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1.
Food-grade microemulsions containing oleic acid, ethanol, Tween 20, and water were formulated as a carrier system for tea seed oil ( Camellia oleifera Abel.). The effect of ethanol on the phase behavior of the microemulsion system was clearly reflected in pseudo-ternary diagrams. The solubilization capacity and solubilization efficiency of tea seed oil dispersions were measured along the dilution line at a 70/30 surfactant/oil mass ratio with Tween 20 as the surfactant and oleic acid and ethanol (1:3, w/w) as the oil phase. The dispersed phase of the microemulsion (1.5% weight ratio of tea seed oil to the total amount of oil, surfactant, and tea seed oil) could be fully diluted with water without phase separation. Differential scanning calorimetry and viscosity measurements indicated that both the carrier and solubilized systems underwent a similar microstructure transition upon dilution. The dispersion phases gradually inverted from the water-in-oil phase (< 35% water) to the bicontinuous phase (40–45% water) and finally to the oil-in-water phase (> 45% water) along the dilution line. 相似文献
2.
Coenzyme Q 10 (CoQ 10) is present in humans in both the reduced (ubiquinol, CoQ 10H 2) and oxidized (ubiquinone, CoQ 10) forms. CoQ 10 is an essential cofactor in mitochondrial oxidative phosphorylation, and is necessary for ATP production. Total, reduced and oxidized CoQ 10 levels in skeletal muscle of 148 children were determined by HPLC coupled with electrochemical detection, and we established three level thresholds for total CoQ 10 in muscle. We defined as “severe deficiency”, CoQ 10 levels falling in the range between 0.82 and 4.88 μmol/g tissue; as “intermediate deficiency”, those ranging between 5.40 and 9.80 μmol/g tissue, and as “mild deficiency”, the amount of CoQ 10 included between 10.21 and 19.10 μmol/g tissue. Early identification of CoQ 10 deficiency has important implications in children, not only for those with primary CoQ 10 defect, but also for patients with neurodegenerative disorders, in order to encourage earlier supplementation with this agent also in mild and intermediate deficiency. 相似文献
3.
Solubilization and structural stability of a membrane protein bacteriorhodopsin (bR) with n-octyl-β-thioglucoside (OTG) was investigated in comparison with a previous study on bR solubilized with n-octyl-β-glucoside (OG). Highly efficient and stable solubilization of bR with OTG was accomplished above the OTG concentration of about 15 m M. In comparison with OG-solubilized bR, the structural stability of OTG-solubilized bR was high in the dark and under light illumination. These results indicate that OTG is a detergent superior to OG for solubilizing bR molecules. 相似文献
4.
The structure-activity relationship of a U-type antimicrobial microemulsion system containing glycerol monolaurate and ethanol at a 1∶1 mass ratio as oil phase and Tween 20 as surfactant were investigated along a water dilution line at a ratio of 80∶20 mass% surfactant/oil phase, based on a pseudo-ternary phase diagram. The differential scanning calorimetry results showed that in the region of up to 33% water, all water molecules are confined to the hydrophilic core of the reverse micelles, leading to the formation of w/o microemulsion. As the water content increases, the water gains mobility, and transforms into bicontinuous in the region of 33–39% water, and finally the microemulsion become o/w in the region of above 39% water. The microstructure characterization was confirmed by the dynamic light scattering measurements and freeze-fracture transmission electron microscope observation. The antimicrobial activity assay using kinetics of killing analysis demonstrated that the microemulsions in w/o regions exhibited relatively high antimicrobial activity against Escherichia coli and Staphylococcus aureus due to the antimicrobial oil phase as the continuous phase, while the antimicrobial activity started to decrease when the microemulsions entered the bicontinuous region, and decreased rapidly as the water content increased in the o/w region, as a result of the dilution of antimicrobial oil droplets in the aqueous continuous phase. 相似文献
5.
