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1.
In an attempt to provide further confirmation of the antioxidant role of reduced form of coenzyme Q homologue (CoQnH2) and α-tocopherol (α-Toc), we incubated isolated rat hepatocytes with a water-soluble radical initiator, 2,2′-azobis(2-amidinopropane)dihydrochloride (AAPH) in the presence or absence of exogenously added coenzyme Q10 (CoQ10) or α-Toc for 3 h at 37°C under an atmosphere of 95% oxygen and 5% carbon dioxide. In the control experiment without adding AAPH it was confirmed that added CoQ10 and α-Toc were incorporated into the cells and some CoQ10 were converted to CoQ10H2. Incubation of hepatocytes with 50 mM AAPH resulted in the formation of thiobarbituric acid-reactive substances and the decrease in cell viability and both were inhibited by exogenously added CoQ10 or α-Toc in a dose-dependent manner. The decrease in endogenous CoQ9H2 and α-Toc levels was observed by the addition of AAPH. Addition of CoQ10 inhibited the oxidation of CoQ9H2 to CoQ9 dose-dependently while the addition of α-Toc did not. These data suggest that both CoQnH2 and α-Toc act as antioxidants and can inhibit free radical-mediated cell injury.  相似文献   

2.
By the optimization of nitrogen source for coenzyme Q10 (ubiquinone, CoQ10) production in Agrobacterium tumefaciens KCCM 10413 culture, the highest CoQ10 production was achieved in medium containing corn steep powder (CSP). Components for a stimulatory effect on the production of CoQ10 in CSP were screened, and lactate was found to increase dry cell weight (DCW) and the specific CoQ10 content. In a fed-batch culture of A. tumefaciens, supplementation with 1.5 g of lactate l−1 further improved DCW, the specific CoQ10 content, and CoQ10 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 CoQ10 content in A. tumefaciens culture, probably by accelerating TCA cycle and energy production as reported previously, leading to the increase of CoQ10 production.  相似文献   

3.
The use of coenzyme Q10 (CoQ10) as a complementary therapy in heart failure will increase in proportion to the growth of the ageing population and the expansion of statins consumption. Economical production of CoQ10 by microbes will become more important due to the growing demands of the pharmaceutical industry. Process simplification and integration might be one desirable pathway for economic production of CoQ10 by microbial fermentation. In this report, the effect of a coupled fermentation–extraction process on CoQ10 production by newly isolated Sphingomonas sp. ZUTEO3 was evaluated. It was found that the CoQ10 yield of the coupled process was significantly higher than that of the traditional process. As optimal conditions in our experiment, 2% soybean oil was added to the original culture to enhance cell membrane permeability, and 50 mL hexane was added to the 30 h culture as an extracting solvent for the subsequent coupled fermentation–extraction process. The maximal yield of CoQ10 reached 43.2 mg/L and 32.5 mg/g dry cell weight after 38 h of total fermentation period. The coupled process represents one potential pathway for CoQ10 production with even higher yield and lower cost. This is the first report of CoQ10 production by Sphingomonas sp. using a coupled fermentation–extraction process.  相似文献   

4.
The cell growth and CoQ10 (coenzyme Q10) formation of Rhizobium radiobacter WSH2601 were investigated in a 7-1 bioreactor under different dissolved oxygen (DO) concentrations. A maximal CoQ10 content (C/B) of 1.91 mg/g dry cell weight (DCW) and CoQ10 concentration of 32.1 mg/l were obtained at the appropriate DO concentration of 40% (of air saturation). High DO concentration was favourable to the cell growth of Rhizobium radiobacter WSH2601. In order to achieve the maximal yield of CoQ10 production, a new DO-stat feeding strategy was proposed, which significantly improved cell growth and CoQ10 formation. With this strategy, the maximal CoQ10 concentration and DCW reached 51.1 mg/l and 23.9 g/l, respectively, which were 67 and 44.8% higher than those obtained in the batch culture with DO concentration controlled.  相似文献   

5.

