Top PDF Reactive oxygen species, apoptosis and cancer

Reactive oxygen species, apoptosis and cancer

Reactive oxygen species, apoptosis and cancer

Intrinsic apoptotic cascade is associated with the changes in permeability of outer mitochondrial membrane, which allows the release of proapototic proteins. ROS are well known triggers of intrinsic apoptotic pathway through interaction with outer mitochondrial membrane proteins 19 . Proteins of the Bcl-2 family determine the susceptibility to apoptosis, shifting the balance between pro-apoptotic (Bax, Bak, Bad, Bim and Bid) and anti-apoptotic (Bcl-2, Bcl-XL and Bcl-w) members of the family in favour of apoptosis or against it. In the presence of apoptotic stimuli like ROS, truncated form of Bid protein causes Bax/Bak oligomeriza- tion which leads to creation of megapores in mitochondrial membrane 20 . Subsequently, apoptosome complex is formed in the cytosol, activating initiator Caspase 9 and than Caspase 3, which executes the final steps of apoptosis. Caspase activation is further enhanced due to neutralization of caspase inhibitors by proteins released from mitochondria, like Smac/Diablo and Omi/HtrA2 19 . In addition, mitochon- drial proteins like apoptesis-inducing factor and Endo G stimulate caspase-independent apoptosis via translocation into nucleus, where they mediate genomic DNA fragmenta- tion 21 .
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N-Acetyl Cysteine Depletes Reactive Oxygen Species and Prevents Dental Monomer-Induced Intrinsic Mitochondrial Apoptosis In Vitro in Human Dental Pulp Cells.

N-Acetyl Cysteine Depletes Reactive Oxygen Species and Prevents Dental Monomer-Induced Intrinsic Mitochondrial Apoptosis In Vitro in Human Dental Pulp Cells.

Owing to their physical and aesthetic properties, resin-based materials are routinely used to restore the structure and function of teeth [1, 2]. However, residual monomers released from resin restorations as a result of incomplete polymerization could have irritating effects on the oral tissues. Several dental monomers, including 2-hydroxyethyl methacrylate (HEMA), methyl methacrylate (MMA), and triethylenglycol dimethacrylate (TEGDMA), have been identified as cytotoxic molecules that disrupt the stable redox balance and result in oxidative stress [3, 4]. The imbalanced redox state of the cells, characterized by the over-production of reactive oxygen species (ROS) and depletion of glutathione (GSH), has been shown to induce cell death via apoptosis [4–6]. However, the exact and detailed mechanism underlying dental monomer-induced apoptosis is still largely unknown. Apoptosis can be triggered by various signals. In particular, ROS can induce oxidative DNA damage, which can subsequently upregu- late p53, and thus trigger intrinsic mitochondrial apoptosis by shifting the balance in the Bcl-2 family [7–9]. Thus, one of the purposes of the present study is to investigate the possible involvement of mitochondrial intrinsic apoptotic pathway in dental monomer-induced cytotoxicity.
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Alpha-synuclein induces lysosomal rupture and cathepsin dependent reactive oxygen species following endocytosis.

Alpha-synuclein induces lysosomal rupture and cathepsin dependent reactive oxygen species following endocytosis.

Previous studies have demonstrated that adenovirus trafficking within, and eventual escape from, specific endosomal compart- ments is largely determined by the receptors used for cell entry [12,35,36]. For human adenovirus 5, several groups have demonstrated that protein VI release from the capsid involves mechanical capsid uncoating [37] and release of protein VI at, or near, the cell surface [18,37,38]. We have previously shown that this early release of protein VI correlates with the rupture of cell membranes prior to, or upon reaching early endosomes [18]. Early escape from endosomes may be favorable for human adenovirus 5, as it results in the release of fewer activated cathepsins into the cytosol and a reduced inflammatory response compared to other human adenovirus serotypes that enter cells by using different receptors [12]. Conversely, vesicle rupture by a- synuclein is likely not a property that provides selective advantage to the organism. Rather, it seems likely that this property may be an indirect and evolutionarily unintended activity of a protein that has likely evolved to perform a function other than vesicle rupture. Although it is possible that the a-synuclein aggregates used in our study do not precisely recapitulate the ability of toxic a-synuclein species to mediate vesicle rupture in PD, a number of other in vitro and in vivo studies collectively suggest lysosomal dysfunction may be a central aspect of PD pathology (reviewed in [39]).
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Geração e desintoxicação enzimática de espécies reativas de oxigênio em plantas.

