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1.
Ubiquinone (UQ) is the only natural compound which was reported both to generate and to scavenge oxygen-derived radicals. Redox-cycling of ubiquinone may yield six different species of the parent compound: UQH2, UQH−, UQ2−, UQH•, UQ•−, and UQ. Ubiquinol (UQH2) is unequivocally considered to be the ubiquinone species capable of scavenging oxygen-derived radicals. In contrast, the ubiquinone species responsible for one e−reduction of dioxygen (O2) thereby initiating the cascade of oxidative stress is still a matter of controversial debate. In the present study this question was approached by following the effect of O2on the stability of the various reduced forms of UQ. For this purpose conditions were designed allowing the selective accumulation of the two protonated and of the two deprotonated forms of reduced ubiquinones. Our results exclude both protonated (ubiquinol, UQH2) and anionic (ubiquinol anion, UQH−, and ubiquinol dianion, UQ2−) fully reduced ubiquinones as the source exerting one e−reduction of O2. Ubisemiquinone (semiquinone radical, UQH•), when protonated, underwent rapid disproportionation, while transition to the semireduced anionic form (semiquinone radical anion, UQ•−) was found to favor autoxidation. The results obtained in this study provide a chemical base for the assessment of one e−transfer from redox-cycling UQ to O2in the respiratory chain and in biomembranes where ubihydroquinol is suggested to exert antioxidant activities. 相似文献
2.
Saito Y Fukuhara A Nishio K Hayakawa M Ogawa Y Sakamoto H Fujii K Yoshida Y Niki E 《The Journal of nutritional biochemistry》2009,20(5):350-357
Coenzyme Q (CoQ) is a well-known electron transporter in the mitochondrial respiratory chain. Furthermore, ubiquinol (UQH(2))--a reduced form of ubiquinone (UQ)--has been shown to act as a radical-scavenging antioxidant. Some studies have reported the beneficial effect of CoQ addition to cultured cells; however, the cellular uptake and distribution of CoQ have not been elucidated. In the present study, we used rat pheochromocytoma PC12 cells to investigate and compare the cellular uptake and distribution of CoQ(10) and alpha-tocopherol (alphaT). UQ(10) or UQ(10)H(2) treatment resulted in an increase in the cellular content of both CoQ(10) in a time- and concentration-dependent manner. A subcellular fractionation study revealed that the added UQ(10) as well as UQ(10)H(2) mainly localized in the mitochondrial fraction, which is similar to the localization of endogenous CoQ but different from that of alphaT. The cellular distribution of alphaT directly corresponded to the lipid distribution, while the CoQ distribution did not show any relationship with the lipid distribution, particularly in the mitochondrial and microsomal fractions. These results indicate that the cellular distribution of CoQ is completely different from that of alphaT; moreover, a certain system which accumulates CoQ preferentially in mitochondria may be suggested. 相似文献
3.
The high-potential iron-sulfur protein (HiPIP) center of succinate dehydrogenase has an electron paramagnetic resonance (epr) signal in the oxidized form, centered at g = 2.01, and under certain conditions this epr signal is accompanied by absorbances at g = 2.04, g = 1.99, and g = 1.96. These absorbances have been attributed to a spin-spin interaction of paramagnetic species, the semiquinone form of ubiquinone being involved (Ruzicka et al., Proc. Nat. Acad. Sci. USA72, 2886). In the present work this magnetic interaction is studied further; it is concluded that of the three possible species (HiPIP, Flavin H and UQ?H (ubiquinone)) which may interact with UQ?H; a second UQ? most likely partner for the interaction. Nonetheless, the HiPIP center of succinate dehydrogenase also plays a role in the interaction by acting as a “magnetic relaxer” of one or both of the interacting UQ?Hs. The physiological reaction of that part of the ubiquinone pool associated with the succinate dehydrogenase (on the matrix side of the inner mitochondrial membrane) is UQH2 ? UQ?H + H+ + e?. This is in line with recent postulates of the mechanism of ubiquinone mediation in electron transfer. 相似文献
4.