Background

Mitochondria are both the cellular powerhouse and the major source of reactive oxygen species. Coenzyme Q10 plays a key role in mitochondrial energy production and is recognized as a powerful antioxidant. For these reasons it can be argued that higher mitochondrial ubiquinone levels may enhance the energy state and protect from oxidative stress. Despite the large number of clinical studies on the effect of CoQ10 supplementation, there are very few experimental data about the mitochondrial ubiquinone content and the cellular bioenergetic state after supplementation. Controversial clinical and in vitro results are mainly due to the high hydrophobicity of this compound, which reduces its bioavailability.

Principal Findings

We measured the cellular and mitochondrial ubiquinone content in two cell lines (T67 and H9c2) after supplementation with a hydrophilic CoQ10 formulation (Qter®) and native CoQ10. Our results show that the water soluble formulation is more efficient in increasing ubiquinone levels. We have evaluated the bioenergetics effect of ubiquinone treatment, demonstrating that intracellular CoQ10 content after Qter supplementation positively correlates with an improved mitochondrial functionality (increased oxygen consumption rate, transmembrane potential, ATP synthesis) and resistance to oxidative stress.

Conclusions

The improved cellular energy metabolism related to increased CoQ10 content represents a strong rationale for the clinical use of coenzyme Q10 and highlights the biological effects of Qter®, that make it the eligible CoQ10 formulation for the ubiquinone supplementation.  相似文献   

6.
The pharmacokinetics of the total pool of coenzyme Q10 (CoQ10), its oxidized (ubiquinone) and reduced (ubiquinol, CoQ10H2) forms have been investigated in rats plasma during 48 h after a single intravenous injection of a solution of solubilized CoQ10 (10 mg/kg) to rats. Plasma levels of CoQ10 were determined by HPLC with spectrophotometric and coulometric detection. In plasma samples taken during the first minutes after the CoQ10 intravenous injection, the total pool of coenzyme Q10 and proportion of CoQ10H2 remained unchanged during two weeks of storage at ?20°C. The kinetic curve of the total pool of coenzyme Q10 corresponds to a one-compartment model (R 2 = 0.9932), while the corresponding curve of its oxidized form fits to the two-compartment model. During the first minutes after the injection a significant portion of plasma ubiquinone undergoes reduction, and after 7 h the concentration of ubiquinol predominates. The decrease in total plasma coenzyme Q10 content was accompanied by the gradual increase in plasma ubiquinol, which represented about 90% of total plasma CoQ10 by the end of the first day. The results of this study demonstrate the ability of the organism to transform high concentrations of the oxidized form of CoQ10 into the effective antioxidant (reduced) form and justify prospects of the development of parenteral dosage forms of CoQ10 for the use in the treatment of acute pathological conditions.  相似文献   

7.
Summary In the production of coenzyme Q10 (CoQ10) by Agrobacterium sp. the culture broth becomes highly viscous. In an attempt to improve the production process, the effects of chemical and physical factors on broth viscosity and CoQ10 production were studied, using Agrobacterium sp. KY-8593. A particular concentration ratio of sugar to ammonium-nitrogen (NH4–N) in the medium could effectively enhance CoQ10 production without increasing broth viscosity. An increase in culture temperature to between 32°C and 34°C lowered broth viscosity without reducing CoQ10 production. NH4–N concentration and temperature had a correlative effect on broth viscosity. At a temperature of about 33°C, there was a wide range of NH4–N concentration which was optimal for both broth viscosity and CoQ10 production. In optimal conditions with 8% sugar the apparent broth viscosity was reduced to less than 10 pseudo-cP and CoQ10 production was increased to more than 80 mg/l.  相似文献   

