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Coenzyme Q10 (CoQ10) is a potent antioxidant that provides multiple health benefits, but its incorporation into foods is challenging due to its high hydrophobicity. This study aimed to develop soy protein isolate (SPI) gels filled with CoQ10-loaded nanoemulsion. Minimum gelation concentration tests were performed at pH 5, 6 and 7, as well as 11, 13 and 15 (SPI% w/w), to determine the best conditions for gel production. Gels with 15% SPI at pH 7 and various aqueous phase replacements by YNano Q10 (25%–85%) were produced. Uniaxial compression tests indicated that oil droplets were active particles interacting with the microgels of SPI, which structured the protein network. According to the confocal laser scanning microscopy (CLSM) micrographs, the gel structure was formed by microgels, common for SPI gels, and nanodroplets occupied the gels' pores, possibly interacting with each other and with the protein matrix, forming a type of "emulsion network"; the scanning electron microscopy data corroborated the CLSM results. The stability of CoQ10 was evaluated using instrumental colorimetry and showed that the bioactive was highly stable after 45 days of storage according to instrumental color measurements. Regarding the release of CoQ10 during in vitro static digestion, the bioactive was present in the final digesta of gastric phase (GP) and intestinal phase (IP), indicating that EFGs protected the active against the harsh conditions of the gastrointestinal tract. Notably, the higher the amount of nanoemulsion, the higher the concentration of CoQ10 present in the digesta, and the presence of nanoemulsion droplets did not influence on protein hydrolysis. [ABSTRACT FROM AUTHOR]

Reperfusion arrhythmia following cardiac surgery has long been studied as part of myocardial damage. Reperfusion injury is thought to be exacerbated by oxygen-free radicals, whereas arrhythmogenic oscillations in membrane potential are mediated by reactive oxygen. Coenzyme Q10 is a lipid-soluble antioxidant that inhibits lipid peroxidation in biological membranes and supplies ATP cell synthesis, required as the organism's primary energy source. This process explains how Coenzyme Q10 helps stabilize membranes and avoids critical metabolite depletion that may relate to reperfusion arrhythmia. There is a reduction of iatrogenic Coenzyme Q10 after coronary artery bypass surgery (CABG). On the other hand, there is an increased inflammatory process and cellular demand post CABG procedure. It leads to ischemia that can be manifested as arrhythmia. Reperfusion arrhythmia was less common in patients who took Coenzyme Q10. These findings suggest that Coenzyme Q10 supplementation might help patients with heart surgery avoid reperfusion arrhythmia. However, a higher-quality randomized controlled study is needed to determine the effect of Coenzyme Q10 in preventing reperfusion arrhythmia in cardiac surgery patients. [ABSTRACT FROM AUTHOR]

Copyright of Revista Oral is the property of Benemerita Universidad Autonoma de Puebla and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

NADH-quinone oxidoreductase (respiratory complex I) is a key player in mitochondrial energy metabolism. The enzyme couples electron transfer from NADH to quinone with the translocation of protons across the membrane, providing a major proton-motive force that drives ATP synthesis. Recently, X-ray crystallography and cryo-electron microscopy provided further insights into the structure and functions of the enzyme. However, little is known about the mechanism of quinone reduction, which is a crucial step in the energy coupling process. A variety of complex I inhibitors targeting the quinone-binding site have been indispensable tools for mechanistic studies on the enzyme. Using biorationally designed inhibitor probes, the author has accumulated a large amount of experimental data characterizing the actions of complex I inhibitors. On the basis of comprehensive interpretations of the data, the author reviews the structural features of the binding pocket of quinone/inhibitors in bovine mitochondrial complex I. ATP: adenosine triphosphate; BODIPY: boron dipyrromethene; complex I: proton-translocating NADH-quinone oxidoreductase; DIBO: dibenzocyclooctyne; EM: electron microscopy; FeS: iron-sulfur; FMN: flavin adenine mononucleotide; LDT: ligand-directed tosylate; NADH: nicotinamide adenine dinucleotide; ROS: reactive oxygen species; SMP: submitochondrial particle; TAMRA: 6-carboxy-N,N,N',N'-tetramethylrhodamine; THF: tetrahydrofuran; TMH: transmembrane helix Chemical modification of respiratory complex I. The author focuses on structural features of the binding pocket of quinone/inhibitors in complex I. [ABSTRACT FROM AUTHOR]

