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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-1ß) 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.
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Antioxidantes , Estresse Oxidativo , Ubiquinona , Animais , Ubiquinona/análogos & derivados , Ubiquinona/farmacologia , Ubiquinona/uso terapêutico , Camundongos , Feminino , Antioxidantes/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Comprometimento Cognitivo Relacionado à Quimioterapia/tratamento farmacológico , Comprometimento Cognitivo Relacionado à Quimioterapia/metabolismo , Disfunção Cognitiva/tratamento farmacológico , Disfunção Cognitiva/induzido quimicamente , Disfunção Cognitiva/metabolismo , Fármacos Neuroprotetores/farmacologia , Fármacos Neuroprotetores/uso terapêutico , Doxorrubicina/efeitos adversos , Fluoruracila/efeitos adversos , Fluoruracila/farmacologia , Modelos Animais de Doenças , Antineoplásicos/farmacologia , Antineoplásicos/efeitos adversos , Ciclofosfamida/efeitos adversos , Ciclofosfamida/farmacologiaRESUMO
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.
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Apoptose , Cromo , Genisteína , Fígado , NAD(P)H Desidrogenase (Quinona) , Fator 2 Relacionado a NF-E2 , Estresse Oxidativo , Floretina , Transdução de Sinais , Sirtuína 1 , Ubiquinona , Animais , Sirtuína 1/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Ubiquinona/análogos & derivados , Ubiquinona/farmacologia , Camundongos , NAD(P)H Desidrogenase (Quinona)/metabolismo , Genisteína/farmacologia , Apoptose/efeitos dos fármacos , Fator 2 Relacionado a NF-E2/metabolismo , Cromo/toxicidade , Fígado/efeitos dos fármacos , Fígado/metabolismo , Fígado/patologia , Floretina/farmacologia , Transdução de Sinais/efeitos dos fármacos , Masculino , Arsênio/toxicidade , Heme Oxigenase (Desciclizante)/metabolismo , Heme Oxigenase-1/metabolismo , Proteínas de MembranaRESUMO
The relationship between amyloid beta (Aß) 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 ß-site amyloid precursor protein cleaving enzyme-1 (BACE-1) and Glycogen synthase kinase-3-beta (GSK-3ß) enzymes initiate the synthesis of Aß, 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-3ß 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, ß-site amyloid precursor protein cleaving enzyme-1 (BACE-1), phosphatase and tensin homolog (Pten), and Glycogen synthase kinase-3-beta (GSK-3ß), 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-3ß. These findings were substantiated by histological and immunohistological examinations of the hippocampus.
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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.
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Antioxidants play a pivotal role in maintaining skin health and integrity, combating the deleterious effects of oxidative stress induced by environmental aggressors such as UV ra-diation, pollution, and lifestyle factors. This paper reviews the contributions of key antioxidants, including Vitamin C, Vitamin E, Vitamin A, green tea extract, Coenzyme Q10, Resveratrol, Selenium, and Polyphenols, in skin health care. Vitamin C, known for its collagen synthesis promotion and photoprotection properties, alongside Vitamin E, a lipid-soluble antioxidant, syn-ergistically works to neutralize free radicals and repair damaged skin cells. Vitamin A, in the form of retinol, plays a critical role in skin cell regeneration and the maintenance of skin integ-rity. Green tea extract, rich in Polyphenols, offers anti-inflammatory and anticarcinogenic prop-erties, making it a potent ingredient for skin protection. Coenzyme Q10, a naturally occurring antioxidant in the body, aids in energy production for cell repair and regeneration, while Resveratrol, found in grapes and berries, provides anti-ageing benefits by enhancing skin's re-sistance to oxidative stress. Selenium, an essential mineral, contributes to the protection of skin cells from oxidative damage. The incorporation of these antioxidants in skincare products and dietary sources is discussed, highlighting the importance of a holistic approach in skincare re-gimes. The paper emphasizes the synergy between topical applications and dietary intake of antioxidants, advocating for a comprehensive strategy for promoting skin health and preventing age-related skin alterations. Method: For the review article, a variety of search engines and databases were used to identify relevant articles. Furthermore, for biomedical literature focusing on antioxidants and their ef-fects on skin health, PubMed was used. Moreover, to access a wide range of scholarly articles, including those related to dermatology and skincare, Google Scholar was used. Scopus provides comprehensive coverage of peer-reviewed literature across various scientific disciplines. Web of Science identifies high-impact articles and research on antioxidants in skincare. In addition, for accessing full-text articles on antioxidants and their applications in dermatology, Science Direct was used. The inclusion criteria for the review paper were as follows: only studies pub-lished in peer-reviewed journals were included to ensure the credibility and reliability of the information. Articles published in English were considered, to avoid language-related biases and ensure comprehension. Studies published within the last 10 years were included to provide the most current insights into antioxidant research in skincare. Articles must specifically focus on the role of antioxidants (Vitamin C, Vitamin E, Vitamin A, green tea extract, Coenzyme Q10, Resveratrol, Selenium, Polyphenols) in skin health care. Both experimental studies (in vivo and in vitro) and clinical trials were included to provide a comprehensive overview of the antioxidant effects. Full-text articles were included to allow for thorough data extraction and analysis. The exclusion criteria for the review paper were as follows: Publications that were not peer-re-viewed, such as editorials, opinion pieces, and non-scholarly articles, were excluded. Articles published in languages other than English were excluded due to potential translation challenges and to maintain consistency. Studies that did not focus on the specified antioxidants or their impact on skin health were excluded. Duplicate publications were excluded to avoid redundancy in the review. Articles with insufficient or incomplete data were excluded to ensure the quality and reliability of the review findings.