The production yield of Coenzyme Q 10 (CoQ 10) from the sucrose consumed by Agrobacterium tumefaciens KCCM 10413 decreased, and high levels of exopolysaccharide (EPS) accumulated after switching from batch culture to fed-batch
culture. Therefore, we examined the effect of sucrose concentration on the fermentation profile by A. tumefaciens. In the continuous fed-batch culture with the sucrose concentration maintained constantly at 10, 20, 30, and 40 g l −1, the dry cell weight (DCW), specific CoQ 10 content, CoQ 10 production, and the production yield of CoQ 10 from the sucrose consumed increased, whereas EPS production decreased as maintained sucrose concentration decreased. The
pH-stat fed-batch culture system was adapted for CoQ 10 production to minimize the concentration of the carbon source and osmotic stress from sucrose. Using the pH-stat fed-batch
culture system, the DCW, specific CoQ 10 content, CoQ 10 production, and the product yield of CoQ 10 from the sucrose consumed increased by 22.6, 13.7, 39.3, and 39.3%, respectively, whereas EPS production decreased by 30.7%
compared to those of fed-batch culture in the previous report (Ha SJ, Kim SY, Seo JH, Oh DK, Lee JK, Appl Microbiol Biotechnol,
74:974–980, 2007). The pH-stat fed-batch culture system was scaled up to a pilot scale (300 l), and the CoQ 10 production results obtained (626.5 mg l −1 of CoQ 10 and 9.25 mg g DCW −1 of specific CoQ 10 content) were similar to those obtained at the laboratory scale. Thus, an efficient and highly competitive process for microbial
CoQ 10 production is available. 相似文献
6.
In a water-organic solvent, two-phase conversion system, CoQ 10 could be produced directly from solanesol and para-hydroxybenzoic acid (PHB) by free cells of Sphingomonas sp. ZUTE03 and CoQ 10 concentration in the organic solvent phase was significantly higher than that in the cell. CoQ 10 yield reached a maximal value of 60.8 mg l −1 in the organic phase and 40.6 mg g −1-DCW after 8 h. CoQ 10 also could be produced by gel-entrapped cells in the two-phase conversion system. Soybean oil and hexane were found to be
key substances for CoQ 10 production by gel-entrapped cells of Sphingomonas sp. ZUTE03. Soybean oil might improve the release of CoQ10 from the gel-entrapped cells while hexane was the suitable solvent
to extract CoQ 10 from the mixed phase of aqueous and organic. The gel-entrapped cells could be re-used to produce CoQ 10 by a repeated-batch culture. After 15 repeats, the yield of CoQ 10 kept at a high level of more than 40 mg l −1. After 8 h conversion under optimized precursor’s concentration, CoQ 10 yield of gel-trapped cells reached 52.2 mg l −1 with a molar conversion rate of 91% and 89.6% (on PHB and solanesol, respectively). This is the first report on enhanced
production of CoQ 10 in a two-phase conversion system by gel-entrapped cells of Sphingomonas sp. ZUTE03. 相似文献
7.
AbstractCoenzyme Q 10 (CoQ 10) is a poorly-water soluble compound that is being investigated for the treatment of carcinomas. The aim of this research was to develop a suitable formulation for pulmonary delivery of this anticancer agent. An appropriate selection of excipients (phospholipids) and a suitable device (Aeroneb Pro® vibrating-mesh nebulizer) were selected initially after reviewing the literature. After characterization of the bulk drug, a feasible manufacturing process was selected to obtain small particle size dispersions of CoQ 10. Following selection of an appropriate process, the parameters affecting drug particle size were studied. Using LD and gravimetrical analysis, nebulization was evaluated to assess the performance of the inhalation system triad: drug–excipients–device. CoQ 10 powder studied was crystalline with a melting point approximately at 51?°C and with a particle size of 30?µm. Microfluidization was found to be a suitable method to prepare submicron drug particles in aqueous dispersions. Increasing microfluidization processing to more than 50 passes did not provide further particle downsizing for both soya phosphatidylcholine (lecithin) and dipalmitoyl phosphatidylcholine (DPPC) dispersions of CoQ 10, presenting Z-average values of approximately 130 and 70?nm, respectively. Nebulization performance of lecithin-stabilized CoQ 10 dispersions varied according to number of passes in the microfluidizer. Formulations processed with 10 passes presented steadier nebulization over time and different rheological behavior compared to those processed with 30 or 50 passes. In conclusion, aqueous dispersions of CoQ 10 were adequately produced using a microfluidizer with characteristics that were suitable for pulmonary delivery with an Aeroneb Pro® nebulizer. Furthermore, the rheology of these dispersions appeared to play a significant role in the aerosol generation from the active vibrating-mesh nebulizer used. 相似文献
8.
