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PubMed2006

Notoginsenoside R1 inhibits TNF-alpha-induced fibronectin production in smooth muscle cells via the ROS/ERK pathway.

The matrix fibronectin protein plays an important role in vascular remodeling. Notoginsenoside R1 is the main ingredient with cardiovascular activity in Panax notoginseng; however, its molecular mechanisms are poorly understood. We report that notoginsenoside R1 significantly decreased TNF-alpha-induced activation of fibronectin mRNA, protein levels, and secretion in human arterial smooth muscle cells (HASMCs) in a dose-dependent manner. Notoginsenoside R1 scavenged hydrogen peroxide (H2O2) in a dose-dependent manner in the test tube. TNF-alpha significantly increased intracellular ROS generation and then ERK activation, which was blocked by notoginsenoside R1 or DPI and apocynin, inhibitors of NADPH oxidase, or the antioxidant NAC. Our data demonstrated that TNF-alpha-induced upregulation of fibronectin mRNA and protein levels occurs via activation of ROS/ERK, which was prevented by treatment with notoginsenoside R1, DPI, apocynin, NAC, or MAPK/ERK inhibitors PD098059 and U0126. Notoginsenoside R1 significantly inhibited H2O2-induced upregulation of fibronectin mRNA and protein levels and secretion; it also significantly inhibited TNF-alpha and H2O2-induced migration. These results suggest that notoginsenoside R1 inhibits TNF-alpha-induced ERK activation and subsequent fibronectin overexpression and migration in HASMCs by suppressing NADPH oxidase-mediated ROS generation and directly scavenging ROS.

Acetophenones↗
PubMed2006

Characterization by theory of H-transfers and onium reactions of CH3CH2CH2N+H=CH2.

H-transfers by 4-, 5-, and 6-membered ring transition states to the pi-bonded methylene of CH3CH2CH2NH+=CH2 (1) are characterized by theory and compared with the corresponding transfers in cation radicals. Four-membered ring H-transfers converting 1 to CH3CH2CH=N+HCH3 (2) and CH3N+H=CH2 to CH2=NH+CH3 are high-energy processes involving rotation of the source and destination RHC= groups (R = H or C2H5) to near bisection by skeletal planes; migrating hydrogens move near these planes. The H-transfer 1 --> CH3C+HCH2NHCH3 (3) has a higher energy transition-state than 1 --> 2, in marked contrast to the corresponding relative energies of 4- and 5-membered ring H-transfers in cation-radicals. Six-membered ring H-transfer-dissociation (1 --> CH2=CH2 + CH2=N+HCH3) is a closed shell analog of the McLafferty rearrangement. It has a lower energy transition-state than either 1 --> 2 or 1 --> 3, but is still a much higher energy process than 6-membered ring H-transfers in aliphatic cation radicals. In contrast to the stepwise McLafferty rearrangement in cation radicals, H-transfer and CC bond breaking are highly synchronous in 1 --> CH3N+H=CH2 + CH2=CH2. H-transfers in propene elimination from 1 are ion-neutral complex-mediated: 1--> [CH3CH2CH2+ ---NH=CH2] --> [CH3C+HCH3 NH=CH2] --> CH3CH = CH2 + CH2=NH2+. Intrinsic reaction coordinate tracing demonstrated that a slight preference for H-transfer from the methyl containing the carbon from which CH2=NH is cleaved is due to CH2=NH passing nearer this methyl than the other on its way to abstracting H, i.e., some memory of the initial orientation of the partners accompanies this reaction.

Energy Transfer↗
PubMed2006

Preparation, structure and thermal stability of onium- and amino-functionalized silicas for the use as catalysts supports.