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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 SpragueâDawley 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.
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Remodelação Óssea , Ratos Sprague-Dawley , Técnicas de Movimentação Dentária , Ubiquinona , Ubiquinona/análogos & derivados , Ubiquinona/farmacologia , Animais , Ratos , Feminino , Remodelação Óssea/efeitos dos fármacos , Fator A de Crescimento do Endotélio Vascular/metabolismo , Ligante RANK/metabolismo , Processo Alveolar/efeitos dos fármacos , Osteoclastos/efeitos dos fármacos , Antioxidantes/farmacologiaRESUMO
BACKGROUND: To quantitatively evaluate the effect of coenzyme Q10 (CoQ10) pretreatment on outcomes of IVF or ICSI in women with diminished ovarian reserve (DOR) based on the existing randomized controlled trials (RCTs). METHODS: Nine databases were comprehensively searched from database inception to November 01, 2023, to identify eligible RCTs. Reproductive outcomes of interest consisted of three primary outcomes and six secondary outcomes. The sensitivity analysis was adopted to verify the robustness of pooled results. RESULTS: There were six RCTs in total, which collectively involved 1529 participants with DOR receiving infertility treatment with IVF/ICSI. The review of available evidence suggested that CoQ10 pretreatment was significantly correlated with elevated clinical pregnancy rate (OR = 1.84, 95%CI [1.33, 2.53], p = 0.0002), number of optimal embryos (OR = 0.59, 95%CI [0.21, 0.96], p = 0.002), number of oocytes retrieved (MD = 1.30, 95%CI [1.21, 1.40], p < 0.00001), and E2 levels on the day of hCG (SMD = 0.37, 95%CI [0.07, 0.66], p = 0.01), along with a reduction in cycle cancellation rate (OR = 0.60, 95%CI [0.44, 0.83], p = 0.002), miscarriage rate (OR = 0.38, 95%CI [0.15, 0.98], p = 0.05), total days of Gn applied (MD = -0.89, 95%CI [-1.37, -0.41], p = 0.0003), and total dose of Gn used (MD = -330.44, 95%CI [-373.93, -286.96], p < 0.00001). The sensitivity analysis indicated that our pooled results were robust. CONCLUSIONS: These findings suggested that CoQ10 pretreatment is an effective intervention in improving IVF/ICSI outcomes for women with DOR. Still, this meta-analysis included relatively limited sample sizes with poor descriptions of their methodologies. Rigorously conducted trials are needed in the future.