Coenzyme Q 10(CoQ 10) in human milk at different stages of maturity in mothers of preterm and full-term infants and its relation to the total antioxidant capacity of milk is described for the first time. Thirty healthy breastfeeding women provided colostrum, transition-milk and mature-milk samples. Coenzyme Q, α-, γ- and δ-tocopherol, fatty acids and the total antioxidant capacity of the milk were analyzed. Coenzyme Q 10 was found at higher concentrations for colostrum (0.81 ± 0.06 vs. 0.50 ± 0.05 μmol/l) and transition milk (0.75 ± 0.06 vs. 0.45 ± 0.05 μmol/l) in the full-term vs. the preterm group (similar results were found for total antioxidant capacity). Concentrations of α- and γ-tocopherol were higher in the full-term group and decreased with time. In conclusion, CoQ 10 is present in breast milk, with higher concentration in mothers of full-term infants. CoQ 10 in breast milk decreases through lactation in mothers delivering full-term infants. Also, CoQ 10, α- and γ-tocopherol concentration in human milk directly correlates with the antioxidant capacity of the milk. 相似文献
9.
BackgroundAlthough causative mutations have been identified for numerous mitochondrial disorders, few disease-modifying treatments are available. Two examples of treatable mitochondrial disorders are coenzyme Q 10 (CoQ 10 or ubiquinone) deficiency and mitochondrial neurogastrointestinal encephalomyopathy (MNGIE). Scope of reviewHere, we describe clinical and molecular features of CoQ 10 deficiencies and MNGIE and explain how understanding their pathomechanisms have led to rationale therapies. Primary CoQ 10 deficiencies, due to mutations in genes required for ubiquinone biosynthesis, and secondary deficiencies, caused by genetic defects not directly related to CoQ 10 biosynthesis, often improve with CoQ 10 supplementation. In vitro and in vivo studies of CoQ 10 deficiencies have revealed biochemical alterations that may account for phenotypic differences among patients and variable responses to therapy. In contrast to the heterogeneous CoQ 10 deficiencies, MNGIE is a single autosomal recessive disease due to mutations in the TYMP gene encoding thymidine phosphorylase (TP). In MNGIE, loss of TP activity causes toxic accumulations of the nucleosides thymidine and deoxyuridine that are incorporated by the mitochondrial pyrimidine salvage pathway and cause deoxynucleoside triphosphate pool imbalances, which, in turn cause mtDNA instability. Allogeneic hematopoetic stem cell transplantation to restore TP activity and eliminate toxic metabolites is a promising therapy for MNGIE. Major conclusionsCoQ 10 deficiencies and MNGIE demonstrate the feasibility of treating specific mitochondrial disorders through replacement of deficient metabolites or via elimination of excessive toxic molecules. General significanceStudies of CoQ 10 deficiencies and MNGIE illustrate how understanding the pathogenic mechanisms of mitochondrial diseases can lead to meaningful therapies. This article is part of a Special Issue entitled: Biochemistry of Mitochondria, Life and Intervention 2010. 相似文献
10.
Coenzyme Q10 (CoQ10) is the main CoQ species in human and is used extensively in food, cosmetic and medicine industries because of its antioxidant properties and its benefit in prophylactic medicine and therapy for a variety of diseases. Among various approaches to increase the production of CoQ10, microbial fermentation is the most effective. As knowledge of the biosynthetic enzymes and regulatory mechanisms modulating CoQ10 production increases, opportunities arise for metabolic engineering of CoQ10 in microbial hosts. In this review, we present various strategies used up to date to improve CoQ10 production and focus on metabolic engineering of CoQ10 overproduction in microbes. General strategies of metabolic engineering include providing sufficient precursors for CoQ10, increasing metabolic fluxes, and expanding storage capacity for CoQ10. Based on these strategies, CoQ10 production has been significantly improved in natural CoQ10 producers, as well as in heterologous hosts. 相似文献
11.