Doxorubicin (dox) is classified as an antineoplastic antibiotic which is known as adriamycin from the anthracycline group. Due to the release of free radicals and lipid peroxidation which can cause acute cardiotoxicity. Coenzyme Q10 is found in many cells of the body, it is an antioxidant that reduces oxidative stress and lipid peroxidation. This scoping review aims to evaluate the cardioprotective effect of coenzyme Q10 in doxorubicin-induced cardiotoxicity in animals. This review was done based on Arksey and O'Malley's methodology, reviewing published articles from October 1978 and September 2023. 14 out of 11,303 articles were included from the initial search, (10 out of 14 articles found that coenzyme Q10 protect has a protection effect against doxorubicin-induced cardiotoxicity). The results of this review found coenzyme Q10 protects against doxorubicin cardiotoxicity. It is a promising supplement that could be used to prevent cardiotoxicity induced by doxorubicin in cancer patients. [ABSTRACT FROM AUTHOR]

Currently, several options are available for the prevention and treatment of cancers; however, many limitations remain with these approaches. Recently, antioxidants have become important preventive and therapeutic alternatives with few adverse events and minimum cost. Coenzyme Q10 (CoQ10) is a naturally occurring component that performs an anticancer function by reducing oxidative stress. CoQ10 supplementation as an adjuvant therapy offers more progress in the elimination and development of cancers. This review aimed to critically assess and summarize the implication of CoQ10 in cancers, highlighting possible mechanisms, and future directions of research for the standardization of the current regimen for cancer prevention and treatment. [ABSTRACT FROM AUTHOR]

Copyright of Parasite (1252607X) is the property of EDP Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

We investigated suppression of the slow growth of an Escherichia coli ispA null mutant lacking farnesyl diphosphate (FPP) synthase (i.e. IspA) by plasmids carrying prenyl diphosphate synthase genes. The growth rates of ispA mutant-transformants harboring a medium-copy number plasmid that carries ispA or ispB were almost the same as that of the wild-type strain. Although the level of FPP in the transformant with the ispA plasmid was almost the same as that in the wild-type strain, the level in the transformant with the ispB plasmid was as low as that in the ispA mutant. Purified octaprenyl diphosphate synthase (IspB) could condense isopentenyl diphosphate (IPP) with dimethylallyl diphosphate (DMAPP) to form octaprenyl diphosphate and nonaprenyl diphosphate. It is possible that suppression of the slow growth of the ispA mutant by ispB was due to condensation of IPP not only with FPP but also with DMAPP by octaprenyl diphosphate synthase. [ABSTRACT FROM AUTHOR]

Prenylquinones are isoprenoid compounds with a characteristic quinone structure and isoprenyl tail that are ubiquitous in almost all living organisms. There are four major prenylquinone classes: ubiquinone (UQ), menaquinone (MK), plastoquinone (PQ), and rhodoquinone (RQ). The quinone structure and isoprenyl tail length differ among organisms. UQ, PQ, and RQ contain benzoquinone, while MK contains naphthoquinone. UQ, MK, and RQ are involved in oxidative phosphorylation, while PQ functions in photosynthetic electron transfer. Some organisms possess two types of prenylquinones; Escherichia coli has UQ8 and MK8, and Caenorhabditis elegans has UQ9 and RQ9. Crystal structures of most of the enzymes involved in MK synthesis have been solved. Studies on the biosynthesis and functions of quinones have advanced recently, including for phylloquinone (PhQ), which has a phytyl moiety instead of an isoprenyl tail. Herein, the synthesis and applications of prenylquinones are reviewed. [ABSTRACT FROM AUTHOR]

Copyright of Arquivos Brasileiros de Oftalmologia is the property of Arquivos Brasileiros de Oftalmologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Coenzyme Q (CoQ) is a component of the electron transport chain that participates in aerobic cellular respiration to produce ATP. In addition, CoQ acts as an electron acceptor in several enzymatic reactions involving oxidation–reduction. Biosynthesis of CoQ has been investigated mainly inEscherichia coliandSaccharomyces cerevisiae, and the findings have been extended to various higher organisms, including plants and humans. Analyses in yeast have contributed greatly to current understanding of human diseases related to CoQ biosynthesis. To date, human genetic disorders related to mutations in eightCOQbiosynthetic genes have been reported. In addition, the crystal structures of a number of proteins involved in CoQ synthesis have been solved, including those of IspB, UbiA, UbiD, UbiX, UbiI, Alr8543 (Coq4 homolog), Coq5, ADCK3, and COQ9. Over the last decade, knowledge of CoQ biosynthesis has accumulated, and striking advances in related human genetic disorders and the crystal structure of proteins required for CoQ synthesis have been made. This review focuses on the biosynthesis of CoQ in eukaryotes, with some comparisons to the process in prokaryotes. The enzymes involved in CoQ synthesis form a complex inS. cerevisiae. At least nine peptides are required for the synthesis of CoQ. [ABSTRACT FROM PUBLISHER]