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Fertilização in vitro , Reserva Ovariana , Taxa de Gravidez , Ensaios Clínicos Controlados Aleatórios como Assunto , Injeções de Esperma Intracitoplásmicas , Ubiquinona , Humanos , Ubiquinona/análogos & derivados , Ubiquinona/uso terapêutico , Ubiquinona/administração & dosagem , Ubiquinona/farmacologia , Feminino , Reserva Ovariana/efeitos dos fármacos , Gravidez , Injeções de Esperma Intracitoplásmicas/métodos , Fertilização in vitro/métodos , Infertilidade Feminina/terapia , Infertilidade Feminina/tratamento farmacológico , Adulto , Indução da Ovulação/métodosRESUMO
The efficacy of mesenchymal stem cell (MSC) transplantation has been reported for various diseases. We previously developed a drug delivery system targeting mitochondria (MITO-Porter) by using a microfluidic device to encapsulate Coenzyme Q10 (CoQ10) on a large scale. The current study aimed to confirm if treatment with CoQ10 encapsulated by MITO-Porter enhanced mitochondrial functions in MSCs, with the potential to improve MSC transplantation therapy. We used highly purified human bone marrow-derived MSCs, described as rapidly expanding clones (RECs), and attempted to control and increase the amount of CoQ10 encapsulated in the MITO-Porter using microfluidic device system. We treated these RECs with CoQ10 encapsulated MITO-Porter, and evaluated its cellular uptake, co-localization with mitochondria, changes in mitochondrial respiratory capacity, and cellular toxicity. There was no significant change in mitochondrial respiratory capacity following treatment with the previous CoQ10 encapsulated MITO-Porter; however, mitochondrial respiratory capacity in RECs was significantly increased by treatment with CoQ10-rich MITO-Porter. Utilization of a microfluidic device enabled the amount of CoQ10 encapsulated in MITO-Porter to be controlled, and treatment with CoQ10-rich MITO-Porter successfully activated mitochondrial functions in MSCs. The MITO-Porter system thus provides a promising tool to improve MSC cell transplantation therapy.
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Células-Tronco Mesenquimais , Mitocôndrias , Ubiquinona , Ubiquinona/análogos & derivados , Ubiquinona/administração & dosagem , Ubiquinona/farmacologia , Células-Tronco Mesenquimais/efeitos dos fármacos , Células-Tronco Mesenquimais/metabolismo , Humanos , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/metabolismo , Sistemas de Liberação de Medicamentos/métodos , Células Cultivadas , Dispositivos Lab-On-A-ChipRESUMO
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 IL1ß, SOD2, and CAT gene expression (p < 0.05) vs. control. Remarkably, Q showed a significant recovery in IL1ß 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.
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Apoptose , Peróxido de Hidrogênio , Estresse Oxidativo , Epitélio Pigmentado da Retina , Ubiquinona , Humanos , Ubiquinona/análogos & derivados , Ubiquinona/farmacologia , Epitélio Pigmentado da Retina/metabolismo , Epitélio Pigmentado da Retina/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Apoptose/efeitos dos fármacos , Peróxido de Hidrogênio/metabolismo , Peróxido de Hidrogênio/farmacologia , Mitocôndrias/metabolismo , Mitocôndrias/efeitos dos fármacos , Antioxidantes/farmacologia , Células Epiteliais/metabolismo , Células Epiteliais/efeitos dos fármacos , Linhagem Celular , Suplementos NutricionaisRESUMO
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.
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Aging results into disruptive physiological functioning and cellular processes that affect the composition and structure of the plasma membrane. The plasma membrane is the major regulator of ionic homeostasis that regulates the functioning of membrane transporters and exchangers. Coenzyme Q10 is a lipid-soluble antioxidant molecule that declines during aging and age-associated diseases. The present study aims to explore the role of Coenzyme Q10 supplementation to rats during aging on membrane transporters and redox biomarkers. The study was conducted on young and old male Wistar rats supplemented with 20â¯mg/kg b.w. of Coenzyme Q10 per day. After a period of 28 days, rats were sacrificed and erythrocyte membrane was isolated. The result exhibits significant decline in biomarkers of oxidative stress in old control rats when compared with young control. The effect of Coenzyme Q10 supplementation was more pronounced in old rats. The functioning of membrane transporters and Na+/H+ exchanger showed potential return to normal levels in the Coenzyme Q10 treated rats. Overall, the results demonstrate that Coenzyme Q10 plays an important role in maintaining redox balance in cells which interconnects with membrane integrity. Thus, Coenzyme Q10 supplementation may play an important role in protecting age related alterations in erythrocyte membrane physiology.
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Infertility, which affects around 70 million couples globally, is the inability to conceive after at least a year of continuous, unprotected sexual activity. Male-related elements are involving half of all infertility cases globally. Male infertility has various characteristics, including oligospermia, asthenozoospermia, and teratozoospermia. The purpose of this study was to assess the impact of antioxidant-rich food supplements on the properties of semen, like concentration of sperm, morphology, motility, fertility rate, and damage of DNA. Terms such as coenzyme Q10, antioxidants, folic acid, vitamin C, vitamin E, male infertility, selenium and others, were used to search for relevant research papers in the PubMed database. The findings of this study demonstrated beneficial improvements in semen parameters among infertile men who consumed dietary supplements, particularly combining antioxidants like coenzyme Q10, vitamin C, and vitamin E.