Coenzyme Q 10 (CoQ 10), an obligatory cofactor in the aerobic respiratory electron transfer for energy generation, is formed from the conjugation
of a benzoquinone ring with a hydrophobic isoprenoid chain. CoQ 10 is now used as a nutritional supplement because of its antioxidant properties and is beneficial in the treatment of several
human diseases when administered orally. Bioprocesses have been developed for the commercial production of CoQ 10 because of its increased demand, and these bioprocesses depend on microbes that produce high levels of CoQ 10 naturally. However, as knowledge of the biosynthetic enzymes and the regulatory mechanisms modulating CoQ 10 production increases, approaches arise for the genetic engineering of CoQ 10 production in Escherichia coli and Agrobacterium tumefaciens. This review focused on approaches for CoQ 10 production, strategies used to engineer CoQ 10 production in microbes, and potential applications of CoQ 10. 相似文献
12.
2,3-Dimethoxy-5-hydroxy-6-phytyl-and-6-farnesyl-1,4-benzoquinones (HPB and HFB) inhibit DPNH- and succin-oxidases of intact mitochondria from yeast. CoQ 2 reversed the inhibition in DPNH-oxidase, but there was little or no reversal in succin-oxidase. CoQ 6, the dominant CoQ of yeast, showed the same relative reversals as CoQ 2. For CoQ 6-deficient DPNH-oxidase, supplementation with: (a) HPB; (b) HFB; (c) HPB and CoQ 6; (d) HPB and CoQ 10 showed unexpected increases in activity indicating coenzymatic activity for HPB and HFB; the inhibitory effects of HPB and HFB were apparent with supplementation with CoQ 2. HPB inhibited the CoQ 6-deficient succin-oxidase, and also in the presence of CoQ 2, CoQ 6 or CoQ 10. 相似文献
13.
The purpose of these studies was to prepare and characterize nanoparticles into which Coenzyme Q 10 (CoQ 10) had been incorporated (CoQ 10-NPs) using a simple and potentially scalable method. CoQ 10-NPs were prepared by cooling warm microemulsion precursors composed of emulsifying wax, CoQ 10, Brij 78, and/or Tween 20. The nanoparticles were lyophilized, and the stability of CoQ 10-NPs in both lyophilized form and aqueous suspension was monitored over 7 days. The release of CoQ 10 from the nanoparticles was investigated at 37°C. Finally, an in vitro study of the uptake of CoQ 10-NPs by mouse macrophage, J774A.1, was completed. The incorporation efficiency of CoQ 10 was approximately 74%±5%. Differential Scanning Calorimetry (DSC) showed that the nanoparticle was not a physical mixture
of its individual components. The size of the nanoparticles increased over time if stored in aqueous suspension. However,
enhanced stability was observed when the nanoparticles were stored at 4°C. Storage in lyophilized form demonstrated the highest
stability. The in vitro release profile of CoQ 10 from the nanoparticles showed an initial period of rapid release in the first 9 hours followed by a period of slower and
extended release. The uptake of CoQ 10-NPs by the J774A.1 cells was over 4-fold higher than that of the CoQ 10-free nanoparticles ( P<.05). In conclusion, CoQ 10-NPs with potential application for oral CoQ 10 delivery were engineered readily from microemulsion precursors. 相似文献
14.