The article discusses a study which aims to boost coenzyme Q 10 (CoQ10) productivity in Schizosaccharomyces pombe (S. pombe) through a group of biosynthetic genes. Topics discussed include the performance of yeast culture media and genetic manipulations, analysis of extracted CoQ, and the individual overexpression of CoQ biosynthetic genes.

CoQ10 is quite possibly the most powerful antioxidant known to scientists, clinicians and researchers alike. It is rich in applications that offer an outstanding array of potential human therapeutic benefit. Some of the more prominent conditions that respond to CoQ10's use, include hypertension, migraine headaches, coronary artery disease and even Parkinson's disease. The purpose of this review is to illustrate the clinically significant findings in a plethora of prominent studies on Coenzyme Q10. [ABSTRACT FROM AUTHOR]

Abstract: Studies in human and animals have demonstrated that nutritionally induced low birth-weight followed by rapid postnatal growth increases the risk of metabolic syndrome and cardiovascular disease. Although the mechanisms underlying such nutritional programming are not clearly defined, increased oxidative-stress leading to accelerated cellular aging has been proposed to play an important role. Using an established rodent model of low birth-weight and catch-up growth, we show here that post-weaning dietary supplementation with coenzyme Q10, a key component of the electron transport chain and a potent antioxidant rescued many of the detrimental effects of nutritional programming on cardiac aging. This included a reduction in nitrosative and oxidative-stress, telomere shortening, DNA damage, cellular senescence and apoptosis. These findings demonstrate the potential for postnatal antioxidant intervention to reverse deleterious phenotypes of developmental programming and therefore provide insight into a potential translatable therapy to prevent cardiovascular disease in at risk humans. [Copyright &y& Elsevier]

Background: Statins are the most commonly prescribed and effective medications for reducing low-density lipoprotein levels. Some patients experience myopathic symptoms during statin treatment. The etiology is not known, but depletion of mevalonate pathway metabolites, including coenzyme Q10 (CoQ10), has been suggested. Despite a lack of conclusive evidence supporting its utility, CoQ10 supplementation has been recommended to patients who experience myalgic symptoms. Objective: The Co-Enzyme Q10 in Statin Myopathy study is designed to examine the effect of CoQ10 supplementation on the extent and intensity of muscle pain during treatment with simvastatin. Methods: We will recruit patients with a documented history of myalgia during statin treatment. The presence of statin-related myalgia will be confirmed in a crossover run-in trial during which the presence and absence of symptoms will be documented during statin and placebo treatment, respectively. Individuals experience myalgic symptoms while taking statins but not placebo will be randomized to receive simvastatin 20 mg daily plus either 600 mg daily of CoQ10 or placebo. Muscle pain intensity will be documented during weekly phone calls via use of the Brief Pain Inventory, Short Form. Treatment will continue for 8 weeks or until muscle symptoms are reported continuously for 1 week or become intolerable, and then subjects will crossover to the alternative treatment (CoQ10 or placebo). Results: This study is an ongoing clinical trial. Conclusions: This study will determine the utility of CoQ10 for reducing pain intensity in myalgic patients and will provide guidance for clinicians treating patients with hypercholesterolemia who are intolerant to statins. [Copyright &y& Elsevier]

The article studies tightly-bound quinone functions in the ubiquinone reaction sites of the quinoprotein alcohol dehydrogenase (ADH) of the Gluconobacter suboxydans bacterium in acetic acid. It includes an in-depth analysis of the solubilization and purification of ADH with dodecyl maltoside, as well as a discussion on the issues' implications for biological chemistry.

