Q10 could be due to its ability to significantly decrease ROS production and lipid peroxidation and significantly increase the motility, plasma membrane integrity, mitochondrial membrane potential, acrosome integrity, DNA integrity and activities of catalase and glutatione. In this study, 37 fatty acids (FAs) were quantified in dwarf surf clam sperm, with 21 FAs being significantly impacted by the cryopreservation with 8% DMSO. Thirteen of these 21 FAs were changed due to the addition of 20 μM Q10 to 8% DMSO, with approximately half of them being improved significantly toward the levels of fresh control, while the remaining half extended further from the trends shown with 8% DMSO treatment. However, no significant difference was found in the percentage of each FA category sum and the ratio of unsaturated/saturated FAs between the two treated groups. In conclusion, the antioxidant Q10 has shown the potential to further improve the sperm cryopreservation technique in bivalves. [ABSTRACT FROM AUTHOR]

Abstract Background The effectiveness and adverse effects of coenzyme Q10 for heart failure remain unclear owing to small sample sizes and variations in the quality of existing studies in literature. Methods The databases of EMBASE, PubMed, Web of Science, CINAHL databases, Scopus, Cochrane Central Register of Controlled Trials, VIP, Wanfang, and CNKI were searched for randomized controlled trials on the coenzyme Q10-assisted treatment of heart failure. Relevant literature was retrieved, data were extracted, and the risk of bias of the included studies was evaluated by two investigators independently using the Review Manager 5.4 software and the STATA 15 software. Results In total, 33 studies were included in this meta-analysis, which showed that all-cause mortality [RR = 0.64, 95% CI (0.48, 0.85), P = 0.002; GRADE: moderate quality], hospitalization for heart failure [RR = 0.50, 95% CI (0.37, 0.67), P

Abstract The most common mutation in southern Chinese individuals with late-onset multiple acyl-coenzyme A dehydrogenase deficiency (MADD; a fatty acid metabolism disorder) is c.250G > A (p.Ala84Thr) in the electron transfer flavoprotein dehydrogenase gene (ETFDH). Various phenotypes, including episodic weakness or rhabdomyolysis, exercise intolerance, and peripheral neuropathy, have been reported in both muscular and neuronal contexts. Our cellular models of MADD exhibit neurite growth defects and excessive apoptosis. Given that axonal degeneration and neuronal apoptosis may be regulated by B-cell lymphoma (BCL)-2 family proteins and mitochondrial outer membrane permeabilization through the activation of proapoptotic molecules, we measured the expression levels of proapoptotic BCL-2 family proteins (e.g., BCL-2-associated X protein and p53-upregulated modulator of apoptosis), cytochrome c, caspase-3, and caspase-9 in NSC-34 cells carrying the most common ETFDH mutation. The levels of these proteins were higher in the mutant cells than in the wide-type cells. Subsequent treatment of the mutant cells with coenzyme Q10 downregulated activated protein expression and mitigated neurite growth defects. These results suggest that the activation of the BCL-2/mitochondrial outer membrane permeabilization/apoptosis pathway promotes apoptosis in cellular models of MADD and that coenzyme Q10 can reverse this effect. Our findings aid the development of novel therapeutic strategies for reducing axonal degeneration and neuronal apoptosis in MADD.

Background: Hyperglycemia-induced oxidative stress can damage the liver and lead to diabetes complications. Coenzyme Q10 (CoQ-10) reduces diabetes-related oxidative stress. However, its molecular mechanisms are still unclear. This study aimed to examine CoQ-10’s antioxidant capabilities against hyperglycemia-induced oxidative stress in the livers of diabetic rats, specifically targeting the Nrf2/Keap1/ARE signaling pathway.Methods: This study was conducted between 2020-2021 at Arak University of Medical Sciences. A total of 30 male adult Wistar rats (8 weeks old) weighing 220-250 g were randomly assigned to five groups (n=6 in each group): control healthy, sesame oil (CoQ-10 solvent), CoQ-10 (10 mg/Kg), diabetic, and diabetic+CoQ-10. Liver oxidative stress indicators, including malondialdehyde, catalase, glutathione peroxidase, and glutathione, were estimated using the spectrophotometry method. Nrf2, Keap1, HO-1, and NQO1 gene expressions were measured using real-time PCR tests in the liver tissue. All treatments were conducted for 6 weeks. Statistical analysis was performed using SPSS software. One-way ANOVA followed by LSD’s or Tukey’s post hoc tests were used to compare the results of different groups. P