Coenzyme Q 10 (CoQ 10), a strong antioxidant, is used extensively in food, cosmetic and medicine industries. A natural producer, Rhodopseudomonas palustris, was engineered to overproduce CoQ 10. For increasing the CoQ 10 content, crtB gene was deleted to block the carotenoid pathway. crtB gene deletion led to 33% improvement of CoQ 10 content over the wild type strain. However, it was found that the yield of hopanoids was also increased by competing for the precursors from carotenoid pathway with CoQ 10 pathway. To further increase the CoQ 10 content, hopanoid pathway was blocked by deleting shc gene, resulting in R. palustris [ Δshc, ΔcrtB] to produce 4·7 mg g −1 DCW CoQ 10, which was 1·2 times higher than the CoQ 10 content in the wild type strain. The common strategy of co-expression of rate-limiting enzymes (DXS, DPS and UbiA) was combined with the pathway blocking method resulted in 8·2 mg g −1 DCW of CoQ 10, which was 2·9 times higher than that of wild type strain. The results suggested a synergistic effect among different metabolic engineering strategies. This study demonstrates the potential of R. palustris for CoQ 10 production and provides viable strategies to increase CoQ 10 titer. 相似文献
15.
BackgroundCoenzyme Q 10 (CoQ 10) and its analogs are used therapeutically by virtue of their functions as electron carriers, antioxidant compounds, or both. However, published studies suggest that different ubiquinone analogs may produce divergent effects on oxidative phosphorylation and oxidative stress. Methodology/Principal FindingsTo test these concepts, we have evaluated the effects of CoQ 10, coenzyme Q 2 (CoQ 2), idebenone, and vitamin C on bioenergetics and oxidative stress in human skin fibroblasts with primary CoQ 10 deficiency. A final concentration of 5 µM of each compound was chosen to approximate the plasma concentration of CoQ 10 of patients treated with oral ubiquinone. CoQ 10 supplementation for one week but not for 24 hours doubled ATP levels and ATP/ADP ratio in CoQ 10 deficient fibroblasts therein normalizing the bioenergetics status of the cells. Other compounds did not affect cellular bioenergetics. In COQ2 mutant fibroblasts, increased superoxide anion production and oxidative stress-induced cell death were normalized by all supplements. Conclusions/SignificanceThese results indicate that: 1) pharmacokinetics of CoQ 10 in reaching the mitochondrial respiratory chain is delayed; 2) short-tail ubiquinone analogs cannot replace CoQ 10 in the mitochondrial respiratory chain under conditions of CoQ 10 deficiency; and 3) oxidative stress and cell death can be counteracted by administration of lipophilic or hydrophilic antioxidants. The results of our in vitro experiments suggest that primary CoQ 10 deficiencies should be treated with CoQ 10 supplementation but not with short-tail ubiquinone analogs, such as idebenone or CoQ 2. Complementary administration of antioxidants with high bioavailability should be considered if oxidative stress is present. 相似文献
16.
Mevalonic aciduria (MVA) and phenylketonuria (PKU) are inborn errors of metabolism caused by deficiencies in the enzymes mevalonate kinase and phenylalanine 4-hydroxylase, respectively. Despite numerous studies the factors responsible for the pathogenicity of these disorders remain to be fully characterised. In common with MVA, a deficit in coenzyme Q 10 (CoQ 10) concentration has been implicated in the pathophysiology of PKU. In MVA the decrease in CoQ 10 concentration may be attributed to a deficiency in mevalonate kinase, an enzyme common to both CoQ 10 and cholesterol synthesis. However, although dietary sources of cholesterol cannot be excluded, the low/normal cholesterol levels in MVA patients suggests that some other factor may also be contributing to the decrease in CoQ 10.The main factor associated with the low CoQ 10 level of PKU patients is purported to be the elevated phenylalanine level. Phenylalanine has been shown to inhibit the activities of both 3-hydroxy-3-methylglutaryl-CoA reductase and mevalonate-5-pyrophosphate decarboxylase, enzymes common to both cholesterol and CoQ 10 biosynthesis.Although evidence of a lowered plasma/serum CoQ 10 level has been reported in MVA and PKU, few studies have assessed the intracellular CoQ 10 concentration of patients. Plasma/serum CoQ 10 is influenced by dietary intake as well as its lipoprotein content and therefore may be limited as a means of assessing intracellular CoQ 10 concentration. Whether the pathogenesis of MVA and PKU are related to a loss of CoQ 10 has yet to be established and further studies are required to assess the intracellular CoQ 10 concentration of patients before this relationship can be confirmed or refuted. 相似文献
17.
