bluuebunny/crossref_metadata_2025_split huggingface dataset:
Kinetic analysis of antioxidant capacity of wine
Authors: Tubaro Franco , Rapuzzi Pierpaolo , Ursini Fulvio 
Published: December 2008

AbstractA competition kinetics procedure for measuring total antioxidant capacity in wine is described. This procedure is based on the &&num;147;crocin bleaching test&&num;148; (Bors et al. Biochim. Biophys. Acta 1984, 796:, 312–319) as modified for analyzing the antioxidant capacity of complex mixtures (Tubaro et al. J. Am. Oil Chem. Soc. 1996,73, 173–179). The antioxidant capacity of white wines ranged from 0.08 to 1.2 mM equivalents of the reference antioxidant (Trolox C), while for red wines values ranging from 6.4 to 41.9 mM have been obtained. Although a correlation exists between antioxidant capacity and total phenol content of wines, due to the variable reactivity of different phenol groups, the analysis of the phenol content provides only a crude indication of the actual antioxidant capacity. The analysis of antioxidant capacity on different polyphenol classes, separated by solid phase extraction, indicated that anthocyanins are the major antioxidants of young red wines, and tannins of old red wines and white wines. Several vintages of the same grape have been analyzed and the expected decrease of antioxidant capacity upon ageing was not observed, although spectrophotometric analysis clearly demonstrated the shift from anthocyanin monomers to polymers. Artificial ageing by stirring under air produced a rapid decrease (30 min) of antioxidant capacity, followed by an increase (up to two weeks), but not any significant modification of the spectrophotometric chemical age factor. Since neither natural nor artificial ageing present a clear‐cut relationship with a decrease of antioxidant capacity, we could conclude that the a priori assumption that an old wine contains less antioxidant capacity, although popular, is not fully correct.
13‐HPODE and 13‐HODE modulate cytokine‐induced expression of endothelial cell adhesion molecules differently
Authors: Friedrichs Bärbel , Toborek Michal , Hennig Bernhard , Heinevetter Lutz , Müller Cordula , Brigelius‐Flohé Regina 
Published: December 2008

AbstractExpression of cellular adhesion molecules (CAMs) at endothelial surfaces represents a physiological response to vascular damage and mediates the initiation of inflammation and possibly of atherogenesis. The cytokines TNFα and IL‐1 are potent inducers of CAMs in endothelial cells. Reactive oxygen species comprising lipid oxidation products have been implicated in the signaling pathways of both TNFα and IL‐1 and accordingly could modulate atherogenic events. We, therefore, investigated the potential role of the lipoxygenase product, 13‐hydroperoxyoctadecadienoic acid (13‐HPODE), which has also been identified in oxidized low density lipoproteins on CAM expression in HUVEC. 13‐HPODE induced the expression of ICAM‐1 in a concentration dependent manner up to 75 μM. Higher concentrations were toxic. Similar effects were observed with H2O2and phosphatidylcholine hydroperoxide. VCAM‐1 and E‐selectin were not induced by 13‐HPODE. 13‐HPODE administered simultaneously with IL‐1 or TNFα induced ICAM‐1 additively, suggesting that hydroperoxides and cytokines act on the same signaling pathways. In contrast, pretreatment of cells with 50 μM 13‐HPODE for 1 hour rather inhibited subsequent cytokine‐induced ICAM‐1 and E‐selectin expression. Surprisingly, the reduction product of 13‐HPODE, 13‐hydroxyoctadecadienoic acid (13‐HODE) proved to be an even better inducer of ICAM‐1 than 13‐HPODE. Pretreatment with 13‐HODE did not show any inhibitory effect on ICAM‐1 expression.Our data show that lipoxygenase products differentially affect CAM expression. 13‐HPODE is stimulatory by itself and can positively or negatively affect cytokine signaling depending on time of exposure. 13‐HODE induces CAM expression by itself but does not inhibit cytokine signaling. Thus, the interplay of lipoxygenase products with proinflammatory cytokines can not simply be explained by an oxidant‐mediated facilitation of cytokine signaling.
A multifunctional hydroquinone oxidase of the external cell surface and sera
Authors: Morré D. James , Pogue Rhea , Morré Dorothy M. 
Published: December 2008