Summary: Context: Hepatic and renal damages manifest in patients with acute or chronic heart failure after the incidence of myocardial infarction (MI). Objective: Our objective in this study was aimed to investigate the protective effects of coenzyme Q10 (CoQ10) and taurine, which are bioactive compounds with protective functions, on liver and kidney toxicity rat exposed to isoprenaline, a popular tool for MI induction. Materials and methods: Following two (2) consecutive days of exposure to isoprenaline (200 mg/kg, i.p.), adult Wistar rats were treated with CoQ10 (10 mg/kg, i.p.) and taurine (100 mg/kg, i.p.) singly and in combination for 19 days. Following 21 days of experimentation, blood, liver and kidney were collected for biochemical and histological studies indicative of hepatic and kidney damage. Results: Our result showed that CoQ10 and taurine significantly decreased serum LDH, AST, ALT, and ALP, indicative of hepatic damage compared to isoprenaline groups. The increased creatinine and urea release suggestive of kidney dysfunction were suppressed by CoQ10 and taurine relative to the isoprenaline group. Additionally, CoQ10 and taurine significantly reversed isoprenaline-mediated oxidative stress-induced liver and kidney damage, which are shown by decreased malondialdehyde and nitrite accompanied by increased antioxidants (SOD, CAT, GST, GSH). Modifications to cellular histoarchitectural and fibrosis of the hepatic and renal tissues were attenuated by CoQ10 and taurine therapy. Discussion and conclusion: The findings from this study suggest that CoQ10 and taurine supplements may prevent isoprenaline-induced hepatorenal dysfunctions, possibly by alleviating oxidative stress and histoarchitectural protective functions of the hepatic and kidney cells.

Background and Objective: Sudden sensorineural hearing loss (SSNHL) is a complication that is usually unilateral and can be accompanied by tinnitus and vertigo. Although various infectious, vascular, and immune etiologies have been proposed for SSNHL, the cause is unknown in most cases. Therefore, this study aimed to determine the effect of coenzyme Q10 in the treatment of SSNHL. Materials and Methods: This study was a double-blind, randomized, controlled clinical trial, which was conducted using the available sampling method. A total of 60 patients with SSNHL (18-70 years old) lasting less than one month were divided into two groups: intervention and control. The routine treatment of both groups included weekly injections of dexamethasone in the middle ear for 3 weeks. The intervention group also received 100 mg of coenzyme Q10 per day for 4 weeks, while the control group received a placebo. Patients were evaluated by basic audiological tests at the baseline and third and sixth months after the treatment. Statistical analysis of findings was done in SPSS26 software. Results: The difference in the mean pure tone hearing thresholds of the intervention and control groups was significant in the third month (29.33±15.96 dB and 35.34±12.24 dB; P=0.02) and sixth month (dB 28.00±16.27 and dB 34.33±11.87; P=0.01). Conclusion: In patients with SSNHL, combined treatment with oral coenzyme Q10 at the rate of 100 mg per day, along with intratympanic injection of dexamethasone for four weeks, can improve pure tone hearing thresholds and facilitate the treatment