Elizabeth M. Covey-Crump Natalia V. Bykova Charles Affourtit Marcel H. N. Hoefnagel Per Gardeström Owen K. Atkin 《Physiologia plantarum》2007,129(1):175-184
In many environments, leaves experience large diurnal variations in temperature. Such short‐term changes in temperature are likely to have important implications for respiratory metabolism in leaves. Here, we used intact leaf, protoplasts and isolated mitochondria to determine the impact of short‐term changes in temperature on respiration rates (R), adenylate concentrations and the redox poise of the ubiquinone (UQ) pool in mitochondria of potato leaves. The Q10 (i.e. proportional change in R for each 10°C rise in temperature) of respiration was 1.8, both for intact leaves and protoplasts. In protoplasts, the redox poise of the extracted UQ pool (UQR/UQT) increased from 0.33 at 22°C, to 0.76 at 15°C. Further decreases in temperature (from 15 to 5°C) resulted in UQR/UQT decreasing to 0.40. Adenylate ratios in protoplasts were also temperature dependent. At high adenosine 5′‐triphosphate (ATP) adenosine 5′‐diphosphate (ADP) ratios (i.e. low ADP concentrations), UQR/UQT values were low, suggesting that adenylates restricted flux via the UQ‐reducing pathways more than they restricted flux via pathways that oxidized UQH2. To assess whether high rates of alternative oxidase (AOX) activity could have uncoupled respiratory flux (and thus UQR/UQT) from adenylate restriction of the cytochrome (Cyt) pathway, we constructed kinetic curves of O2 uptake (via the two pathways) vs UQR/UQT in isolated mitochondria, measured at two temperatures (15 and 25°C); measurements were made for mitochondria operating under state 3 (i.e. +ADP) and state 4 (i.e. −ADP) conditions. In contrast to the Cyt pathway, flux via the AOX was temperature insensitive, with maximal rates of AOX activity representing 21–57% of total O2 uptake in isolated mitochondria. We conclude that temperature‐dependent variations in UQR/UQT are largely dependent on temperature‐dependent changes in adenylate ratios, and that flux via the AOX could in some circumstances help reduce maximal UQ values. 相似文献
5.
Yann Roche 《生物化学与生物物理学报:生物膜》2006,1758(4):468-478
The thermodynamic behavior of representative short (UQ2), middle (UQ4 and UQ6) and long-chain (UQ10) ubiquinones (UQ) mixed with dipalmitoyl-phosphatidylcholine (DPPC) was studied in monolayers at the air-water interface. The influence of isoprenoid chain-length of UQ on miscibility of both lipids was investigated by analysis of surface pressure-area isotherms and using fluorescence microscopy. Analysis of excess areas (Aex) and free energies of mixing (ΔGm), calculated from compression isotherms in the full range of ubiquinones concentrations, has given evidences for UQ-rich constant-size (UQ6, UQ10) or less growth limited (UQ2, UQ4) microdomains formation within mixed films. Fluorescence microscopy observation revealed that ubiquinones are preferentially soluble in the expanded phase. When lateral pressure increased, concomitant evolutions of Aex and ΔGm parameters, and composition dependence of collapse surface pressures, argue for an evolution towards a total segregation, never reached due to expulsion of ubiquinones from the film. The possible significance of these observations is discussed in relation to ubiquinones organization and similar chain length effects in membranes. 相似文献
6.
The redox properties of ubiquinone-10 (UQ) were examined in monolayers of mixtures of dioleoylphosphatidylcholine, palmitoylsphingomyelin, and cholesterol of different compositions, self-assembled on a mercury electrode, over the pH range from 7.5 to 9.5. A detailed analysis of the cyclic voltammograms of UQ in the above lipid environments points to a mechanism consisting of an elementary electron transfer step followed by two protonation (or deprotonation) steps in quasiequilibrium and by a further electron transfer step. In a lipid environment of solid-ordered (so) microdomains in a liquid-disordered (ld) matrix, electron transport across the lipid monolayer takes place in the ld phase. In a pure so phase, UQ tends to segregate into UQ-rich pools, exhibiting reversible electron transfer steps. In a lipid environment consisting of liquid-ordered (lo) microdomains (lipid rafts) in an ld matrix, UQ molecules tend to localize along the edge of the lipid rafts. However, in a lipid environment consisting exclusively of lo and so microdomains, UQ molecules tend to segregate into UQ-rich pools. In all lipid environments, electron transport by UQ occurs with the quinone moiety localized on the solution side with respect to the ester linkages of the dioleoylphosphatidylcholine molecules. 相似文献
7.