AbstractA multifunctional cell surface protein with NADH oxidase (NOX) activity and capable of oxidizing hydroquinones is located at the exterior of the cell and is shed in soluble form into sera. The oxidase appears to function as a terminal oxidase of a trans plasma membrane electron transport chain consisting of a NAD(P)H‐ubiquinone reductase at the cytosolic membrane surface, possibly a b‐type cytochrome, ubiquinone and the oxidase. Hyperactivity or conditions that interrupt ordered 2H+ + 2e− transport from NAD(P)H or hydroquinone to molecular oxygen and other acceptors at the external cell surface may result in the generation of superoxide. The latter may serve to propagate aging‐related redox changes both to adjacent cells and circulating blood components. A circulating NOX activity form associated with aging and the reduction of cytochrome c by sera of aged patients that is partially inhibited by ubiquinone are described.
Cytosolic NADPH‐UQ reductase, the enzyme responsible for cellular ubiquinone redox cycle as an endogenous antioxidant in the rat liver
Authors: Kishi Takeo , Takahashi Takayuki , Usui Akinori , Hashizume Naoko , Okamoto Tadashi 
Published: December 2008

AbstractCellular ubiquinone (UQ) is expected to act as an endogenous antioxidant against oxidative stress. To confirm this, UQ‐reductases which are necessary to regenerate ubiquinol (UQH2) were investigated in rat tissue, and a novel NADPH‐dependent UQ (NADPH‐UQ) reductase was found in cytosol. The cytosolic NADPH‐UQ reductase activity accounted for more than 80% of UQ‐10 reduction by the rat liver homogenate in the presence of NADPH. Furthermore, the NADPH‐UQ reductase activities in various tissues were correlated to the redox states of UQ in the corresponding tissues. Rat liver cytosol with NADPH protected lecithin liposomes containing UQ‐10, as well as UQH2‐10 from AMVN (2,2′‐azobis(2,4‐dimethyl‐valeronitrile))‐induced lipid peroxidation. The enzyme purified from rat liver cytosol, reduced UQ‐10 in lecithin liposomes at approximately the same rate as did cytosol. These results supported that cytosolic NADPH‐UQ reductase is the enzyme responsible for nonmitochondrial UQ reduction acting as an endogenous antioxidant against oxidative stress. The antioxidant role of the UQ redox cycle and NADPH‐UQ reductase was discussed in relation to other cellular NADPH‐dependent antioxidant enzymes.
Mitochondrial coenzyme Q content and aging
Authors: Lass Achim , Kwong Linda , Sohal Rajindar S. 
Published: December 2008

AbstractThe main objective of this study was to determine the nature of the relationship between aging and mitochondrial coenzyme Q (CoQ) content. Mitochondria in the heart, skeletal muscle, kidney and brain of the mouse varied in both the amount of total CoQ (CoQ9+CoQ10) content as well as in the ratio of the CoQ9 to CoQ10. CoQ content declined with age only in the skeletal muscle. Caloric restriction (CR) resulted in an increase in the amount of CoQ9 in skeletal muscle mitochondria. This effect was partially reversible upon termination of the caloric restriction regimen. Results suggest that a decrease in mitochondrial CoQ content is an integral aspect of aging in skeletal muscle.
A role for reduced coenzyme Q in atherosclerosis?
Authors: Thomas Shane R. , Witting Paul K. , Stocker Roland 
Published: December 2008