We explored and compared several synthetic methods of grafting silica with strong (alkyltriphenylphosphonium, tetralkylammonium, propylpyridinium and dialkylimidazolium) and weak (gamma-aminopropyl, gamma-(N-imidazolyl)propyl) anion-exchanging groups starting with commercially available chloroalkyl- and gamma-aminopropylsilanes. Structure of the intermediate and final materials was investigated by elemental analysis, titration, 13C, 29Si, 31P MAS NMR, DRIFT, and TPD MS. The derivatives of alkyltriphenylphosphonium, propylpyridinium and dialkylimidazolium cation can be prepared with satisfactory quaternisation yields (ca. 30-100%) via the nucleophilic substitution of gamma-chloropropyl groups either in the silane or in chloropropylsilica, resulting in bonded phases with moderate densities: 0.2-1.0 group nm(-2) (onium salts) and 0.2-1.5 group nm(-2) (amines). Parallel one-pot end-capping/hydrophobization can be done if a mixture of target silane with end-capping reagent or gamma-chloropropylsilane is used. The grafted layer is highly stable at the level of Si-C bonds and decomposes at ca. 400 degrees C, while the onium functions begin to decompose at ca. 250 degrees C, lowering the thermal stability of materials. Thus, anion-exchanging silicas can be envisaged for the use as catalyst supports at moderate temperatures.

Catalysis↗
PubMed2005

The reactive oxygen species are involved in resistance responses of wheat to the Russian wheat aphid.

The effect of Russian wheat aphid (RWA), Diuraphis noxia (Mordvilko), infestation on the hydrogen peroxide (H(2)O(2)) content and NADPH oxidase (EC 1.6.3.1) activity was studied in the resistant (cv. Tugela DN) and near-isogenic susceptible (cv. Tugela) wheat (Triticum aestivum L.). The objective of this study was to investigate the involvement of the reactive oxygen species (ROS) during the resistance responses against the RWA. Infestation significantly induced an early accumulation of the H(2)O(2) and increase of NADPH oxidase activity to higher levels in the resistant than susceptible plants. Results of inhibitory studies using diphenylene iodonium (DPI), a suicide inhibitor of NADPH oxidase, strongly suggested a possible signalling role for H(2)O(2) during RWA resistance response by activation of downstream defence enzymes [intercellular peroxidase (EC 1.11.1.7) and beta-1,3-glucanase (EC 3.2.1.39)].

Animals↗
PubMed2006

Molecular dynamics study of the fibril elongation of the prion protein fragment PrP106-126.

The present paper aims at exploring the elongation of the PrP106-126 fibril under acid environments through molecular dynamics simulation. It shows that influenced by the edge strands of the fibril, single PrP106-126 peptide forms beta-sheet and becomes a new element of the fibril. Under acidic condition, single PrP106-126 fragment presents a much larger variety of conformations than it does under neural condition. However, acidic condition does not largely affect the stability of the PrP106-126 fibril. Consequently, the speed of the fibril elongation can be dramatically increased by lowering the pH value of the solution. The pH values are adjusted by either altering the protonation state of the residues or adding hydronium ions or hydroxyl ions.

Computer Simulation↗
PubMed2006

Synthetic smooth muscle cell phenotype is associated with increased nicotinamide adenine dinucleotide phosphate oxidase activity: effect on collagen secretion.

OBJECTIVE: Smooth muscle cells (SMCs) from prosthetic vascular grafts secrete higher levels of collagen than aortic SMCs under basal conditions and during incubation with oxidized low-density lipoprotein. We postulated that reactive oxygen species (ROS) contributed to the observed difference. The objective of this study was to assess the effect of ROS on collagen secretion by aortic and graft SMCs and explore the mechanism involved. METHODS: SMCs isolated from canine aorta or Dacron thoracoabdominal grafts were incubated with 6-anilinoquinoline-5,8-quinone (LY83583), an agent that induces superoxide production. Type I collagen in the conditioned medium was measured by enzyme-linked immunosorbent assay, and superoxide anion production was measured by lucigenin assay. RESULTS: LY83583 stimulated a rapid increase in collagen production by graft SMCs that paralleled the LY83583-induced increase in superoxide production. The increase in both collagen and superoxide was greater in graft SMCs than aortic SMCs. Collagen and superoxide production were inhibited by superoxide scavengers. Nicotinamide adenine dinucleotide phosphate (NADPH) induced significantly more superoxide production by graft SMCs than aortic SMCs, suggesting that the NADPH oxidase system was more active in graft SMCs. NADPH oxidase inhibitors blocked the superoxide and collagen production induced by LY83583. CONCLUSION: In SMCs, the synthetic phenotype is associated with increased NADPH oxidase activity and elevated superoxide production in response to an oxidative stress. Superoxide, in turn, leads to increased collagen production. CLINICAL RELEVANCE: The inflammatory process after prosthetic vascular graft implantation causes oxidative stress that can stimulate collagen production by graft SMCs, contributing to the progression of intimal hyperplasia. The exaggerated response of graft SMCs to oxidative stress offers a potential target for therapeutic interventions.