Thomas Grenier-Larouche Anne Galinier Louis Casteilla André C. Carpentier André Tchernof 《Journal of lipid research》2015,56(10):1985-1992
Occurrence of oxidative stress in white adipose tissues contributes to its dysfunction and the development of obesity-related metabolic complications. Coenzyme Q10 (CoQ10) is the single lipophilic antioxidant synthesized in humans and is essential for electron transport during mitochondrial respiration. To understand the role of CoQ10 in adipose tissue physiology and dysfunction, the abundance of the oxidized and reduced (CoQ10red) isoforms of the CoQ10 were quantified in subcutaneous and omental adipose tissues of women covering the full range of BMI (from 21.5 to 53.2 kg/m2). Lean women displayed regional variations of CoQ10 redox state between the omental and subcutaneous depot, despite similar total content. Obese women had reduced CoQ10red concentrations in the omental depot, leading to increased CoQ10 redox state and higher levels of lipid hydroperoxide. Women with low omental CoQ10 content had greater visceral and subcutaneous adiposity, increased omental adipocyte diameter, and higher circulating interleukin-6 and C-reactive protein levels and were more insulin resistant. The associations between abdominal obesity-related cardiometabolic risk factors and CoQ10 content in the omental depot were abolished after adjustment for omental adipocyte diameter. This study shows that hypertrophic remodeling of visceral fat closely relates to depletion of CoQ10, lipid peroxidation, and inflammation. 相似文献
8.
Estela Lorza-Gil Jane C. de Souza Marta García-Arévalo Jean F. Vettorazzi Ana Carolina Marques Alessandro G. Salerno Jose Roberto Trigo Helena C. F. Oliveira 《Journal of cellular physiology》2019,234(7):11047-11059
New onset of diabetes is associated with the use of statins. We have recently demonstrated that pravastatin-treated hypercholesterolemic LDL receptor knockout (LDLr−/−) mice exhibit reductions in insulin secretion and increased islet cell death and oxidative stress. Here, we hypothesized that these diabetogenic effects of pravastatin could be counteracted by treatment with the antioxidant coenzyme Q 10 (CoQ 10), an intermediate generated in the cholesterol synthesis pathway. LDLr −/− mice were treated with pravastatin and/or CoQ 10 for 2 months. Pravastatin treatment resulted in a 75% decrease of liver CoQ 10 content. Dietary CoQ 10 supplementation of pravastatin-treated mice reversed fasting hyperglycemia, improved glucose tolerance (20%) and insulin sensitivity (>2-fold), and fully restored islet glucose-stimulated insulin secretion impaired by pravastatin (40%). Pravastatin had no effect on insulin secretion of wild-type mice. In vitro, insulin-secreting INS1E cells cotreated with CoQ 10 were protected from cell death and oxidative stress induced by pravastatin. Simvastatin and atorvastatin were more potent in inducing dose-dependent INS1E cell death (10–15-fold), which were also attenuated by CoQ 10 cotreatment. Together, these results demonstrate that statins impair β-cell redox balance, function and viability. However, CoQ 10 supplementation can protect the statins detrimental effects on the endocrine pancreas. 相似文献
9.
10.