How does a single amino acid mutation occurring in the blinding disease, Lebers hereditary optic neuropathy (LHON), impair electron shuttling in mitochondria? We investigated changes induced by the m.3460 G>A mutation in mitochondrial protein ND1 using the tools of Molecular Dynamics and Free Energy Perturbation simulations, with the goal of determining the mechanism by which this mutation affects mitochondrial function. A recent analysis suggested that the mutations replacement of alanine A52 with a threonine perturbs the stability of a region where binding of the electron shuttling protein, Coenzyme Q10, occurs. We found two functionally opposing changes involving the role of Coenzyme Q10. The first showed that quantum electron transfer from the terminal Fe/S complex, N2, to the Coenzyme Q10 headgroup, docked in its binding pocket, is enhanced. However, this positive adjustment is overshadowed by our finding that the mobility of Coenzyme Q10 in its oxidized and reduced states, entering and exiting its binding pocket, is disrupted by the mutation in a manner that leads to conditions promoting the generation of reactive oxygen species. An increase in reactive oxygen species caused by the LHON mutation has been proposed to be responsible for this optic neuropathy.

Abstract Backround Metabolic-dysfunction Associated Steatotic Liver Disease (MASLD) has been associated with increased cardiovascular risk. The aim of this Randomized Double-blind clinical Trial was to evaluate the effects of coenzyme-Q10 supplementation in patients with MASLD in terms of endothelial, vascular and myocardial function. Methods Sixty patients with MASLD were randomized to receive daily 240 mg of coenzyme-Q10 or placebo. At baseline and at 6-months, the a)Perfused boundary region of sublingual vessels using the Sideview Darkfield imaging technique, b)pulse-wave-velocity, c)flow-mediated dilation of the brachial artery, d)left ventricular global longitudinal strain, e)coronary flow reserve of the left anterior descending coronary artery and f)controlled attenuation parameter for the quantification of liver steatosis were evaluated. Results Six months post-treatment, patients under coenzyme-Q10 showed reduced Perfused boundary region (2.18 ± 0.23vs.2.29 ± 0.18 μm), pulse-wave-velocity (9.5 ± 2vs.10.2 ± 2.3 m/s), controlled attenuation parameter (280.9 ± 33.4vs.304.8 ± 37.4dB/m), and increased flow-mediated dilation (6.1 ± 3.8vs.4.3 ± 2.8%), global longitudinal strain (-19.6 ± 1.6vs.-18.8 ± 1.9%) and coronary flow reserve (3.1 ± 0.4vs.2.8 ± 0.4) compared to baseline (p 0.05). In patients under coenzyme-Q10, the reduction in controlled attenuation parameter score was positively related to the reduction in Perfused boundary region and pulse wave velocity and reversely related to the increase in coronary flow reserve and flow-mediated dilation (p

Non-alcoholic fatty liver disease (NAFLD), characterized by hepatic fat accumulation in individuals consuming little or no alcohol, has become highly prevalent globally. Oxidative stress plays a central role in instigating inflammation and cell death pathways driving NAFLD progression. This case–control study aimed to elucidate the association between circulating levels of the pivotal non-enzymatic antioxidants – coenzyme Q10 and vitamins E and C – and liver injury parameters among 60 Iraqi NAFLD patients versus 30 healthy controls. NAFLD diagnosis entailed over 5% hepatic steatosis on ultrasound excluding other etiologies. Patients spanned three age groups: 20–29, 30–39, and 40–49. Substantially diminished antioxidant levels concurrent with elevated alkaline phosphatase enzyme were unveiled in NAFLD patients relative to controls (all p < 0.001). Age-based analysis reinforced widespread antioxidant depletion and liver enzyme augmentation across NAFLD patients. Significant correlations also emerged between antioxidants and liver parameters. Our novel observations confirm an antioxidant inadequacy likely perpetuating pathogenic oxidative reactions in NAFLD. Restoring such deficits through lifestyle or therapeutic interventions may confer preventative and disease-modifying value.