8.
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 Q10 (CoQ10) deficiency, suggesting dysregulation of the mevalonate pathway.Secondary CoQ10 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 CoQ10 supplementation. Dysregulated mevalonate pathway in FH, including increased expression of cholesterogenic enzymes and decreased expression of CoQ10 biosynthetic enzymes, was also corrected by CoQ10 treatment.Reduced CoQ10 content and mitochondrial dysfunction may play an important role in the pathophysiology of early atherosclerosis in FH. The diagnosis of CoQ10 deficiency and mitochondrial impairment in FH patients may also be important to establish early treatment with CoQ10.  相似文献   

9.
This report describes the optimization of culture conditions for coenzyme Q10 (CoQ10) production by Agrobacterium tumefaciens KCCM 10413, an identified high-CoQ10-producing strain (Kim et al., Korean patent. 10-0458818, 2002b). Among the conditions tested, the pH and the dissolved oxygen (DO) levels were the key factors affecting CoQ10 production. When the pH and DO levels were controlled at 7.0 and 0–10%, respectively, a dry cell weight (DCW) of 48.4 g l−1 and a CoQ10 production of 320 mg l−1 were obtained after 96 h of batch culture, corresponding to a specific CoQ10 content of 6.61 mg g-DCW−1. In a fed-batch culture of sucrose, the DCW, specific CoQ10 content, and CoQ10 production increased to 53.6 g l−1, 8.54 mg g-DCW−1, and 458 mg l−1, respectively. CoQ10 production was scaled up from a laboratory scale (5-l fermentor) to a pilot scale (300 l) and a plant scale (5,000 l) using the impeller tip velocity (V tip) as a scale-up parameter. CoQ10 production at the laboratory scale was similar to those at the pilot and plant scales. This is the first report of pilot- and plant-scale productions of CoQ10 in A. tumefaciens.  相似文献   

10.
Coenzyme Q10(CoQ10) 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 Q10 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, CoQ10 is present in breast milk, with higher concentration in mothers of full-term infants. CoQ10 in breast milk decreases through lactation in mothers delivering full-term infants. Also, CoQ10, α- and γ-tocopherol concentration in human milk directly correlates with the antioxidant capacity of the milk.  相似文献   

11.
Diabetes-induced cardiac complications include left ventricular (LV) dysfunction and heart failure. We previously demonstrated that LV phosphoinositide 3-kinase p110α (PI3K) protects the heart against diabetic cardiomyopathy, associated with reduced NADPH oxidase expression and activity. Conversely, in dominant negative PI3K(p110α) transgenic mice (dnPI3K), reduced cardiac PI3K signaling exaggerated diabetes-induced cardiomyopathy, associated with upregulated NADPH oxidase. The goal was to examine whether chronic supplementation with the antioxidant coenzyme Q10 (CoQ10) could attenuate LV superoxide and diabetic cardiomyopathy in a setting of impaired PI3K signaling. Diabetes was induced in 6-week-old nontransgenic and dnPI3K male mice via streptozotocin. After 4 weeks of diabetes, CoQ10 supplementation commenced (10 mg/kg ip, 3 times/week, 8 weeks). At study end (12 weeks of diabetes), markers of LV function, cardiomyocyte hypertrophy, collagen deposition, NADPH oxidase, oxidative stress (3-nitrotyrosine), and concentrations of CoQ9 and CoQ10 were determined. LV NADPH oxidase (Nox2 gene expression and activity, and lucigenin-enhanced chemiluminescence), as well as oxidative stress, were increased by diabetes, exaggerated in diabetic dnPI3K mice, and attenuated by CoQ10. Diabetes-induced LV diastolic dysfunction (prolonged deceleration time, elevated end-diastolic pressure, impaired E/A ratio), cardiomyocyte hypertrophy and fibrosis, expression of atrial natriuretic peptide, connective tissue growth factor, and β-myosin heavy chain were all attenuated by CoQ10. Chronic CoQ10 supplementation attenuates aspects of diabetic cardiomyopathy, even in a setting of reduced cardiac PI3K protective signaling. Given that CoQ10 supplementation has been suggested to have positive outcomes in heart failure patients, chronic CoQ10 supplementation may be an attractive adjunct therapy for diabetic heart failure.  相似文献   