AbstractSubstantial evidence implicates oxidative modification of low density lipoprotein (LDL) as an important event contributing to atherogenesis. As a result, the elucidation of the molecular mechanisms by which LDL is oxidized and how such oxidation is prevented by antioxidants has been a significant research focus. Studies on the antioxidation of LDL lipids have focused primarily onα‐tocopherol (α‐TOH), biologically and chemically the most active form of vitamin E and quantitatively the major lipid‐soluble antioxidant in extracts prepared from human LDL. In addition toα‐TOH, plasma LDL also contains low levels of ubiquinol‐10 (CoQ10H2; the reduced form of coenzyme Q10). Recent studies have shown that in oxidizing plasma lipoproteinsα‐TOH can exhibit anti‐ or pro‐oxidant activities for the lipoprotein's lipids exposed to a vast array of oxidants. This article reviews the molecular action ofα‐TOH in LDL undergoing “mild” radical‐initiated lipid peroxidation, and discusses how small levels of CoQ10H2 can represent an efficient antioxidant defence for lipoprotein lipids. We also comment on the levelsα‐TOH, CoQ10H2 and lipid oxidation products in the intima of patients with coronary artery disease and report on preliminary studies examining the effect of coenzyme Q10 supplementation on atherogenesis in apolipoprotein E knockout mice.
Distribution of antioxidants among blood components and lipoproteins: Significance of lipids/CoQ10 ratio as a possible marker of increased risk for atherosclerosis
Authors: Tomasetti Marco , Alleva Renata , Solenghi Maria Diana , Littarru Gian Paolo 
Published: December 2008

AbstractTotal CoQ10 levels were evaluated in whole blood and in plasma obtained from a group of 83 healthy donors. Extraction with light petroleum ether/methanol was more efficient, for whole blood, than the extraction which is often used for plasma and serum, i.e., ethanol hexane. An excellent correlation was present between plasma CoQ10 and whole blood CoQ10. CoQ10 is mainly associated with plasma rather than with cellular components. Positive, significant correlations were found between the LDL‐chol/CoQ10 ratio and the total‐chol/HDL‐chol ratio, which is usually considered a risk factor for atherosclerosis. The proportion of CoQ10 carried by LDL was 58 ± 10%, while the amount carried by HDL was 26 ± 8%. In VLDL + IDL CoQ10 was 16 ± 8%. The content of CoQ10 in single classes of lipoproteins is strictly correlated with CoQ10 plasma concentration. In a parallel study conducted on a population of diabetic patients (one IDDM group and one NIDDM) CoQ10 plasma levels were generally higher compared to the control group, also when normalised to total cholesterol. In particular the LDL fraction showed a CoQ10/chol ratio higher in NIDDM but not in IDDM patients, compared to controls. The CoQ10/triglycerides ratio was lower in NIDDM respect to controls and even lower in IDDM patients.
Plasma ubiquinone to ubiquinol ratio in patients with hepatitis, cirrhosis, and hepatoma, and in patients treated with percutaneous transluminal coronary reperfusion
Authors: Yamamoto Yorihiro , Yamashita Satoshi 
Published: December 2008

AbstractTo assess the degree of oxidative stress, we measured plasma ubiquinone‐10 percentage (%CoQ‐10) in total amounts of ubiquinone‐10 in patients with chronic active hepatitis, liver cirrhosis, and hepatocellular carcinoma, and in age‐matched control subjects. %CoQ‐10 values were 12.9 ± 10.3 (n=28), 10.6 ± 6.8 (n=28), 18.9 ± 11.1 (n=20), and 6.4 ± 3.3 (n=16), respectively, showing a significant increase in oxidative stress in patient groups as compared to control subjects. There were no differences in total amounts of ubiquinone‐10 and ubiquinol‐10 among the four groups. We next measured %CoQ‐10 in plasmas obtained from nine patients treated with percutaneous transluminal coronary angioplasty (PTCA). Plasmas were collected when hospitalized, and at the time (0, 4, 8, 12, 16, and 20 hr, and 1, 2, 3, 4, and 7 days) after the PTCA. %CoQ‐10 values before and right after PTCA were 9.9 ± 2.8 and 11.4 ± 2.0, respectively, reached a maximum (20#150;45) at 1 or 2 days later, and decreased to 7.9 ± 2.7 at 7 days after PTCA, indicating an increase in oxidative stress in patients during coronary reperfusion.
Coenzyme Q10administration and its potential for treatment of neurodegenerative diseases
Authors: Beal M. Flint 
Published: December 2008