Peripheral nerve injuries (PNIs) constitute a significant concern as they predominantly affect young and productive age groups of the population, causing social and economic pressure on patients. PNIs are a global problem that can result in disability because of the disruption of nerve function. PNI leads to a reduction in nerve conduction velocity, which worsens or impairs the mobility of the innervated area. Managing PNI remains a major clinical challenge. Coenzyme Q10 (CoQ10) is a lipid-soluble antioxidant first identified in 1957. It is an important antioxidant necessary for the organs to maintain their normal function and the body’s chemical processes. It scavenges free radicals and reduces oxidative stress. Studies showed that antioxidants such as CoQ10 a potent antioxidant, help the regeneration of PNIs. It has been observed to increase the myelination process in nerve fibres and promote nerve regeneration in rats after injury. Therefore, this review handles the current positive effects of CoQ10 on peripheral nerve regeneration following injury.

Background: Among the three most used anticancer drugs, cyclophosphamide, Adriamycin, and 5-Fluorouracil (CAF), the most significant outcome is chemobrain, caused by increased oxidative stress, inflammatory insult, and mitochondrial dysfunction. Objective: In this study, endogenous antioxidant coenzyme Q10 (CoQ10) was evaluated for its neuroprotective effects in CICI. Materials and methods: The chemobrain was induced in Swiss albino female mice by administering CAF (40 + 4 + 25 mg/kg) intraperitoneal (i.p.) in three cycles (single injection per week) followed by treatment with CoQ10 (40 mg/kg; p.o.) for up to 3 weeks followed by behavioral, biochemical, molecular and histopathological analysis. Results: Treatment with CoQ10 significantly improved cognition by improving exploring time in novel objects recognition test followed by increasing the time spent in the target quadrant in MWM test as compared to CAF-treated animals. Moreover, CoQ10 demonstrated antioxidant properties by reducing the expression of LPO while increasing levels of GSH, SOD, and catalase as compared to CAF-treated animals. While the levels of AChEs were significantly reduced after CoQ10 treatment in CAF-treated animals. In terms of its mechanism, it effectively counteracted the pro-inflammatory substances (TNF-α and IL-1β) triggered by CAF while also enhancing the levels of anti-inflammatory markers (IL-10 and Nrf2). Moreover, CoQ10 showed mitochondrial enhancers and it improved the level of Complex (I, II, and IV). Besides that, mitochondrial morphological analysis was done by TEM, and neuronal morphology along with quantification analysis was performed by H&E staining using Image J software to confirm the neuroprotective effect of CoQ10 over CAF-induced cognitive impairment. Conclusion: This study suggests CoQ10 can protect the mitochondria by imposing antioxidant, and anti-inflammatory properties, which could be a potential therapy for CICI. [ABSTRACT FROM AUTHOR]

The feasibility of incorporating different concentrations (0; 1% – 'Y1'; 7% – 'Y7') of coenzyme Q10 (CoQ10)‐loaded nanoemulsions (Ynano Q10) in yogurts was evaluated, as well as the bioactive's stability during static in vitro digestion. Yogurts were characterised regarding CoQ10 concentrations, physicochemical/rheological properties and sensory acceptability. Ynano Q10 incorporation has not negatively affected yogurts properties, stability and overall acceptance on sensory tests. Bioactive's stability during in vitro digestion was higher in Ynano Q10 than in fortified yogurts; however, CoQ10 concentrations in yogurts after the intestinal phase (0.008% for Y1 and 0.175% for Y7) were sufficiently high, considering CoQ10 recommended daily intake. [ABSTRACT FROM AUTHOR]