Purple, photosynthetic reaction centers from Rhodobacter sphaeroides bacteria use ubiquinone (UQ10) as both primary (QA) and secondary (QB) electron acceptors. Many quinones reconstitute QA function, while a few will act as QB. Nine quinones were tested for their ability to bind and reconstitute QA and QB functions. Only ubiquinone (UQ) reconstitutes both functions in the same protein. The affinities of the non-native quinones for the QB site were determined by a competitive inhibition assay. The affinities of benzoquinones, naphthoquinone (NQ), and 2-methyl-NQ for the QB site are 7 ± 3 times weaker than that at QA site. However, di-ortho-substituted NQs and anthraquinone bind tightly to the QA site (K d ≤ 200 nM), and ≥1,000 times more weakly to the QB site, perhaps setting a limit on the size of the site. With a low-potential electron donor, 2-methyl, 3-dimethylamino-1,4-NQ, (Me-diMeAm-NQ) at QA, QB reduction is 260 meV, more favorable than with UQ as QA. Electron transfer from Me-diMeAm-NQ at the QA site to NQ at the QB site can be detected. In the QB site, the NQ semiquinone is estimated to be ≈60–100 meV higher in energy than the UQ semiquinone, while in the QA site, the semiquinone energy level is similar or lower with NQ than with UQ. Thus, the NQ semiquinone is more stable in the QA than in the QB site. In contrast, the native UQ semiquinone is ≈60 meV lower in energy in the QB than in the QA site, stabilizing forward electron transfer from QA to QB. 相似文献
11.
《Critical reviews in biochemistry and molecular biology》2013,48(1):69-77
Ubiquinone (UQ), also known as coenzyme Q (CoQ), is a redox-active lipid present in all cellular membranes where it functions in a variety of cellular processes. The best known functions of UQ are to act as a mobile electron carrier in the mitochondrial respiratory chain and to serve as a lipid soluble antioxidant in cellular membranes. All eukaryotic cells synthesize their own UQ. Most of the current knowledge on the UQ biosynthetic pathway was obtained by studying Escherichia coli and Saccharomyces cerevisiae UQ-deficient mutants. The orthologues of all the genes known from yeast studies to be involved in UQ biosynthesis have subsequently been found in higher organisms. Animal mutants with different genetic defects in UQ biosynthesis display very different phenotypes, despite the fact that in all these mutants the same biosynthetic pathway is affected. This review summarizes the present knowledge of the eukaryotic biosynthesis of UQ, with focus on the biosynthetic genes identified in animals, including Caenorhabditis elegans, rodents, and humans. Moreover, we review the phenotypes of mutants in these genes and discuss the functional consequences of UQ deficiency in general. 相似文献
12.
Ohishi H Odoko M Zhou DY Tozuka Y Okabe N Nakatani K Ishida T Grzeskowiak K 《Biochemical and biophysical research communications》2008,368(2):382-387
In crystals of complexes of thermine and d(CGCGCG)2 molecules grown at 4, 10, and 20 °C, the numbers of thermine molecules connected to the DNA molecule were dependent on the temperature of the crystallization. Two molecules of thermine and one Mg2+ ion were connected to DNA molecule when thermine and d(CGCGCG)2 were co-crystallized at 4 and at 20 °C. When an increased concentration of magnesium and thermine molecules were co-crystallized with d(CGCGCG)2 molecules at 10 °C, three Mg2+ ions and only one thermine molecule were bound with a d(CGCGCG)2 molecule. The number of polyamines and of Mg2+ ions connected to DNA was dependent on the atomic values of the polyamine and of the metal ion. The binding of more Mg2+ ions occurred when the atomic value of Mg2+ exceeded that of the corresponding mono- or polyamine, and when the Mg2+ ion concentration was elevated. Furthermore, this study is the first documentation of a naturally occurring polyamine bound to the minor groove of DNA in a crystal structure. 相似文献
13.