Geração e desintoxicação enzimática de espécies reativas de oxigênio em plantas.

The biotic and abiotic stress conditions imposed on plants induces overproduction of reactive oxygen species (ROS), which can cause damage to cellular structures and even lead to the death of the plant. The biochemical and physiological responses of higher plants to oxidative stress includes an effi cient antioxidant defense system, which involves the activity of the enzymes superoxide dismutase, catalase, ascorbate peroxidase, peroxiredoxines, among others, in addition to non-enzymatic metabolites, which, together, work on eliminating the ROS and in reducing oxidative damage. This review will address the main production sites of ROS and the action of some enzymes of antioxidative defense system in plants.
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Relação entre a toxicidade de manganês e a tolerância ao alagamento em plantas de Zea

Relação entre a toxicidade de manganês e a tolerância ao alagamento em plantas de Zea

When exposed to prolonged low-oxygen stress, plants typically overproduce reactive oxygen species (ROS), which can cause oxidative damage to plant cells at high concentrations (Shabala, 2011). This damage is the result of ROS reacting with macromolecules, such as proteins, lipids and nucleic acids, leading to a loss of enzyme activity, altered membrane fluidity and genomic damage (Mittler et al., 2004). Efficient antioxidant systems that involve both nonenzymatic and enzymatic molecules can provide some protection against the deleterious effects of ROS (Mittler et al., 2004). For example, superoxide dismutases (SODs) are (uniquely) capable of scavenging O 2 - , producing
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Macrophage migration inhibitory factor induces autophagy via reactive oxygen species generation.

Macrophage migration inhibitory factor induces autophagy via reactive oxygen species generation.

rMIF Induces Autophagy in Human Hepatoma Cells We used rMIF to treat a human hepatoma cell line HuH-7 cells to determine if MIF can induce autophagy. Using PI/Annexin V double staining, we found no significant change of cell death in the presence of rMIF for 24-h (data not shown). However, Western blotting analysis of the cell lysates indicated rMIF induced the conversion of the cytosolic LC3-I to LC3-II after 3-h, 6-h, and 24- h of incubation (Fig. 1A). In addition, MIF specific inhibitor ISO-1 reduced LC3-II conversion. Previous studies have shown that 3- MA (an inhibitor of type III PI3K), NAC (a ROS scavenger) inhibits autophagy. Herein, we found 3-MA and NAC showed ability to inhibit MIF-induced LC3-II conversion. In addition, an NADPH oxidase inhibitor, DPI, also inhibited MIF-induced LC3 conversion. Furthermore, pEGFPC1-LC3 plasmid was transfected into HuH-7 cells (HuH-7-LC3-EGFP) to observe EGFP-LC3 punctae formation by fluorescent microscopy. Treatment of rMIF to HuH-7-LC3-EGFP for 6-h resulted in ,33 punctae formation per cell that was reduced to ,15 punctae in the presence of ISO-1 or 3-MA (Fig. 1B, 1C). Serum starvation induced by HBSS and rapamycin were used as positive controls here. In addition, in the presence of bafilomycin A1 (a vacuolar ATPase inhibitor that blocks fusion of autophagosome and lysosome), the LC3-II expression was increased in HuH-7 cells treated with or without rMIF (Fig. 1D). These results suggest an increase of autophagic flux in the cells treated with rMIF. To further clarify whether MIF induced autophagic flux, mRFP-GFP tandem fluorescence-tagged LC3 plasmid (ptfLC3) was transfected into HuH-7 cells to monitor the progression of the autophagic flux. The GFP tag is acid sensitive while the RFP tag is acid-insensitive. The double tagged LC3 was used to label autophagosomes, amphisomes, and autolysosomes [6,26]. In autophagosomes both tags emit fluorescent light resulting in yellow fluorescent dots. However, fusion of autophagosomes to late endosomes or lysosomes results in acidic amphisomes or autolysosomes where the green fluorescence from GFP is lost resulting in red fluorescent dots. After 24-h rMIF treatment, red LC3 punctae were increased in treated HuH-7 cells while more yellow LC3 punctae were found in untreated HuH-7 cells (Fig. 1E). Furthermore, using bafilomycin A1 to block autophagic flux before autophagosome-lysosome fusion, an increase of yellow LC3 punctae was noticed in rMIF treated cells. Therefore, these results indicate that MIF induced an autophagic flux.
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Effects of reactive oxygen and nitrogen species on actomyosin and their implications for muscle contractility