Objective: This study provides histological evidence of the combined effects of L-Carnitine, and Coenzyme Q10 on gliosis and anhedonia in a rat model of multiple sclerosis (MS). Methods: Fifty male Sprague Dawley rats were randomly divided into 5 groups of 10 rats each. Group 1 was the control group. The rest of the groups were disease models and were given 0.2% cuprizone w/w to induce MS. After 4 weeks, Group 3 started receiving L-Carnitine, Group 4 was given Coenzyme Q10, and Group 5 received both, while cuprizone poisoning continued. After 12 weeks sucrose preference test and tail suspension test were performed for anhedonia. Rats were euthanized and brains were dissected, and assessed for astrocytes, oligodendrocytes, and microglial count. Results: A significant increase in oligodendrocyte count, while a reduction in astrocyte and microglial count was seen in the synergistic group (p < 0.05). Synergism could not be proved in anhedonia. Conclusion: The combination of Coenzyme Q10 and L-Carnitine has a synergistic effect in controlling gliosis in a rat model of MS, but synergism could not be demonstrated on anhedonia. [ABSTRACT FROM AUTHOR]

BACKGROUND: Coenzyme Q10 (CoQ10) is a naturally produced, lipid-soluble molecule crucial for cellular energy production and antioxidant activity. It diminishes with age and under external stress factors in skin, leading to signs of aging. Beyond its role in cellular energy production within the mitochondria, CoQ10 is vital to skin's defense against oxidative stress, a key contributor to premature aging. Use of topical skincare products with CoQ10 can be effective to replenish levels of CoQ10 and reverse skin aging. OBJECTIVE: This publication discusses the role of CoQ10 in skin aging along with the benefits of topical skincare products that incorporate CoQ10 as an ingredient. METHODS: We searched the PubMed database using terms "Coenzyme Q10" and "skin" and "aging." Overall, the search yielded 80 results, but a limitation of 10 years was then applied to restrict publications to those with the most up-to-date science. RESULTS: A total of 36 publications were identified and included as background for this article. These 36 publications encompassed both original research articles and review articles. DISCUSSION: Applying topical skincare products with CoQ10 replenishes CoQ10 cellular levels, helping to normalize cellular energy homeostasis and providing antioxidative effects to support and repair cutaneous damage including signs of skin aging. In ex vivo and in vivo studies, application of CoQ10 increased CoQ10 levels both on the skin surface (i.e., stratum corneum) and even more in deeper levels of the skin. Clinically, topical application of CoQ10-formulated products reduces the depth of cutaneous wrinkles, a sign associated with aging. CONCLUSION: Aging and stressed skin are, in part, the result of alterations in cellular metabolic homeostasis, which can be reversed via the benefits of topical application of CoQ10-enriched formulations that stimulate cutaneous energy metabolism and reduce free radicals via antioxidant function. By restoring physiological homeostasis, topical skincare products with CoQ10 replenish the skin's antioxidant levels, increase cellular (energy) metabolism, and reduce the signs of skin aging. [ABSTRACT FROM AUTHOR]

Age-related macular degeneration (AMD) and diabetic retinopathy (DR) are common retinal diseases responsible for most blindness in working-age and elderly populations. Oxidative stress and mitochondrial dysfunction play roles in these pathogenesis, and new therapies counteracting these contributors could be of great interest. Some molecules, like coenzyme Q10 (CoQ10), are considered beneficial to maintain mitochondrial homeostasis and contribute to the prevention of cellular apoptosis. We investigated the impact of adding CoQ10 (Q) to a nutritional antioxidant complex (Nutrof Total®; N) on the mitochondrial status and apoptosis in an in vitro hydrogen peroxide (H2O2)-induced oxidative stress model in human retinal pigment epithelium (RPE) cells. H2O2 significantly increased 8-OHdG levels (p < 0.05), caspase-3 (p < 0.0001) and TUNEL intensity (p < 0.01), and RANTES (p < 0.05), caspase-1 (p < 0.05), superoxide (p < 0.05), and DRP-1 (p < 0.05) levels, and also decreased IL1β, SOD2, and CAT gene expression (p < 0.05) vs. control. Remarkably, Q showed a significant recovery in IL1β gene expression, TUNEL, TNFα, caspase-1, and JC-1 (p < 0.05) vs. H2O2, and NQ showed a synergist effect in caspase-3 (p < 0.01), TUNEL (p < 0.0001), mtDNA, and DRP-1 (p < 0.05). Our results showed that CoQ10 supplementation is effective in restoring/preventing apoptosis and mitochondrial stress-related damage, suggesting that it could be a valid strategy in degenerative processes such as AMD or DR. [ABSTRACT FROM AUTHOR]