Ion homeostasis is essential for plant cell resistance to salt stress. Under salt stress, to avoid cellular damage and nutrient deficiency, plant cells need to maintain adequate K nutrition and a favorable K to Na ratio in the cytosol. Recent observations revealed that both nitric oxide (NO) and hydrogen peroxide (H2O2) act as signaling molecules to regulate K to Na ratio in calluses from Populus euphratica under salt stress. Evidence indicated that NO mediating H2O2 causes salt resistance via the action of plasma membrane H+-ATPase but that activity of plasma membrane NADPH oxidase is dependent on NO. Our study demonstrated the signaling transduction pathway. In this addendum, we proposed a testable hypothesis for NO function in regulation of H2O2 mediating salt resistance.Key Words: hydrogen peroxide, nitric oxide, signaling molecule, salt resistanceUnder salinity conditions, tolerant plant cells achieve ion homeostasis by extruding Na to the external medium and/or compartmentalizing into vacuoles, maintaining K uptake and high K and low Na in the cytosol.1,2 Control of Na movement across the plasma membrane (PM) and tonoplast in order to maintain a low Na concentration in the cytoplasm is a key factor of cellular adaptation to salt stress.3,4 Na transport across the PM is dependent on the electrochemical gradient created by the PM H+-ATPase.5,6 It has been proven that the activity of the PM H+-ATPase is a key index of plant adaptation to salt stress.7 Therefore, the regulation of expression of the PM H+-ATPase may represent an important cellular mechanism for salt resistance. In contrast to our understanding of the regulation of PM H+-ATPase by other factors, the roles of NO and H2O2 act as signals under salt stress have been less known.Previous studies have shown that both NO and H2O2 function as stress signals in plants, mediating a range of resistance mechanisms in plants under stress conditions.8–10 We have previously shown that NO serves as a signal in inducing salt resistance by increasing the K to Na ratio, which is dependent on the increased PM H+-ATPase activity in calluses from reed.11 Although NO acts as a signal molecule under salt stress and induces salt resistance by increasing PM H+-ATPase activity, our research results also indicated NO can not activate purified PM H+-ATPase activity, at least in vitro. Subsequently, we set out to find the other signal molecules and factors between NO and PM H+-ATPase activity. Since our studies have indicated that NO can not induce salt resistance directly, what roles dose it play in salt resistance in tolerant cells under salt stress? We initially hypothesized ABA or H2O2 might be downstream signal molecules to regulate the activity of PM H+-ATPase. Further results indicated H2O2 content increased greatly under salt stress. Since H2O2 might be the candidate downstream signal molecule, we tested PM H+-ATPase activity and K to Na ratio in calluses by adding H2O2. The results suggested that H2O2 inducing an increased PM H+-ATPase activity resulted in an increased K to Na ratio. Summing up this new assay that allows us to speculate NO maybe regulate the H2O2 generation.Since H2O2 is involved in downstream signal molecule of NO, PM NADPH oxidase, the main source of H2O2 production, might be the regulated target of NO. We took a pharmacological approach to examine the speculation. The results indicated that PM NADPH oxidase is required for H2O2 accumulation and PM NADPH oxidase activity could attribute to NO in calluses under salt stress. These results also raised another question regarding what concentrations of NO can induce such effects. In our experiments, NO content was induced 1.6 times higher than the control values under salt treatment. We speculated there exists an effective balance point in NO signal system similar to previous reports by Delledonne et al.12 in disease resistance.Further research work is required to decipher the mechanism through which NO and H2O2 acts and how K and Na elements uptake might be connected with salt resistance. We would like to propose a simple testable model that accounts for the results reported in this paper (Fig. 1). According to our model, H2O2 rather than NO is the major signaling molecular that mediated directly PM H+-ATPase under salt stress. Normally, NO generated from nitric oxide synthase (NOS) acts as a signal molecule to regulate other mechanisms. Under salt stress, accumulated NO activates PM NADPH oxidase activity. Then, a number of H2O2 is produced from PM NADPH oxidase. The PM H+-ATPase is activated greatly by the accumulated H2O2. Eventually, the transmembrane electrochemical gradient is created and K to Na ratio increases. The model we have proposed here is testable and should provide further insights into salt resistance mechanism regulated by NO and H2O2 signal molecules.Open in a separate windowFigure 1Hypothetical model for the potential function of NO and H2O2 as signaling molecules in inducing salt resistance. Salt stress activates a signal transduction cascade that leads to the increased activity of PM H+-ATPase, whose expression produces salt resistance. NO is generated by NOS, and H2O2 is produced by NADPH oxidase attributed to NO. The activity of PM H+-ATPase is regulated by H2O2 directly under salt stress. The model is based on the recent results in calluses from P. euphratica12 and those previously reported on the NO function in reed.11Research on roles of NO and H2O2 under stress conditions in plant is advancing rapidly. Further analysis of salt resistance mechanism with novel technology will certainly increase our knowledge in this field. 相似文献
14.