Abstract: Background: The hydroxymethylglutaryl coenzyme A reductase inhibitors (statins) are effective cholesterol lowering medications, however, statins may interfere with CoQ10 biosynthesis. We examined the effect of statin therapy as well as nutritional supplements on plasma, cardiac and skeletal muscle concentrations of CoQ10. Methods: Forty patients with left ventricular dysfunction had fasting blood samples collected at baseline and following four weeks of supplementation (150mg/day of CoQ10). Cardiac and skeletal muscle biopsies were collected at the time of surgery and frozen in liquid nitrogen until analyzed for CoQ10 levels by high performance liquid chromatography. Results: Nutrient supplementation significantly increased plasma [(1.8 (1.2, 2.7) vs 0.8 (0.6, 0.94) μg/ml plasma, median+IQR; p =0.001)] and cardiac tissue concentrations of CoQ10 [(120.5 (76.5, 177.1) vs 87.3 (60.5, 110.8) nmol/g wet weight, p =0.04)]. No effect of supplementation was seen on samples of skeletal muscle from the chest wall. Statin therapy was not found to influence plasma, cardiac or chest wall levels of CoQ10. Conclusion: Nutrient supplementation significantly increased plasma and cardiac tissue levels of CoQ10 but did not influence chest wall muscle concentrations. Statin therapy did not significantly influence tissue concentrations of CoQ10. Longer term studies are needed to confirm this observation. [Copyright &y& Elsevier]

Abstract: Background: Coenzyme Q10 (CoQ10) is an endogenous cofactor in the mitochondrial energy production. CoQ10 has been touted to improve heart failure, but its effect on systolic function is controversial. Several small, randomized controlled trials evaluating CoQ10 showed variable results and were largely underpowered. We conducted a meta-analysis of these trials to evaluate the impact of CoQ10 therapy on ejection fraction and cardiac output. Methods and Results: A systematic literature search was conducted to identify randomized, controlled trials of CoQ10 in heart failure between 1966 and June 2005. Subgroup analysis was conducted to assess clinical heterogeneity between trials. Of the 11 trials identified, 10 evaluated ejection fraction (n = 277) and 2 evaluated cardiac output (n = 42). Doses ranged from 60 to 200 mg/day with treatment periods ranging from 1 to 6 months. There was a 3.7% net improvement in ejection fraction (95% CI 1.59–5.77; P< .00001 for statistical heterogeneity). A more profound effect among patients not receiving angiotensin-converting enzyme inhibitors was observed (6.74% [95% CI 2.63–10.86]). Cardiac output increased an average of 0.28 L/minute (95% CI 0.03–0.53; P = .96 for statistical heterogeneity). Conclusion: CoQ10 enhances systolic function in chronic heart failure, but its effectiveness may be reduced with concomitant use of current standard therapies. [Copyright &y& Elsevier]

Summary: Pediatric cardiomyopathy (PCM) represents a group of rare and heterogeneous disorders that often results in death. While there is a large body of literature on adult cardiomyopathy, all of the information is not necessarily relevant to children with PCM. About 40% of children who present with symptomatic cardiomyopathy are reported to receive a heart transplant or die within the first two years of life. In spite of some of the advances in the management of PCM, the data shows that the time to transplantation or death has not improved during the past 35 years. Coenzyme Q10 is a vitamin-like nutrient that has a fundamental role in mitochondrial function, especially as it relates to the production of energy (ATP) and also as an antioxidant. Based upon the biochemical rationale and a large body of data on patients with adult cardiomyopathy, heart failure, and mitochondrial diseases with heart involvement, a role for coenzyme Q10 therapy in PCM patients is indicated, and preliminary results are promising. Additional studies on the potential usefulness of coenzyme Q10 supplementation as an adjunct to conventional therapy in PCM, particularly in children with dilated cardiomyopathy, are therefore warranted. [Copyright &y& Elsevier]

Discusses the functional analysis of two solanesyl diphosphate (SPP) synthases from Arabidopsis thaliana. Isolation of cDNA for A. thaliana SPP synthase (At-SPS2); Substrate and product specificities of At-SPS2; Kinetic analysis; Subcellular localization of two SPP synthases; Real-time polymerase chain reaction analysis of two SPP synthases.

In this article, the authors focus on the role of coenzyme (CoA) Q10 on the suppression of hepatic hydroxymethylglutaryl-CoA reductase (HMGR) activity in laying hens. They inform that dietary CoA Q10 reduces egg yolk cholesterol content and HMGR activity. They mention that dietary atorvastatin, a drug for hyperlipidemia, is transferred into the egg yolk in laying hens.