Objectives: Coenzyme Q10 (CoQ10) or ubiquinone is one of a cell’s most important electron carriers during oxidative phosphorylation and many other cellular processes. As a strong anti-oxidant with further anti-inflammatory effects CoQ10 is of potential therapeutical value. The aim of this randomized controlled clinical trial was to investigate the effect of topical CoQ10 on early wound healing after recession coverage surgery using the modified coronally advanced tunnel (MCAT) and palatal connective tissue graft (CTG). Materials and methods: Thirty patients with buccal gingival recessions were evaluated after being randomly allocated to: 1) MCAT and CTG with topical application of a coenzyme Q10 spray for 21 days or 2) MCAT and CTG with placebo spray. Wound healing was evaluated by the early wound healing index (EHI). Patient-reported pain was analyzed by a 100-mm visual analogue scale (VAS) at day 2, 7, 14 and 21 post-surgically. Mean recession coverage, gain of keratinized tissue and esthetic outcomes were assessed at 6 months. Results: EHI and pain scores showed no significant differences. Time to recovery defined as VAS<10 mm was shorter in the test group. Mean root coverage after 6 months was 84.62 ± 26.57% and 72.19 ± 26.30% for test and placebo, p=0.052. Complete root coverage was obtained in 9 (60%) test and in 2 (13.3%) placebo patients. Increase in keratinized tissue width and esthetical outcomes were similar for both groups. Conclusion: CoQ10 had no significant effect on early wound healing and on mean root coverage after 6 months. Clinical relevance: Early wound healing: in young healthy patients with no inflammatory oral conditions topical CoQ10 does not improve early healing. [ABSTRACT FROM AUTHOR]

Rational: Patients experience post-stroke cognitive impairment during aging. To date, no specific treatment solution has been reported for this disorder. Objective: The purpose of this study was to evaluate the effects of exercise training and coenzyme Q10 supplementation on middle cerebral artery occlusion (MCAO) induced behavioral impairment, long-term potentiation inhibition and cerebral infarction size in aging rats. Methods: Fifty aging male rats underwent MCAO surgery and were randomly distributed in to the following groups: 1-Sham, 2- control, 3- Coenzyme Q10, 4- Exercise training and 5- Exercise training with Q10 supplementation (Ex + Q10). Aerobic training groups were allowed to run on a treadmill for 12 weeks. Q10 (50 mg/kg) was administered intragastrically by gavage. Morris water maze, shuttle box and elevated plus maze tests were used to evaluate cognitive function. The population spike (PS) amplitude and slope of excitatory postsynaptic potentials (EPSP) in the dentate gyrus area were recorded as a result of perforant pathway electrical stimulation. Results: Our study showed that Q10 and aerobic training alone ameliorate spatial memory in the acquisition phase, but have no effect on spatial memory in the retention phase. Q10 and exercise training synergistically promoted spatial memory in the retention phase. Q10 and exercise training separately and simultaneously mitigated cerebral ischemia-induced passive avoidance memory impairment in acquisition and retention phases. The EPSP did not differ between the groups, but exercise training and Q10 ameliorate the PS amplitude in hippocampal responses to perforant path stimulation. Exercising and Q10 simultaneously reduced the cerebral infarction volume. Conclusion: Collectively, the findings of the present study imply that 12 weeks of aerobic training and Q10 supplementation alone can simultaneously reverse cerebral ischemia induced neurobehavioral deficits via amelioration of synaptic plasticity and a reduction in cerebral infarction volume in senescent rats. [ABSTRACT FROM AUTHOR]