Giulio Kleiner Emanuele Barca Marcello Ziosi Valentina Emmanuele Yimeng Xu Agustin Hidalgo-Gutierrez Changhong Qiao Saba Tadesse Estela Area-Gomez Luis C. Lopez Catarina M. Quinzii 《生物化学与生物物理学报:疾病的分子基础》2018,1864(11):3708-3722
Nephrotic syndrome (NS), a frequent chronic kidney disease in children and young adults, is the most common phenotype associated with primary coenzyme Q10 (CoQ10) deficiency and is very responsive to CoQ10 supplementation, although the pathomechanism is not clear. Here, using a mouse model of CoQ deficiency-associated NS, we show that long-term oral CoQ10 supplementation prevents kidney failure by rescuing defects of sulfides oxidation and ameliorating oxidative stress, despite only incomplete normalization of kidney CoQ levels and lack of rescue of CoQ-dependent respiratory enzymes activities. Liver and kidney lipidomics, and urine metabolomics analyses, did not show CoQ metabolites. To further demonstrate that sulfides metabolism defects cause oxidative stress in CoQ deficiency, we show that silencing of sulfide quinone oxido-reductase (SQOR) in wild-type HeLa cells leads to similar increases of reactive oxygen species (ROS) observed in HeLa cells depleted of the CoQ biosynthesis regulatory protein COQ8A. While CoQ10 supplementation of COQ8A depleted cells decreases ROS and increases SQOR protein levels, knock-down of SQOR prevents CoQ10 antioxidant effects. We conclude that kidney failure in CoQ deficiency-associated NS is caused by oxidative stress mediated by impaired sulfides oxidation and propose that CoQ supplementation does not significantly increase the kidney pool of CoQ bound to the respiratory supercomplexes, but rather enhances the free pool of CoQ, which stabilizes SQOR protein levels rescuing oxidative stress. 相似文献
15.
A. Baccarini-Melandri N. Gabellini B.A. Melandri K.R. Jones A.W. Rutherford A.R. Crofts E. Hurt 《Archives of biochemistry and biophysics》1982,216(2):566-580
In chromatophores from the facultative photosynthetic bacterium, Rhodopseudomonas sphaeroides, Ga, the function of ubiquinone-10 (UQ-10) at two specialized binding sites (QB and QZ) has been determined by kinetic criteria. These were the rate of rereduction of flash-oxidized [BChl]2+ through the back reaction, or the binary pattern of cytochrome b561 (for the Qb site), and the rapid rate of rereduction of flash-oxidized cytochrome c, or the relative amplitude of the antimycin-sensitive Phase III () of the carotenoid spectral shift induced by a single turnover flash at Eh ~ 100 mV (for the QZ site). The phenomenon associated with the two binding sites behaved differently on extraction of UQ from lyophilized chromatophores using isooctane. By this selective extraction procedure it has been possible to show that UQ-10 molecules are required at different concentrations in the membrane for specific redox events in secondary electron transfer. The reduction of cytochrome b occurs in particles which no longer show the phenomena associated with QZ, but still possess a large proportion of Qb, while rapid rereduction of flash-oxidized cytochrome c requires an additional complement of UQ-10 (QZ). Extracted particles lacking QZ and a large amount of QB have been reconstituted with different UQ homologs (UQ-1, UQ-3, and UQ-10). Specific redox events have been studied in reconstituted particles. All UQ homologs act as secondary acceptors from the reaction center; UQ-3 and UQ-10, but not UQ-1, are also able to reconstitute the function of QZ as electron donor to cytochrome c. Only UQ-10, however, is able to restore normal rates of the overall cyclic electron transfer induced by a train of flashes, and maximal rates of the light-induced ATP synthesis. The results are interpreted in terms of Q-cycle mechanisms in which quinone and quinol at both the QZ and Qb sites are in rapid equilibrium with the quinone pool. 相似文献
16.