Effects of reactive oxygen and nitrogen species on actomyosin and their implications for muscle contractility

order rate constant of (4-7) ·10 9 M -1 ·s -1 close to the diffusion limit for chemical reactions. This reaction is three times more efficient than SOD in scavenging superoxide and therefore is preferred where ever both species are present [83]. It is important to recall that peroxynitrite “dosage” should be calculated as a concentration x time product. In some pathophysiological conditions such as during ischemia/reperfusion syndrome and inflammation, generations rates of 0.1-1µM/min peroxynitrite have been reported to be reached in tissues [75,84], where the duration of the tissue insult can last from 30 min to several hours. (a) Modified residues on myosin. Thiol oxidation by peroxynitrite has been previously attributed to loss of function in a number of proteins. On the other hand, the decrease in the free cysteine content of myosin has been previously associated with age-related inhibition of the actomyosin ATPase activity. Skeletal muscle myosin contains 40 cysteines including two highly reactive cysteines, Cys-707 (SH1) and Cys-697 (SH2). These critical residues are located close to the nucleotide binding site and its modification has shown to have functional consequences to the actomyosin complex and to force development of muscle contraction. Oxidation of SH1 is known to inactivate the K + -EDTA ATPase while simultaneously activates the Ca 2+ -dependent ATPase activity. In contrast, oxidation of both reactive cysteine residues inhibits all the myosin ATPase activities including the physiological actin- activated Mg 2+ -ATP hydrolysis activity [85]. The observed decrease of both physiological and non-physiological ATPase activities upon exposure of purified myosin to the peroxynitrite releasing agent SIN-1 indicates that both Cys707 and Cys697 are oxidized by this reagent [57] (Figure 3). Moreover, the obtained IC 50 values were very close to that found for the inhibition of the
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TLR 2, TLR 4, ROS, óxido nítrico, P38 e IKK em células mononucleares de cães com leishmaniose Visceral tratadas com o imunomodulador P-MAPA: Larissa Martins Melo. -

TLR 2, TLR 4, ROS, óxido nítrico, P38 e IKK em células mononucleares de cães com leishmaniose Visceral tratadas com o imunomodulador P-MAPA: Larissa Martins Melo. -

Leishmania (L.) chagasi is the etiologic agent of visceral leishmaniasis (VL) that can be transmitted to humans and dogs. VL in Brazil represents a serious public health problem; therefore, it is important to study new alternatives to treat infected dogs. In dogs, the therapeutic arsenal against canine VL is limited. The immunomodulator protein aggregate magnesium-ammonium phospholinoleate- palmitoleate anhydride (P-MAPA) improves immunocompetence when the immune system is impaired, but its dependence on Toll-like receptors (TLRs) and the mechanisms involved in the immune response remain unclear. The in vitro action of P-MAPA on the expression of TLR2 and TLR4, reactive oxygen species (ROS), nitric oxide (NO) and p38 mitogen-activated protein kinase (p38MAPK) and IKK phosphorylation were studied in mononuclear cells from peripheral blood and macrophages from healthy and Leishmania-infected dogs. The PBMC or macrophages were isolated and cultured with different concentrations of P-MAPA (20,100 and 200μg/mL) in a humid environment at 37°C with 5% CO 2 .
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Diazoxide prevents reactive oxygen species and mitochondrial damage, leading to antihypertrophic effects