Aminoquinolines↗
PubMed2006

The effects of exogenous antioxidants on lifespan and oxidative stress resistance in Drosophila melanogaster.

We used the fruit fly Drosophila melanogaster to test the effects of feeding the superoxide dismutase (SOD) mimetic drugs Euk-8 and -134 and the mitochondria-targeted mitoquinone (MitoQ) on lifespan and oxidative stress resistance of wild type and SOD-deficient flies. Our results reaffirm the findings by other workers that exogenous antioxidant can rescue pathology associated with compromised defences to oxidative stress, but fail to extend the lifespan of normal, wild type animals. All three drugs showed a dose-dependent increase in toxicity in wild type flies, an effect that was exacerbated in the presence of the redox-cycling drug paraquat. However, important findings from this study were that in SOD-deficient flies, where the antioxidant drugs increased lifespan, the effects were sex-specific and, for either sex, the effects were also variable depending on (1) the stage of development from which the drugs were given, and (2) the magnitude of the dose. These findings place significant constraints on the role of oxidative stress in normal ageing.

Aging↗
PubMed2006

Activation of nicotinamide adenine dinucleotide phosphate (reduced form) oxidase by advanced glycation end products links oxidative stress to altered retinal vascular endothelial growth factor expression.

Increasing evidence indicates that advanced glycation end products (AGEs) promote retinal alterations through oxidative stress. However, the pathways involved in AGE-induced generation of reactive oxygen species (ROS) in retinal cells are poorly defined. In the present study, we investigated the role of nicotinamide adenine dinucleotide phosphate (reduced form) (NADPH) oxidase in AGE-induced ROS intracellular generation and vascular endothelial growth factor (VEGF) expression in bovine retinal endothelial cells (BRECs). Incubation of BRECs with 100 microg/mL AGEs increased ROS generation and VEGF expression in these cells. Treatment of the cells with the NADPH oxidase inhibitors, apocynin and diphenylene iodonium, inhibited these effects. In retinal endothelial cells exposed to AGEs, translocation of protein kinase C (PKC)-beta2 and p47phox was observed. Inhibition of PKC by treatment of the cells with calphostin C, GF10923X, and LY379196 totally suppressed AGE-mediated p47phox translocation and ROS generation. Incubation of BRECs with gliclazide inhibited AGE-induced PKC-beta2 and p47phox translocation and totally abrogated AGE-mediated ROS generation and VEGF expression. Overall, these results demonstrate that AGEs induce intracellular ROS generation and VEGF expression in retinal endothelial cells through a PKC-dependent activation of NADPH oxidase. Inhibition of retinal NADPH oxidase expression and ROS generated by this system provides a new potential mechanism by which gliclazide may affect retinal VEGF expression and exert a beneficial effect on diabetic retinopathy.

Acetophenones↗
PubMed2006

Is the reactive oxygen species-dependent-NF-kappaB activation observed in iron-loaded BALB/c mice a key process preventing growth of Leishmania major progeny and tissue-damage?