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Coenzyme Q10 (CoQ10) is an essential medicinal ingredient. In this study, we obtained a high-yielding mutant strain of CoQ10, VK-2-3, by subjecting R. sphaeroides V-0 (V-0) to a 12C6+ heavy ion beam and high-voltage prick electric field treatment. To investigate the mutation mechanism, the complete genomes of VK-2-3 and V-0 were sequenced. Collinearity analysis revealed that the nicotinamide adenine dinucleotide-dependent dehydrogenase (NAD) gene underwent rearrangement in the VK-2-3 genome. The NAD gene was overexpressed and silenced in V-0, and this construct was named RS.NAD and RS.ΔNAD. The results showed that the titers of CoQ10 in the RS.NAD and RS.ΔNAD increased and decreased by 16.00 and 33.92%, respectively, compared to those in V-0, and these differences were significant. Our results revealed the mechanism by which the VK-2-3 CoQ10 yield increases through reverse metabolic engineering, providing insights for genetic breeding and mechanistic analysis.
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BACKGROUND: 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. OBJECTIVE: 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 Q10 supplementation on SELENOP. METHODS: 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 Q10 (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. RESULTS: 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. CONCLUSION: 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.
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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.
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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.
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Tecido Conjuntivo , Retração Gengival , Ubiquinona , Cicatrização , Humanos , Ubiquinona/análogos & derivados , Ubiquinona/uso terapêutico , Ubiquinona/farmacologia , Cicatrização/efeitos dos fármacos , Masculino , Feminino , Retração Gengival/cirurgia , Adulto , Projetos Piloto , Tecido Conjuntivo/transplante , Resultado do Tratamento , Medição da Dor , Administração Tópica , Pessoa de Meia-IdadeRESUMO
Researchers have studied the effects of exercise on serum methyl-arginine and vitamin D metabolites; however, the effects of exercise combined with antioxidants are not well documented. Since oxidative stress affects the metabolism of vitamin D and methyl-arginine, we hypothesised that the antioxidant coenzyme Q10 (CoQ10) might modulate exercise-induced changes. A group of twenty-eight healthy men participated in this study and were divided into two groups: an experimental group and a control group. The exercise test was performed until exhaustion, with gradually increasing intensity, before and after the 21-day CoQ10 supplementation. Blood samples were collected before, immediately after, and 3 and 24 h after exercise. CoQ10, vitamin D metabolites, asymmetric dimethylarginine (ADMA), symmetric dimethylarginine, methylarginine, dimethylamine, arginine, citrulline, and ornithine were analysed in serum samples. CoQ10 supplementation caused a 2.76-fold increase in the concentration of serum CoQ10. Conversely, the 25(OH)D3 concentration increased after exercise only in the placebo group. ADMA increased after exercise before supplementation, but a decrease was observed in the CoQ10 supplementation group 24 h after exercise. In conclusion, our data indicate that CoQ10 supplementation modifies the effects of exercise on vitamin D and methyl-arginine metabolism, suggesting its beneficial effects. These findings contribute to the understanding of how antioxidants like CoQ10 can modulate biochemical responses to exercise, potentially offering new insights for enhancing athletic performance and recovery.
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Background: Available evidence from randomized clinical trials is contrasting and definitely inconclusive in determining whether or not CoQ10 dietary supplementation is advisable in patients with statin intolerance or poor statin tolerability. Methods: This randomized, double-blind, placebo-controlled clinical study aimed at investigating the effect of chronic dietary supplementation with coenzyme Q10 (CoQ10) phytosome on physical performance in older adults with a ≥3-month history of statin-associated asthenia. The study's participants were randomized to either a placebo or 300 mg daily CoQ10 phytosome (equivalent to 60 mg CoQ10; Ubiqsome®, Indena SpA, Milan, Italy). Asthenia, handgrip strength (HGs), 2-min step test (2MST), and 1-min sit-to-stand (STS) repetitions were assessed at baseline and at 8-week follow-up. Results: After the first 4 weeks of dietary supplementation, individuals taking CoQ10 phytosome showed a greater improvement in asthenia compared to the placebo group (p < 0.05). Even more significantly, at 8-week follow-up, participants receiving CoQ10 showed substantial improvements in asthenia (-30.0 ± 20.0%), HGS (+29.8 ± 3.6%), 2MST (+11.1 ± 1.8%), and 1-min STS repetitions (+36.4 ± 3.9%) compared to both baseline and placebo (p < 0.05). Conclusions: According to our findings, chronic dietary supplementation with CoQ10 phytosome significantly enhances physical performance in older adults with statin-associated asthenia. This could have relevant implications for improving the compliance of older adults with statin treatment.