AbstractCoenzyme Q10(CoQ10) is an essential cofactor of the electron transport chain as well as an important antioxidant. Previous studies have suggested that it may exert therapeutic effects in patients with known mitochondrial disorders. We investigated whether it can exert neuroprotective effects in a variety of animal models. We have demonstrated that CoQ10can protect against striatal lesions produced by both malonate and 3‐nitropropionic acid. It also protects against MPTP toxicity in mice. It extended survival in a transgenic mouse model of amyotrophic lateral sclerosis. We demonstrated that oral administration can increase plasma levels in patients with Parkinson's disease. Oral administration of CoQ10significantly decreased elevated lactate levels in patients with Huntington's disease. These studies therefore raise the prospect that administration of CoQ10may be useful for the treatment of neurodegenerative diseases.
Coenzyme Q10 depletion and mitochondrial energy disturbances in rejection development in patients after heart transplantation
Authors: Gvozdjáková Anna , Kucharská Jarmila , Mizera Stanislav , Braunová Zuzana , Schreinerová Zlatica , Schrameková Eva , Pecháň Ivan , Fabián Juraj 
Published: December 2008

AbstractSixty endomyocardial biopsies (EMB) and whole blood or plasma samples from 34 patients after heart transplantation (HTx‐pts) were studied. Acute rejection of the transplanted heart was histologically graded as: 0 (without), 0‐1 (incipient), 1 (mild), 2 (moderate). The level of coenzyme Q10 (CoQ10) in 28 EMB was estimated by HPLC. Mitochondrial respiratory chain function and energy production were measured in 60 EMB. This study is the first report showing a correlation between: (a) histological signs of rejection in the human transplanted heart and (b) CoQ10 level of EMB, CoQ10 blood level, and mitochondrial bioenergetic processes: inhibition in FAD‐part, but not in NAD‐part of respiratory chain. In all patients after heart transplantation (HTx‐pts) the dynamic balance between total antioxidant status and degree of oxidative stress was disturbed.Conclusions: CoQ10 level and mitochondrial bioenergetic functions of EMB contribute to the explanation of pathobiochemical mechanisms of origin and development rejection of human transplanted heart. We suppose that estimation of EMB CoQ10 level could be used as a bioenergetic marker of rejection development in human transplanted heart. CoQ10 therapy could contribute to the prevention of rejection of the transplanted heart.
The effect of coenzyme Q10 administration on metabolic control in patients with type 2 diabetes mellitus
Authors: Eriksson J. G. , Forsén T. J. , Mortensen S. A. , Rohde M. 
Published: December 2008

AbstractA possible relationship between the pathogenesis of type 2 diabetes and coenzyme Q10 (CoQ10) deficiency has been proposed. The aim of this study was to assess the effect of CoQ10 on metabolic control in 23 type 2 diabetic patients in a randomized, placebo‐controlled trial. Treatment with CoQ10 100 mg bid caused a more than 3‐fold rise in serum CoQ10 concentration (p<0.001). No correlation was observed between serum CoQ10 concentration and metabolic control. No significant changes in metabolic parameters were observed during CoQ10 supplementation. The treatment was well tolerated and did not interfere with glycemic control, therefore CoQ10 may be used as adjunctive therapy in patients with associated cardiovascular diseases.
Monounsaturated diet lowers LDL oxidisability in type IIb and type IV dyslipidemia without affecting coenzyme Q10 and vitamin E contents
Authors: Baroni Silvia Svegliati , Amelio Mauro , Fiorito Alessia , Gaddi Antonio , Littarru Gianpaolo , Battino Maurizio 
Published: December 2008