Systemic iron delivery to BALB/c mice, at time points surrounding the inoculation of 1000 Leishmania major metacyclic promastigotes intradermally in the ear results in the complete absence of onset and further development of ear lesion. In these iron-protected mice, the L. major intracellular progeny remains very low in both the ear and the draining lymph node. The iron-induced protective status is associated with a diphenyleneiodonium-sensitive sustained increased oxidative burst. We showed that iron-loaded mice developed no lesions at the site of the primary inoculation and were also resistant to reinoculation at a distant site (intradermal re-inoculation of 1000 metacyclic promastigotes in the contra-lateral ear). Interestingly, in the lymph node cell population recovered from iron-loaded mice at weeks 8 and 12 after the second parasite inoculation, and whatever the protective status studied--primary or resistant to re-inoculation--three potentially related features were observed: (i) NF-kappaB activation, (ii) enhanced TCR-mediated T lymphocyte proliferation, and (iii) high number of IFN-gamma-positive CD4(+)T cells. These results show a putative role of an iron-induced reactive oxygen species-dependent activation of NF-kappaB in the development of protective immunity against L. major.

Animals↗
PubMed2006

The prevention of the growth of Leishmania major progeny in BALB/c iron-loaded mice: a process coupled to increased oxidative burst, the amplitude and duration of which depend on initial parasite developmental stage and dose.

BALB/c mice were given or not iron around the time of intradermal parasite inoculation, in their ears, of either 10(6) stationary-phase (designated "high-dose model") or 10(3)Leishmania major metacyclic promastigotes (designated "low-dose model"). Iron-loaded mice in the high-dose model displayed delayed and limited pathogenic processes, whereas in the low-dose model, the mice remained ear lesion-free over 12 months post-parasite inoculation. These phenotypes were coupled to an increased leukocyte oxidative burst displayed mainly by neutrophils: it was early and transient in the high-dose model, whereas it was sustained in the low-dose model. In the latter model, injection of an antioxidant (diphenyleneiodonium chloride) at week 2 post-L. major inoculation resulted in a significant decrease in oxidative burst and reversed the protective status. The increased and sustained oxidative burst displayed by the neutrophils, the sustained presence of IL-12 (p40/p70)-positive leukocytes in the ear dermis, the low number of inflammatory leukocytes in the ear dermis and their concomitant high number in the draining lymph node are three related features that likely contribute to the shaping of the protective status, the onset and dynamic maintenance of which are antioxidant sensitive.

Animals↗
PubMed2004

Bacterial cytoplasmic membrane permeability assay using ion-selective electrodes.

We used K(+) and tetraphenylphosphonium (TPP(+)) electrodes simultaneously to evaluate the ability of antimicrobial peptides to form channels (or more generally to increase permeability) and to abolish membrane potential in bacterial cytoplasmic membranes in situ. Such evaluations are usually made independently by colorimetric monitoring of the hydrolysis of a chromogenic substrate by a cytoplasmic enzyme or by fluorimetric determination of membrane depolarization using a membrane potential-sensitive dye. In the present study, the K(+) electrode was used to evaluate channel-forming ability by monitoring the efflux of K(+) originally present in the cytoplasm of bacteria, while the TPP(+) electrode was used to examine membrane depolarization causing the efflux of TPP(+) accumulated in the cytoplasm of bacteria dependent on membrane potential. Thus, the combination of these two electrodes enabled us to clarify how the peptide-induced formation of ion channels is involved in disrupting the energy-generating system in situ.

Anti-Bacterial Agents↗
PubMed2005

A key role for the microglial NADPH oxidase in APP-dependent killing of neurons.

Reactive oxygen species (ROS) and deposition of cleaved products of amyloid precursor protein (APP) are thought to contribute to neuronal loss observed in Alzheimer's disease (AD). The relationship between these factors was studied in a neuroblastoma and microglia co-culture system. Overexpression of wild-type APP (APP-wt) or APP with three mutations typical of familial AD (APP-3m) in SH-SY5Y neuroblastoma cells did not directly alter their morphology, growth rate, cell cycle or H(2)O(2) sensitivity. In a co-culture of APP-wt neuroblastoma cells with microglia, microglial cells generated ROS and neuronal cells died. The cell death was more pronounced in APP-3m-expressing neurons. Neuroblastoma cell death was attenuated by ROS-scavengers and was dose-dependently inhibited by the NADPH oxidase inhibitor diphenyleneiodonium chloride (DPI). Macrophage cell lines behaved similarly to microglia in the co-culture model. However, a macrophage cell line deficient in the NADPH oxidase subunit, gp91phox, failed to kill neurons. These results suggest that APP-dependent microglia activation and subsequent ROS generation by the phagocyte NADPH oxidase play a crucial role in neuronal killing in a cellular model of AD.