Sanjay Singh Parmar Anjali Jaiwal Om Parkash Dhankher 《Critical reviews in biotechnology》2015,35(2):152-164
Coenzyme Q10 (CoQ10) or Ubiquinone10 (UQ10), an isoprenylated benzoquinone, is well-known for its role as an electron carrier in aerobic respiration. It is a sole representative of lipid soluble antioxidant that is synthesized in our body. In recent years, it has been found to be associated with a range of patho-physiological conditions and its oral administration has also reported to be of therapeutic value in a wide spectrum of chronic diseases. Additionally, as an antioxidant, it has been widely used as an ingredient in dietary supplements, neutraceuticals, and functional foods as well as in anti-aging creams. Since its limited dietary uptake and decrease in its endogenous synthesis in the body with age and under various diseases states warrants its adequate supply from an external source. To meet its growing demand for pharmaceutical, cosmetic and food industries, there is a great interest in the commercial production of CoQ10. Various synthetic and fermentation of microbial natural producers and their mutated strains have been developed for its commercial production. Although, microbial production is the major industrial source of CoQ10 but due to low yield and high production cost, other cost-effective and alternative sources need to be explored. Plants, being photosynthetic, producing high biomass and the engineering of pathways for producing CoQ10 directly in food crops will eliminate the additional step for purification and thus could be used as an ideal and cost-effective alternative to chemical synthesis and microbial production of CoQ10. A better understanding of CoQ10 biosynthetic enzymes and their regulation in model systems like E. coli and yeast has led to the use of metabolic engineering to enhance CoQ10 production not only in microbes but also in plants. The plant-based CoQ10 production has emerged as a cost-effective and environment-friendly approach capable of supplying CoQ10 in ample amounts. The current strategies, progress and constraints of CoQ10 production in plants are discussed in this review. 相似文献
17.
Quinone and inhibitor binding to Rhodopseudomonas sphaeroides (R-26 and GA) reaction centers were studied using spectroscopic methods and by direct adsorption of reaction centers onto anion exchange filters in the presence of 14C-labelled quinone or inhibitor. These measurements show that as secondary acceptor, QB, ubiquinone (UQ) is tightly bound in the semiquinone form and loosely bound in the quinone and quinol forms. The quinol is probably more loosely bound than the quinone. o-Phenanthroline and terbutryn, a triazine inhibitor, compete with UQ and with each other for binding to the reaction center. Inhibition by o-phenanthroline of electron transfer from the primary to the secondary quinone acceptor (QA to QB) occurs via displacement of UQ from the QB binding site. Displacement of UQ by terbutryn is apparently accessory to the inhibition of electron transfer. Terbutryn binding is lowered by reduction of QB to Q?B but is practically unaffected by reduction of QA to Q?A in the absence of QB. UQ-9 and UQ-10 have a 5- to 6-fold higher binding affinity to the QB site than does UQ-1, indicating that the long isoprenoid chain facilitates the binding to the QB site. 相似文献
18.
The reaction center-light harvesting complex 1 (RC-LH1) purified from the photosynthetic bacterium Rhodobacter sphaeroides has been studied with respect to the kinetics of charge recombination and to the phospholipid and ubiquinone (UQ) complements tightly associated with it. In the antenna-RC complexes, at 6.5 < pH < 9.0, P+QB− recombines with a pH independent average rate constant <k> more than three times smaller than that measured in LH1-deprived RCs. At increasing pH values, for which <k> increases, the deceleration observed in RC-LH1 complexes is reduced, vanishing at pH > 11.0. In both systems kinetics are described by a continuous rate distribution, which broadens at pH > 9.5, revealing a strong kinetic heterogeneity, more pronounced in the RC-LH1 complex. In the presence of the antenna the QAQB− state is stabilized by about 40 meV at 6.5 < pH < 9.0, while it is destabilized at pH > 11. The phospholipid/RC and UQ/RC ratios have been compared in chromatophore membranes, in RC-LH1 complexes and in the isolated peripheral antenna (LH2). The UQ concentration in the lipid phase of the RC-LH1 complexes is about one order of magnitude larger than the average concentration in chromatophores and in LH2 complexes. Following detergent washing RC-LH1 complexes retain 80-90 phospholipid and 10-15 ubiquinone molecules per monomer. The fractional composition of the lipid domain tightly bound to the RC-LH1 (determined by TLC and 31P-NMR) differs markedly from that of chromatophores and of the peripheral antenna. The content of cardiolipin, close to 10% weight in chromatophores and LH2 complexes, becomes dominant in the RC-LH1 complexes. We propose that the quinone and cardiolipin confinement observed in core complexes reflects the in vivo heterogeneous distributions of these components. Stabilization of the charge separated state in the RC-LH1 complexes is tentatively ascribed to local electrostatic perturbations due to cardiolipin. 相似文献
19.
