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Intracellular ROS (intracellular + ro)
Terms modified by Intracellular ROS Selected AbstractsFluorescent Nanoprobes: Fluorescent Gold Nanoprobe Sensitive to Intracellular Reactive Oxygen Species (Adv. Funct.ADVANCED FUNCTIONAL MATERIALS, Issue 12 2009Mater. On page 1884, H. Lee and co-workers report fluorescent gold nanoprobes sensitive to reactive oxygen species (ROS). Using nanoparticle surface energy transfer between gold nanoparticles and end-dopamine modified fluorescein-hyaluronic acid conjugates, gold nanoprobes are created with extreme sensitivity to intracellular ROS. The cover image shows real time monitoring of intracellular ROS generation within macrophage cells via fluorescence recovery of the nanoprobes. [source] Fluorescent Gold Nanoprobe Sensitive to Intracellular Reactive Oxygen SpeciesADVANCED FUNCTIONAL MATERIALS, Issue 12 2009Hyukjin Lee Abstract Gold nanoprobes immobilized with fluorescein-hyaluronic acid (HA) conjugates are fabricated and utilized for monitoring intracellular reactive oxygen species (ROS) generation in live cells via nanoparticle surface energy transfer. A bio-inspired adhesive molecule, dopamine, is used to robustly end-immobilize HA onto the surface of gold nanoparticles (AuNPs) for securing intracellular stability against glutathione. ROS induces cleavage and fragmentation of the HA chains immobilized on the surface of the AuNPs allows rapid and specific detection of intracellular ROS by emitting strong fluorescence-recovery signals. In particular, fluorescence-quenched gold nanoprobes exhibit selective and dose-dependent fluorescence-recovery signals upon exposure to certain oxygen species such as superoxide anion () and hydroxyl radical (·OH). The fluorescent gold nanoprobe is usefully exploited for real-time intracellular ROS detection and antioxidant screening assay, and has exciting potential for various biomedical applications as a new class of ROS imaging probes. [source] Naturally occurring polyphenolic antioxidants modulate IgE-mediated mast cell activationIMMUNOLOGY, Issue 4 2000S.-S. Chen Summary Reactive oxygen species (ROS) are known to modulate activities of a host of kinases, phosphatases and transcription factors. Rutin and chlorogenic acid (CGA) are the major polyphenolic antioxidants present in the small molecular fraction of smokeless tobacco leaf extracts, as ascertained by reverse-phase high-pressure liquid chromatography (HPLC) and mass spectrometry. Levels of intracellular ROS in resting versus antigen,immunoglobulin E (IgE)-challenged murine mast cells were measured at 510 nm by fluorescence-activated cell sorting (FACS) using carboxy-dichlorofluorescein (DCFH-DA). Enhanced ROS production was observed in IgE-sensitized mast cells following antigenic challenge. Rutin and CGA reduced ROS levels in antigen,IgE-activated mast cells. Concomitantly, they also profoundly inhibited histamine release by these activated mast cells. In contrast, rutin and CGA augmented the inducible cytokine messages, i.e. interleukin (IL)-10, IL-13, interferon-, (IFN-,), IL-6 and tumour necrosis factor-, (TNF-,) in IgE-sensitized mast cells following antigen challenge. This study indicates that tobacco polyphenolic antioxidants that quench intracellular ROS, differentially affect two effector functions of antigen,IgE-activated mast cells. This model system may be employed to determine the molecular target of polyphenols. The potential role of these polyphenolic antioxidants on IgE-mediated allergy in vivo depends on a balance of their differential effects on mast cell activation. [source] Reactive Oxygen Species and Signal TransductionIUBMB LIFE, Issue 1 2001Toren Finkel Abstract Increasing evidence suggests a role for intracellular reactive oxygen species (ROS) as mediators of normal and pathological signal transduction pathways. In particular, a growing list of recent reports have demonstrated a rapid and significant increases in intracellular ROS following growth factor or cytokine stimulation. These ROS appear essential for a host of downstream signaling