Diazoxide prevents reactive oxygen species and mitochondrial damage, leading to antihypertrophic effects

inhibition of calcium-induced mitochondrial swelling. Our data, taken together with other studies [16,24,25] suggest that protecting mitochondria by mitoKATP opening can be a valuable tool to avoid cardiac hypertrophy and associated functional loss. Evidence for this hypothesis emerged in 2004 when Xia and colleagues [24] demonstrated that diazoxide inhibited phenylefrine-induced hy- pertrophy in isolated rat cardiomyocytes by modulation of Na-H exchanger isoform 1. Moreover, mitoKATP opening has been asso- ciated with the antihypertrophic effect of K-opioid receptor acti- vation [25]. Our study extends these observations by showing that mitoKATP exert anti-hypertrophic effects in a manner associated to the maintenance of intracellular redox balance and mitochondrial function.
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Abieslactone induces cell cycle arrest and apoptosis in human hepatocellular carcinomas through the mitochondrial pathway and the generation of reactive oxygen species.

Abieslactone induces cell cycle arrest and apoptosis in human hepatocellular carcinomas through the mitochondrial pathway and the generation of reactive oxygen species.

Akt is a critical kinase involved in cell signal transduction cascades promoting cell survival by inhibiting apoptosis through its ability to phosphorylate and inactivate several proapoptotic proteins [43]. It has been reported that some clinical chemotherapeutic agents could induce cancer cell apoptosis by regulating Akt signal pathway [44]. NF-kB, a pro-inflammatory nuclear transcription factor, regulates genes important for tumor invasion, metastasis, angiogenesis, and chemoresistance [45]. Exposure of cancer cells to anticancer drugs can induce the activation of the NF-kB pathway, leading to the expression of anti-apoptotic genesand resistance to apoptosis. Recent studies have shown that downregulation of Akt and NF-kB activity is involved in mitochondria-mediated apoptosis, and Akt and NF-kB signals appear to be a downstream regulator of ROS generation. To determine if abieslactone-induced apoptosis was mediated by regulating Akt and NF-kB activity, we treated HepG2 cells with increasing concentrations of abieslactone. Our results show that abieslactone inhibited total and phosphory- lated Akt activities. However, abieslactone applied to HepG2 cells did not change p65/RelA protein levels. Thus, we concluded that abieslactone induced HepG2 cell apoptosis via the ROS/Akt pathway.
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Reactive oxygen species regulate protrusion efficiency by controlling actin dynamics.

Reactive oxygen species regulate protrusion efficiency by controlling actin dynamics.

paraformaldehyde, permeabilized in PBS containing 0.5% Triton X-100 and blocked with 2% BSA in PBS. Cells were then immunolabeled for the following antibodies: myosin IIA heavy chain (Sigma-Aldrich, St. Louis, MO), pMLC (Ser 19 , a gift from Y. Sasaki, Kitasato University, Tokyo, Japan), long isoforms of tropomyosin (TM311, Sigma-Aldrich, St. Louis, MO), p34-Arc/ ARPC2 (Millipore, Bedford, MA), phosphorylated-cofilin (P- cofilin, a gift from J. Bamburg, Colorado State University, Fort Collins, CO), phosphorylated-ERK (9101, Cell Signaling, Beverly, MA) by using the appropriate Alexa Fluor 488-conjugated secondary antibodies (Molecular Probes, Eugene, OR). F-actin was detected by using Alexa Fluor 568-conjugated phalloidin (Molecular Probes, Eugene, OR). Cells were mounted on slides with ProLong Gold antifade reagent (Invitrogen, Carlsbad, CA). To localize and quantify the relative number of actin filament free barbed ends, live cells were permeabilized with 0.25 mg/ml saponin in the presence of 0.5 m M X-rhodamine actin and fixed as previously described [69]. Epifluorescence images of fixed cells were acquired on an inverted microscope (Eclipse TE 2000-U, Nikon) equipped with an electronically controlled shutter, filter wheels, and a 14-bit cooled CCD camera (Cool SNAP HQ, Photometrics) controlled by MetaMorph software (Universal Imaging Corp.) with a 60X/1.4 NA Plan Apo DIC objective lens (Nikon).
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Production of reactive oxygen species in Dalbergia nigra seeds under thermal stress