12.
Summary.  Wistar rats were fed with different diets with or without supplement coenzyme Q10 (CoQ10) and with oil of different sources (sunflower or virgin olive oil) for six or twelve months. Ubiquinone contents (CoQ9 and CoQ10) were quantified in homogenates of livers and brains from rats fed with the four diets. In the brain, younger rats showed a 3-fold higher amount of ubiquinone than older ones for all diets. In the liver, however, CoQ10 supplementation increased the amount of CoQ9 and CoQ10 in both total homogenates and plasma membranes. Rats fed with sunflower oil as fat source showed higher amounts of ubiquinone content than those fed with olive oil, in total liver homogenates, but the total ubiquinone content in plasma membranes was similar with both fat sources. Older rats showed a higher amount of ubiquinone after diets supplemented with CoQ10. Two ubiquinone-dependent antioxidant enzyme activities were measured. NADH-ferricyanide reductase activity in hepatocyte plasma membranes was unaltered by ubiquinone accumulation, but this activity increased slightly with age. Both cytosolic and membrane-bound dicumarol-sensitive NAD(P)H:(quinone acceptor) oxidoreductase (DT-diaphorase, EC 1.6.99.2) activities were decreased by diets supplemented with CoQ10. Animals fed with olive oil presented lower DT-diaphorase activity than those fed with sunflower oil, suggesting that the CoQ10 antioxidant protection is strengthened by olive oil as fat source. Received May 22, 2002; accepted September 20, 2002; published online May 21, 2003 RID="*" ID="*" Correspondence and reprints: Departamento de Biología Celular, Fisiología e Inmunología, Universidad de Córdoba Edificio Severo Ochoa, Campus de Rabanales, 14071 Córdoba, Spain.  相似文献   

13.
The neurotoxic effects of cocaine and methamphetamine (METH) were studied in mice brain with a primary objective to determine the neuroprotective potential of coenzyme Q10 (CoQ10) in drug addiction. Repeated treatment of cocaine or METH induced significant reduction in the striatal dopamine and CoQ10 in mice. Cocaine or METH-treated mice exhibited increased thiobarbituric acid reactive substances (TBARs) in the striatum and cerebral cortex without any significant change in the cerebellum. Complex I immunoreactivity was inhibited in both cocaine and METH-treated mice, whereas tyrosine hydroxylase (TH) immunoreactivity was decreased in METH-treated mice and increased in cocaine-treated mice. Neither cocaine nor METH could induce significant change in α-synuclein expression at the doses and duration we have used in the present study. CoQ10 treatment attenuated cocaine and METH-induced inhibition in the striatal 18F-DOPA uptake as determined by high-resolution microPET neuroimaging. Hence exogenous administration of CoQ10 may provide neuroprotection in drug addiction.  相似文献   

14.
The study was conducted to determine the effects of dietary L-carnitine and coenzyme Q10 (CoQ10) supplementation on growth performance and ascites mortality of broilers. A 3 × 3 factorial arrangement was employed with three levels (0, 75 and 150 mg/kg) of L-carnitine and three levels of CoQ10 (0, 20 and 40 mg/kg) supplementation during the experiment. Five hundred and forty one-day-old Arbor Acre male broiler chicks were randomly allocated into nine groups with six replicates each. All birds were fed with the basal diets from day 1 to 7 and changed to the experimental diets from day 8. During day 15 to 21 all the birds were exposed to low ambient temperature (15 - 18°C) to induce ascites. The results showed that under this condition, growth performance of broilers were not significantly affected by CoQ10 or L-carnitine + CoQ10 supplementation during week 0 - 3 and 0 - 6, but body weight gain (BWG) of broilers was significantly reduced by 150 mg/kg L-carnitine during week 0 - 6. Packed cell volume (PCV) of broilers was significantly decreased by L-carnitine and L-carnitine + CoQ10 supplementation (P < 0.05). Erythrocyte osmotic fragility (EOF), ascites heart index (AHI) and ascites mortality of broilers were significantly decreased by L-carnitine, CoQ10 and L-carnitine + CoQ10 supplementation. Though no significant changes were observed in total antioxidative capability (T-AOC), total superoxide dismutase (T-SOD) was increased by L-carnitine, CoQ10 and L-carnitine + CoQ10 supplementation (P < 0.05). Malonaldehyde (MDA) content was significantly decreased by CoQ10 and L-carnitine + CoQ10 supplementation. The results indicate that dietary L-carnitine and CoQ10 supplementation reduce ascites mortality of broilers; the reason may be partially associated with their antioxidative effects.  相似文献   