events. Biochemical characterization of this ligand-activated ROS production has revealed important information regarding the molecular composition of the cellular oxidases and the regulation of their activity by small GTPases. Work is proceeding on identifying strategies to identify how ROS might specifically regulate signaling pathways by altering the activity of direct target molecules. This review will focus on the progress in the rapid emerging area of oxidant or redox-dependent signal transduction and speculate how these insights might alter our view and treatment of diseases thought to be caused by oxidative stress. [source] Zeolite Encapsulation Decreases TiO2 -photosensitized ROS Generation in Cultured Human Skin Fibroblasts,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 1 2006Biao Shen ABSTRACT Sunscreens protect skin against sunburn. However, studies have demonstrated that UV-irradiated sunscreen components such as titanium dioxide (TiO2) promote the photogeneration of reactive oxygen species (ROS). Because encapsulation of TiO2 within zeolites alters its photocatalytic activity, supra-molecular composites based on NaY zeolite hosts containing TiO2 guests were prepared, and the effects on ROS formation in cells under UVA-irradiation evaluated. DCFH-DA (2,,7,-dichlorofluorescein diacetate) was used as a profluorescent probe to monitor intracellular ROS. The detection of in-tracellular 2,,7,-dichlorofluorescein (DCF) fluorescence by confocal microscopy revealed that DCFH-DA was taken up, hydrolyzed and oxidized by yeast cells and cultured human skin fibroblasts within 20 and 6 min, respectively. Higher DCF fluorescence was observed in fibroblasts following UVA irra-diation in the absence but not in the presence of the radical nitroxide, TEMPOL (4-hydroxy-2,2,6,6-tetramethylpipery-dine-1-oxyl), which exhibits superoxide dismutase-mimetic and catalase-mimetic activity. UVA-induced fluorescence increased by -50% in the presence of 32-nm anatase TiO2 particles and decreased by essentially an equal amount in the presence of TiO2 encapsulated within NaY zeolites (TiO2@NaY). Addition of the uncomplexed NaY host also decreased (by ,30%) the amount of UVA-induced fluorescence but, un-expectedly, the combination of the free guest and host (TiO2@NaY) caused a doubling of the fluorescence. Protection of cells against TiO2 -induced intracellular ROS by encapsulation suggests that supramolecular species may be beneficial in photoprotection of the skin. In contrast, the potentiation of TiO2 -induced ROS by uncomplexed NaY points to a critical role for formulation when free TiO2 is used as a sun screen ingredient. [source] Effects of H2O2 exposure on human sperm motility parameters, reactive oxygen species levels and nitric oxide levelsANDROLOGIA, Issue 3 2010S. S. Du Plessis Summary Research has revealed that reactive oxygen species (ROS) negatively affect sperm function, both in vivo and in vitro. Sperm preparation techniques for assisted reproductive technologies (ART) are potential causes for additional ROS production. This study aimed to correlate the concentration of exogenous H2O2 with sperm motility parameters and intracellular ROS and nitric oxide (NO) levels to reiterate the importance of minimising ROS levels in ART. Human spermatozoa from 10 donors were incubated and exposed to different exogenous H2O2 concentrations (0, 2.5, 7.5 and 15 ,m). Subsequently, motility was determined using computer-aided semen analysis, while ROS (2,7-dichlorofluorescin diacetate) and NO (diaminofluorescein-2/diacetate) were analysed using fluorescence-activated cell sorting. Results showed that H2O2 did affect the sperm parameters. Exogenous H2O2 was detrimental to motility and resulted in a significant increase in overall ROS and NO levels. A significant increase in static cells was seen as well. It is important to elucidate the mechanisms between intracellular ROS levels with sperm motility parameters. While this experiment demonstrated a need to reduce exogenous ROS levels during ART, it did not illustrate the cause and effect relationship of intracellular