By the optimization of nitrogen source for coenzyme Q 10 (ubiquinone, CoQ 10) production in Agrobacterium tumefaciens KCCM 10413 culture, the highest CoQ 10 production was achieved in medium containing corn steep powder (CSP). Components for a stimulatory effect on the production
of CoQ 10 in CSP were screened, and lactate was found to increase dry cell weight (DCW) and the specific CoQ 10 content. In a fed-batch culture of A. tumefaciens, supplementation with 1.5 g of lactate l −1 further improved DCW, the specific CoQ 10 content, and CoQ 10 production by 16.0, 5.8, and 22.8%, respectively. It has been reported that lactate stimulates cell growth and acts as an
accelerator driving the tricarboxylic acid (TCA) cycle (Roberto et al. 2002, Biotechnol Let 24:427–431; Matsuoka et al. 1996, Biosci Biotechnol Biochem 60:575–579). In this study, lactate supplementation increased DCW and the specific CoQ 10 content in A. tumefaciens culture, probably by accelerating TCA cycle and energy production as reported previously, leading to the increase of CoQ 10 production. 相似文献
18.
Coenzyme Q 10 (CoQ 10) is an important mitochondrial electron transfer component and has been postulated to function as a powerful antioxidant protecting LDL from oxidative damage. It could thus reduce the risk of cardiovascular disease. Thus far, beneficial effects of supplementation with CoQ 10 have been reported. To study the relation between unsupplemented concentrations of plasma CoQ 10 and coronary atherosclerosis, we performed a case-control study among 71 male cases with angiographically documented severe coronary atherosclerosis and 69 healthy male controls free from symptomatic cardiovascular disease and without atherosclerotic plaques in the carotid artery.Plasma CoQ 10 concentrations (mean ± SE) were 0.86 ± 0.04 vs. 0.83 ± 0.04 μmol/l for cases and controls, respectively. The CoQ 10/LDL-cholesterol ratio (μmol/mmol) was slightly lower in cases than in controls (0.22 ± 0.01 vs. 0.26 ± 0.03). Differences in CoQ 10 concentrations and CoQ 10/LDL-cholesterol ratio did not reach significance. The odds ratios (95% confidence interval) for the risk of coronary atherosclerosis calculated per μmol/l increase of CoQ 10 was 1.12 (0.28–4.43) after adjustment for age, smoking habits, total cholesterol and diastolic blood pressure.We conclude that an unsupplemented plasma CoQ 10 concentration is not related to risk of coronary atherosclerosis. 相似文献
19.
Familial Hypercholesterolemia (FH) is an autosomal co-dominant genetic disorder characterized by elevated low-density lipoprotein (LDL) cholesterol levels and increased risk for premature cardiovascular disease. Here, we examined FH pathophysiology in skin fibroblasts derived from FH patients harboring heterozygous mutations in the LDL-receptor.Fibroblasts from FH patients showed a reduced LDL-uptake associated with increased intracellular cholesterol levels and coenzyme Q 10 (CoQ 10) deficiency, suggesting dysregulation of the mevalonate pathway.Secondary CoQ 10 deficiency was associated with mitochondrial depolarization and mitophagy activation in FH fibroblasts. Persistent mitophagy altered autophagy flux and induced inflammasome activation accompanied by increased production of cytokines by mutant cells. All the pathological alterations in FH fibroblasts were also reproduced in a human endothelial cell line by LDL-receptor gene silencing.Both increased intracellular cholesterol and mitochondrial dysfunction in FH fibroblasts were partially restored by CoQ 10 supplementation. Dysregulated mevalonate pathway in FH, including increased expression of cholesterogenic enzymes and decreased expression of CoQ 10 biosynthetic enzymes, was also corrected by CoQ 10 treatment.Reduced CoQ 10 content and mitochondrial dysfunction may play an important role in the pathophysiology of early atherosclerosis in FH. The diagnosis of CoQ 10 deficiency and mitochondrial impairment in FH patients may also be important to establish early treatment with CoQ 10. 相似文献
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