AbstractThe purpose of the present study was to evaluate the effects of MUFA vs PUFA enriched diets on the plasma and LDL lipid profile and antioxidant contents in mild hypercholesterolemic and triglyceridemic subjects. The study was divided in two consecutive diet periods. Two groups of 11 dyslipidemic patients each (type IIb and type IV) were recruited and during the first period (lasting four weeks) received a linoleic rich diet while during the following four weeks took an oleate rich diet.Both groups showed no significant changes in cholesterol and TG concentration either in plasma or in LDL. Coenzyme Q10 and vitamin E were also unaffected by the dietary treatments. LDL proneness to be oxidatively modified increased after dietary PUFA administration and markedly decreased following the virgin olive oil enriched diet. In fact, LDL from hypertrigliceridemic subjects on a oleate‐enriched diet displayed a 26% (p<0.05) longer lag‐phase in conjugated dienes generation than during linoleate‐enriched diet and at recruitment. In hypecholesterolemic subjects similar results were obtained: the lag‐phase was 28% longer after MUFA diet that after PUFA diet. No differences were found in the maximum propagation rate and maximum concentration of conjugated dienes among dietary periods and at recruitment. Since we found that the vit. E and CoQ10 levels in plasma and in LDL particles remained unchanged during the course of the study, we may conclude that LDL proneness to undergo oxidative modifications is mainly the result of compositional change due to the enrichment from the different diets of the relative fats.
Virgin olive oil and coenzyme Q10 protect heart mitochondria from peroxidative damage during aging
Authors: Huertas J. R. , Martinez‐Velasco E. , Ibáñez S. , López‐Frias M. , Ochoa J. J. , Quiles J. , Castelli G. Parenti , Mataix J. , Lenaz G. 
Published: December 2008

AbstractThe mitochondrial theory of aging suggests that this phenomenon is the consequence of random somatic mutations in mitochondrial DNA, induced by long‐term exposure to free radical attack. There are two potential dietary means of delaying the effects of free radicals on cellular aging, i.e., enrichment of mitochondrial membranes with monounsaturated fatty acids and supplementation with antioxidants. We have performed a preliminary study on male rats, 6 or 12 month old, fed with diets differing in the nature of the fat (virgin olive oil or sunflower oil) and/or with antioxidant supplementation (coenzyme Q10), analysing hydroperoxide and coenzyme Q9 and Q10 in heart mitochondria. Preliminary results allow us to conclude that the CoQ10 dietetic supplementation as well as the enrichment of the cellular membranes with monounsaturated fatty acids, successfully protect mitochondrial membranes from aged rats against the free radical insult.
Coenzyme Q10, a cutaneous antioxidant and energizer
Authors: Hoppe U. , Bergemann J. , Diembeck W. , Ennen J. , Gohla S. , Harris I. , Jacob J. , Kielholz J. , Mei W. , Pollet D. , Schachtschabel D. , Sauermann G. , Schreiner V. , Stäb F. , Steckel F. 
Published: December 2008

AbstractThe processes of aging and photoaging are associated with an increase in cellular oxidation. This may be in part due to a decline in the levels of the endogenous cellular antioxidant coenzyme Q10 (ubiquinone, CoQ10). Therefore, we have investigated whether topical application of CoQ10 has the beneficial effect of preventing photoaging.We were able to demonstrate that CoQ10 penetrated into the viable layers of the epidermis and reduce the level of oxidation measured by weak photon emission. Furthermore, a reduction in wrinkle depth following CoQ10 application was also shown. CoQ10 was determined to be effective against UVA mediated oxidative stress in human keratinocytes in terms of thiol depletion, activation of specific phosphotyrosine kinases and prevention of oxidative DNA damage. CoQ10 was also able to significantly suppress the expression of collagenase in human dermal fibroblasts following UVA irradiation. These results indicate that CoQ10 has the efficacy to prevent many of the detrimental effects of photoaging.
Fructose‐2,6‐bisphosphate and control of carbohydrate metabolism in eukaryotes
Authors: Okar David A. , Lange Alex J. 
Published: December 2008