ROS and NO levels with sperm motility. Further research needs to be conducted to define a pathological level of ROS. [source] Antiapoptotic Cardioprotective Effect of Hypothermia Treatment Against Oxidative Stress InjuriesACADEMIC EMERGENCY MEDICINE, Issue 9 2009Chien-Hua Huang MD Abstract Objectives:, The effect of hypothermia on cardiomyocyte injury induced by oxidative stress remains unclear. The authors investigated the effects of hypothermia on apoptosis and mitochondrial dysfunction in cardiomyocytes exposed to oxidative stress. Methods:, Cardiomyocytes (H9c2) derived from embryonic rat heart cell culture were exposed to either normothermic (37°C) or hypothermic (31°C) environments before undergoing oxidative stress via treatment with hydrogen peroxide (H2O2). The degree of apoptosis was determined by annexin V and terminal deoxynucleotidyl transferase (TUNEL) staining. The amount of reactive oxygen species (ROS) was compared after H2O2 exposure between normo- and hypothermic-pretreated groups. Mitochondrial dysfunction in both groups was measured by differential reductase activity and transmembrane potential (,,m). Results:, Hydrogen peroxide induced significant apoptosis in both normothermic and hypothermic cardiomyocytes. Hypothermia ameliorated apoptosis as demonstrated by decreased annexin V staining (33 ± 1% vs. 49 ± 4%; p < 0.05) and TUNEL staining (27 ± 17% vs. 80 ±25%; p < 0.01). The amount of intracellular ROS increased after H2O2 treatment and was higher in the hypothermic group than that in the normothermic group (237.9 ± 31.0% vs. 146.6 ± 20.6%; p < 0.05). In the hypothermic group, compared with the normothermic group, after H2O2 treatment mitochondrial reductase activity was greater (72.0 ± 17.9% vs. 27.0 ± 13.3%; p < 0.01) and the mitochondria ,,m was higher (101.0 ± 22.6% vs. 69.7 ± 12.9%; p < 0.05). Pretreatment of cardiomyocytes with the antioxidant ascorbic acid diminished the hypothermia-induced increase in intracellular ROS and prevented the beneficial effects of hypothermia on apoptosis and mitochondrial function. Conclusions:, Hypothermia at 31°C can protect cardiomyocytes against oxidative stress,induced injury by decreasing apoptosis and mitochondrial dysfunction through intracellular ROS-dependent pathways. [source] Outer membrane vesicles from Neisseria meningitidisAPMIS, Issue 3 2002Effects on leukocyte adhesion molecules, reactive oxygen species Flow cytometry was used to study the expression of leukocyte adhesion molecules CD11a, CD11b, CD11c, CD14, and CD62L (L-selectin) and production of reactive oxygen species (ROS) in an ex vivo human whole-blood system stimulated with lipopolysaccharide-containing outer membrane vesicles (LPS-OMV) from N. meningitidis. Results demonstrated a dose-dependent increase in surface expression of CD11a, CD11b, CD11c and CD14 in granulocytes and monocytes (maximal at 30,120 min) upon OMV-LPS challenge, whereas CD62L expression was heavily downregulated (maximal at 30,120 min). The OMV-associated LPS was almost as potent (on a weight basis) as purified LPS from E. coli in inducing adhesion molecule modulation but the response was delayed. Upon stimulation with OMV-LPS or E. coli -LPS, the production of intracellular ROS increased in both granulocytes and monocytes when dihydroethidium (DHE, mainly reflecting superoxide anion) was used as a probe, whereas peroxynitrite production monitored with dihydrorhodamine 123 (DHR) was not significantly changed. The OMV-mediated modulation of leukocyte adhesion molecule expression and increased ROS production may certainly lead to increased entrapment of leukocytes in the microcirculation and contribute to untoward inflammatory reactions as seen in systemic meningococcal disease. [source] Ergosterol peroxide from an edible mushroom suppresses inflammatory responses in RAW264.7 macrophages and growth of HT29 colon adenocarcinoma cellsBRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2007M Kobori Background and purpose: 5,,8,-Epidioxy-22E -ergosta-6, 22-dien-3,-ol (ergosterol peroxide) is a major antitumour sterol produced by edible or medicinal