15.
The major coenzyme Q species in humans is the decaprenyl quinoid derivative coenzyme Q10 (CoQ10), and its measurement is somewhat challenging owing to its hydrophobicity and tendency to be oxidized. There are three major methods which are suited for analysis of CoQ10: HPLC-coupled UV or electrochemical detection, and tandem mass spectrometry. The techniques are discussed, and results of these applications to determine CoQ10 concentrations in various human fluids and tissues are summarized.  相似文献   

16.

Background

Coenzyme Q10 (CoQ10) 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 Findings

To test these concepts, we have evaluated the effects of CoQ10, coenzyme Q2 (CoQ2), idebenone, and vitamin C on bioenergetics and oxidative stress in human skin fibroblasts with primary CoQ10 deficiency. A final concentration of 5 µM of each compound was chosen to approximate the plasma concentration of CoQ10 of patients treated with oral ubiquinone. CoQ10 supplementation for one week but not for 24 hours doubled ATP levels and ATP/ADP ratio in CoQ10 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/Significance

These results indicate that: 1) pharmacokinetics of CoQ10 in reaching the mitochondrial respiratory chain is delayed; 2) short-tail ubiquinone analogs cannot replace CoQ10 in the mitochondrial respiratory chain under conditions of CoQ10 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 CoQ10 deficiencies should be treated with CoQ10 supplementation but not with short-tail ubiquinone analogs, such as idebenone or CoQ2. Complementary administration of antioxidants with high bioavailability should be considered if oxidative stress is present.  相似文献   

17.
《Free radical research》2013,47(9):1125-1134
Abstract

Endogenous coenzyme Q10 (CoQ10) is a lipid-soluble antioxidant and essential for the electron transport chain. We previously demonstrated that hydrogen peroxide enhanced CoQ10 levels, whereas disruption of mitochondrial membrane potential by a chemical uncoupler suppressed CoQ10 levels, in human 143B cells. In this study, we investigated how CoQ10 levels and expression of two PDSS and eight COQ genes were affected by oligomycin, which inhibited ATP synthesis at Complex V without uncoupling the mitochondria. We confirmed that oligomycin increased the production of reactive oxygen species (ROS) and decreased mitochondria-dependent ATP production in 143B cells. We also demonstrated that CoQ10 levels were decreased by oligomycin after 42 or 48 h of treatment, but not at earlier time points. Expression of PDSS2 and COQ2–COQ9 were up-regulated after 18-hour oligomycin treatment, and the expression of PPARGC1A (PGC1-1α) elevated concurrently. Knockdown of PPARGC1A down-regulated the basal mRNA levels of PDSS2 and five COQ genes and suppressed the induction of COQ8 and COQ9 genes by oligomycin, but did not affect CoQ10 levels under these conditions. N-acetylcysteine suppressed the augmentation of ROS levels and the enhanced expression of COQ2, COQ4, COQ7, and COQ9 induced by oligomycin, but did not modulate the changes in CoQ10 levels. These results suggested that the condition of mitochondrial dysfunction induced by oligomycin decreased CoQ10 levels independent of oxidative stress. Up-regulation of PDSS2 and several COQ genes by oligomycin might be regulated by multiple mechanisms, including the signaling pathways mediated by PGC-1α and ROS, but it would not restore CoQ10 levels.  相似文献   