Abstract: Although the importance of coenzyme Q10 (CoQ10) in health and disease and its critical role in cellular bioenergetics have been well established in various species, there is a total lack of information on the role of CoQ10 in horses. Therefore, the present study was undertaken first to ascertain the occurrence of CoQ10 and/or possibly other homologs of coenzyme Q (CoQ) in horse serum, and then to examine the response to CoQ10 supplementation on serum CoQ10 concentration. The study was carried out with 2-year-old Thoroughbred horses. Total CoQ (reduced and oxidized forms) in serum was assayed by high-performance liquid chromatography. The data show that horse serum contains CoQ as CoQ10, at a much lower concentration as compared with that of humans and several other species. There is no evidence for the presence of coenzyme Q9 or other homologs of CoQ. On supplementation with CoQ10 at 800 mg a day (1.47 mg/kg body weight), there was a significant increase in serum CoQ10 concentration, approximately 2.7-fold at 60 days. CoQ10 supplementation at this dosage was found to be safe and well tolerated. Additional studies are needed to examine whether maintaining higher serum CoQ10 concentrations is of potential health benefit to the horses, as assessed by selected biochemical markers and also in terms of performance. [Copyright &y& Elsevier]

The article offers information on a study which aims to efficiently produce Coenzyme Q10 in rice by introducing the gene for decaprenyl diphosphate synthase (DdsA) into rice sugary and shrunken mutants. It says that the study utilized the rice cultivar Nipponbare and the DdsA gene was isolated from Gluconobacter suboxydans. The result is a genetically modified rice cultivar that produces 1.3 to 1.6 times coenzyme Q10 as earlier enriched rice did.

During semen cryopreservation, the sensitivity of equine sperm to oxidative stress is increased by the eliminated seminal plasma. Thus, antioxidant addition to the semen extender can be helpful to the sperm survival after freezing and thawing. This work aimed to test whether coenzyme Q10 (CoQ10) added in different concentrations to the INRA 82 freezing extender has antioxidant function on equine sperm to improve its fertilizing ability. Semen samples from five stallions were frozen with the extenders: (T1) INRA 82, control, (T2) T1+ 5 μM CoQ10, (T3) T1+ 25 μM CoQ10, and (T4) T1+ 50 μM CoQ10. After sample thawing, sperm motility and kinetics characteristics were evaluated using a computer-assisted sperm analysis and sperm membrane functionality and integrity were evaluated with a hypo-osmotic swelling test and an epifluorescence microscopy, respectively. The nitrite (NO 2 -) and hydrogen peroxide (H 2 O 2) concentrations of the semen samples were measured with spectrophotometry. There was no difference on the sperm characteristics among all treatments (P >.05). However, the 25 μM CoQ10 (T3) decreased NO 2 − concentration (6.7 ± 2.2 μM/μg protein) compared with the treatments T1, T2, and T4 (64.3 ± 3.7, 59.4 ± 5.3, 45.1 ± 8.6 μM/μg protein), respectively, as well H 2 O 2 concentration (1.8 ± 0.3 μM/μg protein) compared with the control (4.6 ± 0.4 μM/μg protein) and 5 μM CoQ10 treatments (4.8 ± 0.2 μM/μg protein, P <.05). In conclusion, 25 μM CoQ10 plays a significant role as antioxidant to the frozen equine sperm, decreasing NO 2 − and H 2 O 2 concentrations. Thus, its addition to the INRA 82 freezing extender may be beneficial to the fertilizing ability of equine semen. • Addition of CoQ10 to frozen-thawed semen of equine does not influence sperm motility. • Sperm membrane functionality and integrity of equine were not influenced by CoQ10 addition. • However, 25 μM CoQ10 decreased NO 2 − and H 2 O 2 concentration compared with the control. • Coenzyme Q10 added to the INRA 82 freezing extender has antioxidant function on equine sperm. [ABSTRACT FROM AUTHOR]

Summary Mitochondrial respiratory supercomplexes, comprising complexes I, III, and IV, are the minimal functional units of the electron transport chain. Assembling the individual complexes into supercomplexes may stabilize them, provide greater spatiotemporal control of respiration, or, controversially, confer kinetic advantages through the sequestration of local quinone and cytochrome c pools (substrate channeling). Here, we have incorporated an alternative quinol oxidase (AOX) into mammalian heart mitochondrial membranes to introduce a competing pathway for quinol oxidation and test for channeling. AOX substantially increases the rate of NADH oxidation by O 2 without affecting the membrane integrity, the supercomplexes, or NADH-linked oxidative phosphorylation. Therefore, the quinol generated in supercomplexes by complex I is reoxidized more rapidly outside the supercomplex by AOX than inside the supercomplex by complex III. Our results demonstrate that quinone and quinol diffuse freely in and out of supercomplexes: substrate channeling does not occur and is not required to support respiration. [ABSTRACT FROM AUTHOR]