mushrooms. However, its molecular mechanism of action has yet to be determined. Here, we examine the anticancer and anti-inflammatory effects of ergosterol peroxide. Experimental approach: After treating RAW264.7 macrophages with LPS and purified ergosterol peroxide or ergosterol, we determined LPS-induced inflammatory cytokines, nuclear DNA binding activity of transcription factors and phosphorylation of MAP kinases (MAPKs). HT29 colorectal adenocarcinoma cells were treated with ergosterol peroxide for 5 days. To investigate the antitumour properties of ergosterol peroxide, we performed DNA microarray and RT-PCR analyses and determined the reactive oxygen species (ROS) in HT29 cells. Key results: Ergosterol peroxide suppressed LPS-induced TNF-, secretion and IL-1,/, expression in RAW264.7 cells. Ergosterol peroxide and ergosterol suppressed LPS-induced DNA binding activity of NF-,B and C/EBP,, and inhibited the phosphorylation of p38, JNK and ERK MAPKs. Ergosterol peroxide down-regulated the expression of low-density lipoprotein receptor (LDLR) regulated by C/EBP, and HMG-CoA reductase (HMGCR) in RAW264.7 cells. In addition, ergosterol peroxide showed cytostatic effects on HT29 cells and increased intracellular ROS. Furthermore, ergosterol peroxide induced the expression of oxidative stress-inducible genes, and the cyclin-dependent kinase inhibitor CDKN1A, and suppressed STAT1 and interferon-inducible genes. Conclusion and Implication: Our results suggest that ergosterol peroxide and ergosterol suppress LPS-induced inflammatory responses through inhibition of NF-,B and C/EBP, transcriptional activity, and phosphorylation of MAPKs. Moreover, ergosterol peroxide appears to suppress cell growth and STAT1 mediated inflammatory responses by altering the redox state in HT29 cells. British Journal of Pharmacology (2007) 150, 209,219. doi:10.1038/sj.bjp.0706972 [source] Level of reactive oxygen species induced by p21WAF(1)/CIP(1) is critical for the determination of cell fateCANCER SCIENCE, Issue 7 2009Takafumi Inoue p21WAF(1)/CIP(1) is a well-known cell cycle regulatory protein which is overexpressed in several cancer cell lines, and known to determine cell fate. We generated three recombinant adenovirus vectors that expressed either the full-length p21 (Ad-p21F), a p21 mutant with a deletion of the C-terminal proliferative cell nuclear antigen (PCNA) binding domain (Ad-p21N), or a p21 mutant with a deletion of the N-terminal cyclin-dependent kinase binding domain (Ad-p21C). We transfected these vectors into five cancer cell lines. Premature senescence was induced in all of the lines only following transfection with Ad-p21N and Ad-p21F. In addition, apoptosis was also induced in LoVo and HCT116 cells that harbored wild-type p53 and the reactive oxygen species (ROS) level was higher than in senescent cells. Finally, the induction of apoptosis was inhibited by using siRNA to downregulate p53. This observation implies that there is a feedback signaling loop involving p21/ROS/p53 in apoptotic responses. It appears to be, at least in part, driven by high levels of p21 protein. Next, we investigated the cell death effect of endogenous p21 protein on cell fate using sodium butyrate (NaB). Treatment with 1 mM NaB or 2 to 5 mM NaB induced senescence or apoptosis, respectively. The level of intracellular ROS in 5 mM NaB treated cells was 2-fold higher, compared with that in 1 mM NaB treated cells. We also demonstrated that DNA damage response signals including ataxia telangiectasia mutated, ,H2AX, and p38 MAPK were involved in NaB-induced cell death. The magnitude of intracellular ROS levels in response to p21 elicited either senescence or apoptosis in the cancer cell lines. (Cancer Sci 2009; 100: 1275,1283) [source] Phytoglycoprotein (75,kDa) inhibits expression of interleukin-1, stimulated by DEHP in human mast cellsCELL BIOCHEMISTRY AND FUNCTION, Issue 5 2010Phil-Sun Oh Abstract The purpose of this study is to investigate the inhibitory effect of a glycoprotein (CTB glycoprotein, 75,kDa) isolated from Cudrania tricuspidata Bureau (CTB) on the di-(2-ethylhexyl)phthalate (DEHP) induced expression of allergic-inflammation-related mediators in human mast cells. The changes on the levels of intracellular reactive oxygen species (ROS), mitogen-activated protein kinase (MAPK), transcription factor [nuclear factor (NF)- ,B], and allergic inflammatory mediators [cyclooxygenase (COX)-2 and interleukin (IL)-1,] were evaluated using Western blot and RT-PCR. Our results showed that the CTB glycoprotein in the presence of DEHP inhibits the production of intracellular ROS, the phosphorylation of ERK1/2, and p38 MAPK in HMC-1 cells. In addition, the CTB glycoprotein has suppressive effects on the transcriptional activation of NF- ,B, and on the expression levels of COX-2 and IL-1, in DEHP-treated HMC-1 cells. In conclusion, the CTB glycoprotein has a strong anti-inflammatory effect on the activities of allergic inflammatory mediators indirectly caused by DEHP in HMC-1 cells. Copyright © 2010 John Wiley & Sons, Ltd. [source] Coenzyme Q10 prevents human lens epithelial cells from light-induced apoptotic cell death by reducing oxidative stress and stabilizing BAX,/,Bcl-2 ratioACTA OPHTHALMOLOGICA, Issue 3 2010Marcus Kernt Abstract. Background:, Cataract is one of the most prevalent eye disease and a major cause for legal blindness in the world. Beside others, cumulative light-exposure and apoptotic cell death are significantly associated with cataract development. In contrast, supplementation with antioxidants has been suggested to prevent premature cataractogenesis. This study investigates possible protective effects of Coenzyme Q10 (CoQ10) regarding light-induced stress and apoptotic cell death in human lens epithelial cells (LEC). Methods:, Human LEC were either pre-incubated with CoQ10 or not and then exposed to white light. After 10,40 min of irradiation viability, induction of intracellular reactive oxygen species (ROS), apoptosis and cell death was determined. Expression of apoptotic BAX and anti-apoptotic Bcl-2 protein and their mRNA were determined by RT-PCR and Western blot analysis. Results:, Light exposure decreased LEC viability and Bcl-2 expression and increased intracellular ROS, apoptotic cell death, and BAX expression in a time-of-irradiation-dependent manner. Phototoxic cell death and apoptosis, as well as decrease of Bcl-2 and increase in BAX expression was significantly reduced, when cells were pre-incubated with CoQ10. Conclusions:, In this study, CoQ10 significantly reduced light-induced LEC-damage and attenuated phototoxic effects on BAX and Bcl-2 expression. Therefore, CoQ10 supplementation might also be useful in preventing LEC death and consecutive cataract formation in vivo. [source] EFFECT OF HYDROGEN SULPHIDE ON ,-AMYLOID-INDUCED DAMAGE IN PC12 CELLSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2 2008Xiao-Qing Tang SUMMARY 1Hydrogen sulphide (H2S) is a well-known cytotoxic gas. Recently, H2S has been shown to protect neurons against oxidative stress caused by glutamate, peroxynitrite and HOCl. Considerably lower H2S levels have been reported in the brain of Alzheimer's disease (AD) patients with accumulation of ,-amyloid (A,). 2The aim of present study was to explore the cytoprotection by H2S against A,25,35 -induced apoptosis and the molecular mechanisms underlying this effect in PC12 cells. 3Our findings indicated that A,25,35 significantly reduced cell viability and induced apoptosis of PC12 cells, along with dissipation of the mitochondrial membrane potential (MMP) and overproduction of reactive oxygen species (ROS). 4Sodium hydrosulphide (NaHS), an H2S donor, protected PC12 cells against A,25,35 -induced cytotoxicity and apoptosis not only by reducing the loss of MMP, but also by attenuating the increase in intracellular ROS. 5The results of the present study suggest that the cytoprotection by H2S is related to the preservation of MMP and attenuation of A,25,35 -induced intracellular ROS generation. These findings could significantly advance therapeutic approaches to the neurodegenerative diseases that are associated with oxidative stress, such as AD. [source] | ||||||||||||||||||||||