The relationship between amyloid beta (Aβ) and oxidative stress (OS), both prominent factors in Alzheimer's disease-related neural degeneration, is deeply interconnected. The cleavage of the extracellular domain of Amyloid precursor protein (APP) and phosphorylating different substrates, respectively, the β-site amyloid precursor protein cleaving enzyme-1 (BACE-1) and Glycogen synthase kinase-3-beta (GSK-3β) enzymes initiate the synthesis of Aβ, which causes cognitive deficits in AD. This study aimed to explore the protective potential of Coenzyme Q10 (CoQ10). It also sought to uncover any synergistic effects when combined with donepezil, an acetylcholinesterase inhibitor, in treating Alzheimer's disease in male albino rats, focusing on the modulation of the BACE-1/GSK-3β pathway. The experiment involved 70 rats categorized into different groups: control, donepezil alone, CoQ10 alone, AD-model, donepezil co-treatment, CoQ10 co-treatment, and CoQ10 + donepezil combination. Various assessments, such as cholinesterase activity, oxidative stress, serum iron profile, Brain Derived Neurotrophic Factor (BDNF), Tau protein, β-site amyloid precursor protein cleaving enzyme-1 (BACE-1), phosphatase and tensin homolog (Pten), and Glycogen synthase kinase-3-beta (GSK-3β), were conducted on behavioral and biochemical aspects. CoQ10 treatment demonstrated memory improvement, enhanced locomotion, and increased neuronal differentiation, mainly through the inhibition of the dual BACE-1/GSK-3β. These findings were substantiated by histological and immunohistological examinations of the hippocampus. Highlights Alzheimer's disease (AD) led to the alteration of BACE-1/GSK-3β. Coenzyme Q10 (CoQ10) alleviated D-Gal and AlCl3-induced passive avoidance memory deficits in rats. CoQ10 counteracts Alzheimer's disease by inhibiting acetylcholine esterase. CoQ10 significantly increases levels of BDNF and diminishes Tau burden. CoQ10 acts as a dual BACE1/GSK3β inhibitor. The combination of CoQ10 treatment and donepezil demonstrated potential as a therapeutic approach. [ABSTRACT FROM AUTHOR]

Coenzyme Q10 (CoQ) is a ubiquitous lipid with different biological functions. In blood, there is a close relationship between CoQ status and cholesterol, which strongly supports the study of both molecules simultaneously. The objective of this study was to evaluate plasma CoQ, lipoprotein concentrations and CoQ/Chol ratio in a cohort of paediatric patients with different types of dyslipidaemias. A total of 60 paediatric patients were recruited (age range: 7 months–18 years), including 52 with different types of hypercholesterolemia, 2 with isolated hypertriglyceridemia and 6 with hypobetalipoproteinemia. Plasma CoQ was analysed by HPLC with electrochemical detection, and lipoprotein and cholesterol concentrations by standard automated methods. The lowest CoQ values were detected in patients with hypobetalipoproteinemia and in two cases of liver cirrhosis. Mean CoQ values were significantly higher in hypercholesterolemic patients compared to controls (average values 1.07 µmol/L and 0.63 µmol/L) while the CoQ/cholesterol ratio did not show differences (170 vs. 163, respectively). Mean CoQ values were significantly lower in the group of patients with hypobetalipoproteinemia compared to controls (mean CoQ values of 0.22 µmol/L vs. 0.63 µmol/L, respectively), while those of CoQ/cholesterol did not show differences. Pearson's correlation test showed a positive correlation between the CoQ and cholesterol values (r = 0.565, p < 0.001) and between the CoQ and the LDL cholesterol values (r = 0.610, p < 0.001). Our results suggest that it is advisable to analyse plasma CoQ and cholesterol concentrations in patients with hypobetalipoproteinemia and hypercholesterolemia associated with liver damage. [ABSTRACT FROM AUTHOR]