AbstractFructose‐2,6‐bisphosphate is an important intracellular biofactor in the control of carbohydrate metabolic fluxes in eukaryotes. It is generated from ATP and fructose‐6‐phosphate by 6‐phosphofructo‐2‐kinase and degraded to fructose‐6‐phosphate and phosphate ion by fructose‐2,6‐bisphosphatase. In most organisms these enzymatic activities are contained in a single polypeptide. The reciprocal modulation of the kinase and bisphosphatase activities by post‐translational modifications places the level of the biofactor under the control of extra‐cellular signals. In general, these signals are generated in response to changing nutritional states, therefore, fructose‐2,6‐bisphosphate plays a role in the adaptation of organisms, and the tissues within them, to changes in environmental and metabolic states. Although the specific mechanism of fructose‐2,6‐bisphosphate action varies between species and between tissues, most involve the allosteric activation of 6‐phosphofructo‐1‐kinase and inhibition of fructose‐1,6‐bisphosphatase. These highly conserved enzymes regulate the fructose‐6‐phosphate/fructose‐1,6‐bisphosphate cycle, and thereby, determine the carbon flux. It is by reciprocal modulation of these activities that fructose‐2,6‐bisphosphate plays a fundamental role in eukaryotic carbohydrate metabolism.
Evidence for A1and A2Badenosine receptors in baby hamster kidney (BHK) cells
Authors: Mittal Rashmi A. , Tan Chee‐Hong , Khoo Hoon‐Eng 
Published: December 2008

AbstractAdenosine is known to produce biphasic effects in the renal tissues via adenosine receptors. However, the presence of more than one subtype of adenosine receptor on a type of kidney cell or tissue has not been conclusively demonstrated. To address this issue, we investigated the presence of A1and A2adenosine receptors in baby hamster kidney (BHK) cells by use of radioligand binding and the reverse transcription‐polymerase chain reaction. Ligand binding studies with (3H)‐DPCPX revealed a single class of binding site with a KDof 9.2 ± 2.0 nM, a Bmaxof 1.7 ± 0.2 pmol/mg protein and a pharmacological profile characteristic of A1adenosine receptor on the BHK cell membrane. As the presence of A2adenosine receptors could not be conclusively determined by ligand binding studies, the more sensitive method of RT‐PCR was employed. The presence of A1and A2Badenosine receptors was detected by RT‐PCR with specific primers and the subsequent sequencing of the resultant amplification product. The sequences obtained were 75—90% homologous to the respective adenosine receptor mRNA of rat, mouse and human.
Captopril increased mitochondrial coenzyme Q10 level, improved respiratory chain function and energy production in the left ventricle in rabbits with smoke mitochondrial cardiomyopathy
Authors: Gvozdjáková Anna , Šimko Fedor , Kucharská Jarmila , Braunová Zuzana , Pšenek Peter , Kyselovič JÁN 
Published: December 2008

AbstractThe aim of the study was to show whether the ACE inhibitor captopril is able to protect the heart against the deleterious effect of passive cigarette smoking on left ventricular mitochondria. Four groups of rabbits were investigated: control (C), passive smoking of three cigarettes twice daily/30 minutes (S), control + captopril (7.5 mg/kg body weight twice daily) (Cap), and smoking + captopril (SCap) as in group 2 and 3. Three weeks lasting passive smoking impaired oxidative phosphorylation, diminished cytochrome oxidase activity and increased the mitochondrial F1‐ATPase protein concentration. Moreover, the level of coenzyme Q10 (CoQ10) and coenzyme Q9 were decreased. Simultaneous treatment with captopril prevented partly the decrease of CoQ10 level, deterioration of oxidative phosphorylation, diminution of cytochrome oxidase activity and enhancement of F1‐ATPase level. We conclude that captopril protected the myocardium against the harmful effect of passive smoking in rabbits.