Alzheimer Disease↗
PubMed2005

NMR and IR studies of bis((perfluoroalkyl)sulfonyl)imides.

The influence of water on the NMR and IR spectra of bis((perfluoroalkyl)sulfonyl)imides has been investigated. The large effects of water on the observed spectra suggest that the proton is predominantly bound to the nitrogen of the perfluorosulfonimide acid in the absence of water, while it protonates water to form an onium salt in the presence of water.

Hydrogen↗
PubMed2005

Water trapped in dibenzo-18-crown-6: theoretical and spectroscopic (IR, Raman) studies.

Experimental (IR and Raman) and theoretical (Kohn-Sham calculations) methods are used in a combined analysis aimed at refining the available structural data concerning the molecular guests in channels formed by stacked dibenzo-18-crown-6 (DB18C6) crown ether. The calculations are performed for a simplified model comprising isolated DB18C6 unit and its complexes with either H2O or H3O+ guests, which are the simplest model ingredients of a one-dimensional diluted acid chain, to get structural and energetic data concerning the formation of the complex and to assign the characteristic spectroscopic bands. The oxygen centers in the previously reported crystallographic structure are assigned to either H2O or protonated species.

Crown Ethers↗
PubMed2004

Carvedilol-mediated antioxidant protection against doxorubicin-induced cardiac mitochondrial toxicity.

The cardiotoxicity associated with doxorubicin (DOX) therapy limits the total cumulative dose and therapeutic success of active anticancer chemotherapy. Cardiac mitochondria are implicated as primary targets for DOX toxicity, which is believed to be mediated by the generation of highly reactive free radical species of oxygen from complex I of the mitochondrial electron transport chain. The objective of this study was to determine if the protection demonstrated by carvedilol (CV), a beta-adrenergic receptor antagonist with strong antioxidant properties, against DOX-induced mitochondrial-mediated cardiomyopathy [Toxicol. Appl. Pharmacol. 185 (2002) 218] is attributable to its antioxidant properties or its beta-adrenergic receptor antagonism. Our results confirm that DOX induces oxidative stress, mitochondrial dysfunction, and histopathological lesions in the cardiac tissue, all of which are inhibited by carvedilol. In contrast, atenolol (AT), a beta-adrenergic receptor antagonist lacking antioxidant properties, preserved phosphate energy charge but failed to protect against any of the indexes of DOX-induced oxidative mitochondrial toxicity. We therefore conclude that the cardioprotective effects of carvedilol against DOX-induced mitochondrial cardiotoxicity are due to its inherent antioxidant activity and not to its beta-adrenergic receptor antagonism.

Adrenergic beta-Antagonists↗
PubMed2005

Respiratory burst and NAD(P)H oxidase activity are involved in capacitation of cryopreserved bovine spermatozoa.

Heparin (a glycosaminoglycan) and quercetin (a calcium-ATPase plasma membrane specific inhibitor) induce bovine sperm capacitation. Mitochondria from frozen semen are capable of generating oxidative energy. The aim of the study was to determine oxygen uptake variation and the participation of diphenileneiodonium (DPI)-sensitive oxidases from spermatozoa capacitated with heparin or quercetin. Oxygen uptake was measured polarographically and 2 microM diphenileneiodonium (DPI) was used as a specific inhibitor of NAD(P)H-oxidases. Sperm capacitation was determined by the chlorotetracycline technique. Heparin produced a respiratory burst (17.0+/-3.2 microL O2/h/10(8) spermatozoa; mean+/-S.D.) versus control (11.3+/-0.9 microL O2/h/10(8) spermatozoa; P<0.05). Oxygen uptake and sperm hypermotility were inhibited by cyanide. Treatment with DPI blocked heparin capacitation and oxygen uptake (cyanide-sensitive) decreased to control levels. Respiration of quercetin-treated samples (cyanide-sensitive; 9.7+/-0.7 microL O2/h/10(8) spermatozoa) was not significantly different from the controls; oxygen uptake was not modified by DPI, but quercetin capacitation was inhibited (P<0.05). The effect of DPI with heparin confirmed that oxidases participate in capacitation induction. The addition of superoxide dismutase and/or catalase to heparin- or quercetin-treated samples, failed to modify oxygen uptake and blocked capacitation (P<0.05), suggesting that the superoxide anion (O2*-) participates in the capacitation induction. High mitochondrial activity from heparin-treated samples indicated that energy requirements, especially for hypermotility, were supported by the respiratory chain. Although a respiratory burst was not produced by quercetin, DPI-sensitive-oxidases (O2*- source) were necessary for capacitation. In cryopreserved bovine spermatozoa, heparin- or quercetin-induced capacitation required different levels of mitochondrial energy and DPI-sensitive oxidase activity.