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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). The placebo group exhibited no improvement during the 6-month follow-up period (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 < 0.05 for all relations). CONCLUSIONS: Six-month treatment with high-dose coenzyme-Q10 reduces liver steatosis and improves endothelial, vascular and left ventricle myocardial function in patients with MASLD, demonstrating significant improvements in micro- and macro-vasculature function. TRIAL REGISTRATION: NCT05941910.
Assuntos
Endotélio Vascular , Ubiquinona , Função Ventricular Esquerda , Humanos , Método Duplo-Cego , Ubiquinona/análogos & derivados , Ubiquinona/administração & dosagem , Masculino , Feminino , Pessoa de Meia-Idade , Resultado do Tratamento , Função Ventricular Esquerda/efeitos dos fármacos , Endotélio Vascular/fisiopatologia , Endotélio Vascular/efeitos dos fármacos , Fatores de Tempo , Suplementos Nutricionais , Idoso , Vasodilatação/efeitos dos fármacos , Adulto , Hepatopatia Gordurosa não Alcoólica/fisiopatologia , Hepatopatia Gordurosa não Alcoólica/tratamento farmacológico , Hepatopatia Gordurosa não Alcoólica/diagnóstico , Circulação Coronária/efeitos dos fármacos , Análise de Onda de Pulso , Fígado Gorduroso/fisiopatologia , Fígado Gorduroso/tratamento farmacológico , Fígado Gorduroso/diagnósticoRESUMO
OBJECTIVE: To evaluate the impact of coenzyme Q-10 (CoQ-10) on the dysregulated synthesis of extracellular matrix proteins mediated by transforming growth factor beta 3 (TGF-ß3) in uterine leiomyomas. DESIGN: Laboratory study. SETTING: University. PATIENTS: None. INTERVENTIONS: Treatment of immortalized uterine myometrial and leiomyoma cells to TGF-ß3 and CoQ-10. MAIN OUTCOME MEASURES: The protein concentrations of collagen 1A1 (COL1A1), collagen 3A1 (COL3A1), collagen 11A1 (COL11A1), and fibronectin (FN1) were assessed through western blot analysis after treatment of immortalized uterine myometrial and leiomyoma cells with both transforming growth factor beta (TGF-ß) 3 and concentrations of CoQ-10 at 10, 50, and 100 µM concurrently for 24 hours. RESULTS: Immortalized uterine leiomyoma and myometrial cells exposed to TGF-ß3 for 24 hours demonstrated a significant up-regulation of COL1A1, COL3A1, COL11A1, and FN1 compared with untreated cells. In leiomyoma cells, concurrent treatment with CoQ-10 over the same timeframe revealed a dose-dependent decrease in these protein concentrations compared with those in cells treated with TGF-ß3 alone. At the highest concentration of 100 µM of CoQ-10, significant decreases in the amounts of COL1A1 (0.59 ± 0.10-fold), COL3A1 (0.46 ± 0.09-fold), COL11A1 (0.53 ± 0.09-fold), and FN1 (0.56 ± 0.09-fold) were observed. Similarly, myometrial cells exposed to both TGF-ß3 and CoQ-10 demonstrated a dose-responsive decline in the amount of extracellular matrix protein compared with cells exposed to TGF-ß3 alone. Significant reductions in the amounts of COL1A1 (0.75 ± 0.03-fold), COL3A1 (0.48 ± 0.06-fold), COL11A1 (0.38 ± 0.06), and FN1 (0.69 ± 0.04-fold) were appreciated at 100-µM CoQ-10. CONCLUSION: Coenzyme Q-10 mitigated the aberrant production of key biomarkers of the extracellular matrix mediated by TGF-ß3 in uterine leiomyomas. Our findings highlight a promising nonhormonal compound that can counteract the fibroproliferative process inherent to leiomyomas.