Mario Durán-Prado Javier Fronti?án Raquel Santiago-Mora Juan Ramón Peinado Cristina Parrado-Fernández María Victoria Gómez-Almagro María Moreno José Alberto López-Domínguez José Manuel Villalba Francisco J. Alcaín 《PloS one》2014,9(10)
Neuropathological symptoms of Alzheimer''s disease appear in advances stages, once neuronal damage arises. Nevertheless, recent studies demonstrate that in early asymptomatic stages, ß-amyloid peptide damages the cerebral microvasculature through mechanisms that involve an increase in reactive oxygen species and calcium, which induces necrosis and apoptosis of endothelial cells, leading to cerebrovascular dysfunction. The goal of our work is to study the potential preventive effect of the lipophilic antioxidant coenzyme Q (CoQ) against ß-amyloid-induced damage on human endothelial cells. We analyzed the protective effect of CoQ against Aβ-induced injury in human umbilical vein endothelial cells (HUVECs) using fluorescence and confocal microscopy, biochemical techniques and RMN-based metabolomics. Our results show that CoQ pretreatment of HUVECs delayed Aβ incorporation into the plasma membrane and mitochondria. Moreover, CoQ reduced the influx of extracellular Ca2+, and Ca2+ release from mitochondria due to opening the mitochondrial transition pore after β-amyloid administration, in addition to decreasing O2
.− and H2O2 levels. Pretreatment with CoQ also prevented ß-amyloid-induced HUVECs necrosis and apoptosis, restored their ability to proliferate, migrate and form tube-like structures in vitro, which is mirrored by a restoration of the cell metabolic profile to control levels. CoQ protected endothelial cells from Aβ-induced injury at physiological concentrations in human plasma after oral CoQ supplementation and thus could be a promising molecule to protect endothelial cells against amyloid angiopathy. 相似文献
20.
Maryam Dowlatabadi Mansour Jahangiri 《Journal of biomolecular structure & dynamics》2013,31(14):3616-3626
AbstractMolecular dynamics (MD) simulation was applied to investigate the adsorption mechanism of chlortetracycline (CTC) antibiotic molecule as the aqueous pollutant on the Fe3O4 nanoparticle (NP). Two different NP sizes with a diameter of about 1.4?nm and 3.5?nm were selected. Initially, the stability of both NPs in water was investigated by calculating radial distribution function curves of NP atoms. Simulation results confirmed the stable crystallographic structures of both NPs. However, small NP induce greater structural stabilization. Then, CTC molecules were adsorbed on NPs surface in various pollutant concentrations. Electrostatic and hydrogen bond were the major types of interactions between CTC molecules and the adsorbent surface. CTC molecules formed a complex with NP surface from their amine side chains; while they were parallel to each other in their aromatic rings and π-π bond between two CTC molecules was formed. Diffusion rate of CTC molecules could predict the adsorption mechanism. At lower concentration of CTC, CTC molecules tend to adsorb on the NP surface. At these concentrations, the diffusion rate of CTC was high. By increasing the CTC concentration, the pollutant agglomeration was enhanced which decreased the diffusion rate. At this time, the surface of NP was saturated. In addition, the results of isotherm curves showed that CTC adsorption on small NPs could be defined with both Langmuir and Freundlich isotherm models, while Freundlich isotherm model was more appropriate for larger NPs. In conclusion, observations confirmed that MD simulation could successfully predict the behavior of CTC adsorption on the Fe3O4 NP surface.Communicated by Ramaswamy H. Sarma 相似文献