Animals↗
PubMed2005

Influence of lead (Pb2+) on the reactions of in vitro cultured rat aorta to 5-hydroxytryptamine.

Although several studies demonstrated that lead induced abnormal vascular responses in low level lead exposed animals, investigations of the direct effects of lead on blood vessels are limited. In this study we tested the hypothesis that lead was able to directly affect the contractile reactivities of vessels. Male Wistar rat aortae were removed and cultured in PMRI 1640 with 1 ppm lead acetate for 0.5, 6, 12, 24 and 48 h, and then their responses to norepinephrine bitartrate (NE) and serotonin (5-hydroxytryptamine, 5-HT) were examined. The contractile responses to 5-HT of lead exposed aortae were significantly increased when the aortae were cultured for 24 and 48 h. Denudation of endothelium was able to abolish the increased contractile response completely. Diphenyleneiodonium (DPI), an inhibitor of the NAD(P)H oxidase, could abolish the increased contractile response to 5-HT. However, Vitamin C (VC) enhanced the contractile response of both groups to higher dosages of 5-HT. The expression of 5-HT(2B) receptor was not significantly altered by incubation with 1 ppm lead for 24 h. These data suggest that exposure to low levels of lead can directly increase the contraction of aorta to 5-HT. This effect is endothelium dependent, which is not mediated by increased expression of the 5-HT 2B receptor. The increased contraction to 5-HT may be related to increased production of superoxide (O2*-) induced by lead exposure.

Animals↗
PubMed2006

Aspirin and PPAR-alpha activators inhibit monocyte chemoattractant protein-1 expression induced by high glucose concentration in human endothelial cells.

Activated endothelial cells express monocyte chemoattractant protein-1 (MCP-1), a chemokine which is reportedly involved in the recruitment of plasma monocytes in the early stages of atherosclerosis. Since accelerated atherosclerosis is the main complication of diabetes and both diseases encompass an inflammatory reaction, we hypothesized that the anti-inflammatory drugs, aspirin and peroxisome proliferator-activated receptor (PPAR-alpha) activators (fenofibrate and clofibrate), could have an effect on the high glucose-induced MCP-1 expression in endothelial cells. To test this assumption, as well as the possible mechanisms involved, the MCP-1 expression and secretion, the reactive oxygen species levels, nuclear factor-kB (NF-kB) and activator protein-1 (AP-1) expression were determined in human endothelial cells exposed to high glucose concentrations in the presence of aspirin, fenofibrate and clofibrate. Human endothelial cells kept in normal glucose concentration in the absence of drugs were used as control. The results showed that (i) aspirin, fenofibrate and clofibrate decrease significantly the MCP-1 expression and secretion in human endothelial cells; (ii) the high glucose up-regulated expression of MCP-1 in endothelial cells was significantly reduced by inhibitors of NF-kB and reactive oxygen species; (iii) all drugs notably decrease the level of the reactive oxygen species and activation of NF-kB and AP-1. Together, the findings indicate that in endothelial cells aspirin and PPAR-alpha activators reduce the high glucose-increased expression of MCP-1 by a mechanism that includes the inhibition of reactive oxygen species, and decrease of AP-1 and NF-kB activation.

Anti-Inflammatory Agents, Non-Steroidal↗