18.
BackgroundThe Coq protein complex assembled from several Coq proteins is critical for coenzyme Q6 (CoQ6) biosynthesis in yeast. Secondary CoQ10 deficiency is associated with mitochondrial DNA (mtDNA) mutations in patients. We previously demonstrated that carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP) suppressed CoQ10 levels and COQ5 protein maturation in human 143B cells.MethodsThis study explored the putative COQ protein complex in human cells through two-dimensional blue native-polyacrylamide gel electrophoresis and Western blotting to investigate its status in 143B cells after FCCP treatment and in cybrids harboring the mtDNA mutation that caused myoclonic epilepsy with ragged-red fibers (MERRF) syndrome. Ubiquinol-10 and ubiquinone-10 levels were detected by high-performance liquid chromatography. Mitochondrial energy status, mRNA levels of various PDSS and COQ genes, and protein levels of COQ5 and COQ9 in cybrids were examined.ResultsA high-molecular-weight protein complex containing COQ5, but not COQ9, in the mitochondria was identified and its level was suppressed by FCCP and in cybrids with MERRF mutation. That was associated with decreased mitochondrial membrane potential and mitochondrial ATP production. Total CoQ10 levels were decreased under both conditions, but the ubiquinol-10:ubiquinone-10 ratio was increased in mutant cybrids. The expression of COQ5 was increased but COQ5 protein maturation was suppressed in the mutant cybrids.ConclusionsA novel COQ5-containing protein complex was discovered in human cells. Its destabilization was associated with reduced CoQ10 levels and mitochondrial energy deficiency in human cells treated with FCCP or exhibiting MERRF mutation.General significanceThe findings elucidate a possible mechanism for mitochondrial dysfunction-induced CoQ10 deficiency in human cells.  相似文献   

19.
In this work, Escherichia coli was engineered to produce a medically valuable cofactor, coenzyme Q10 (CoQ10), by removing the endogenous octaprenyl diphosphate synthase gene and functionally replacing it with a decaprenyl diphosphate synthase gene from Sphingomonas baekryungensis. In addition, by over-expressing genes coding for rate-limiting enzymes of the aromatic pathway, biosynthesis of the CoQ10 precursor para-hydroxybenzoate (PHB) was increased. The production of isoprenoid precursors of CoQ10 was also improved by the heterologous expression of a synthetic mevalonate operon, which permits the conversion of exogenously supplied mevalonate to farnesyl diphosphate. The over-expression of these precursors in the CoQ10-producing E. coli strain resulted in an increase in CoQ10 content, as well as in the accumulation of an intermediate of the ubiquinone pathway, decaprenylphenol (10P-Ph). In addition, the over-expression of a PHB decaprenyl transferase (UbiA) encoded by a gene from Erythrobacter sp. NAP1 was introduced to direct the flux of DPP and PHB towards the ubiquinone pathway. This further increased CoQ10 content in engineered E. coli, but decreased the accumulation of 10P-Ph. Finally, we report that the combined over-production of isoprenoid precursors and over-expression of UbiA results in the decaprenylation of para-aminobenzoate, a biosynthetic precursor of folate, which is structurally similar to PHB.  相似文献   

20.
The production yield of Coenzyme Q10 (CoQ10) 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 CoQ10 content, CoQ10 production, and the production yield of CoQ10 from the sucrose consumed increased, whereas EPS production decreased as maintained sucrose concentration decreased. The pH-stat fed-batch culture system was adapted for CoQ10 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 CoQ10 content, CoQ10 production, and the product yield of CoQ10 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 CoQ10 production results obtained (626.5 mg l−1 of CoQ10 and 9.25 mg g DCW−1 of specific CoQ10 content) were similar to those obtained at the laboratory scale. Thus, an efficient and highly competitive process for microbial CoQ10 production is available.  相似文献   

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