Production of reactive oxygen species in Dalbergia nigra seeds under thermal stress

precision and cut in half in the transversal direction in two segments and incubated in 2.0 mL of reaction medium consisting of disodium salt of 100 µM Ethylenediamine tetraacetic acid (Na 2 EDTA), 20 µM β-Nicotinamide adenine dinucleotide reduced (NADH), and 20 mM sodium phosphate buffer, pH 7.8 (Mohammadi and Karr, 2001) in hermetically sealed tubes. The reaction was started by the introduction of 100 µL of 25.2 mM epinephrine in 0.1N HCl, using a chromatography syringe. Samples were incubated at 28 °C, remaining under shaking for 5 minutes. After that, the segments were removed and, as of the seventh minute, reading of absorbance at 480 nm was begun in a Thermo Scientific EVOLUTION 60S spectrophotometer, which was carried out for five minutes. The blank was performed under the same conditions, but without plant tissue. Production of superoxide anion was assessed by determination of the amount of accumulated adrenochrome (Misra and Fridovich, 1971), using the molar absorption coefficient of 4.0 x 10 3 M -1 (Boveris, 1984).
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2,3-Diarylxanthones as strong scavengers of reactive oxygen and nitrogen species: A structure–activity relationship study

2,3-Diarylxanthones as strong scavengers of reactive oxygen and nitrogen species: A structure–activity relationship study

in the aryl groups. However, in this assay, the presence of phenol groups seems to be extremely important for the scavenging effect. The highest ORAC value was obtained for compound 2b, a xan- thone bearing two phenol groups as substituents. The introduction of an additional OH substituent drastically decreases the scaveng- ing activity as it is evident by the results of compounds 3a–c. 2,3-Diarylxanthone 3c, a derivative with two ortho-dihydroxyl groups, provided the lowest ORAC value from all the tested hydroxyxanthone. These observations are not in accordance to the knowledge about structure–activity relationship of flavonoids and phenolic compounds. The ortho-dihydroxyl substitution is particularly important to the ROO  absorbing activity of those
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Reference Values of Oxidative Stress Parameters in Adult Iranian Fat-Tailed Sheep

Reference Values of Oxidative Stress Parameters in Adult Iranian Fat-Tailed Sheep

A stressful condition leads to the excessive production of the radicals, which results in oxidative stress, an imbalance in the oxidant/antioxidant system (Khadija et al., 2009). Generation of free radicals is an integral feature of normal cellular function. In contrast, excessive generation and/or inadequate removal of free radicals results in destructive and irreversible damage to the cell (Lopaczyski and Zeisel, 2001). Reactive oxygen species (ROS) including superoxide radical, hydrogen peroxide and hydroxyl radical have a great impact on the normal function of biomolecules like nucleic acids, proteins and cell membrane phospholipids. Free radicals are generated during stepwise reduction of molecular oxygen (Singh et al., 1999). Hallwell and Gutteridge (1999) described several lines of defense against reactive oxygen species in animals.
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Angiotensin II induces NF-κB, JNK and p38 MAPK activation in monocytic cells and increases matrix metalloproteinase-9 expression in a PKC- and Rho kinase-dependent manner

Angiotensin II induces NF-κB, JNK and p38 MAPK activation in monocytic cells and increases matrix metalloproteinase-9 expression in a PKC- and Rho kinase-dependent manner

Angiotensin II (ANG II), the main effector of the renin-angiotensin system, is implicated in endothelial permeability, recruitment and activation of immune cells, and also vascular remodeling through induction of inflammatory genes. Matrix metalloprotei- nases (MMPs) are considered to be important inflammatory factors. Elucidation of ANG II signaling pathways and of possible cross-talks between their components is essential for the development of efficient inhibitory medications. The current study investigates the inflammatory signaling pathways activated by ANG II in cultures of human monocytic U-937 cells, and the ef- fects of specific pharmacological inhibitors of signaling intermediates on MMP-9 gene (MMP-9) expression and activity. MMP-9 expression was determined by real-time PCR and supernatants were analyzed for MMP-9 activity by ELISA and zymography methods. A multi-target ELISA kit was employed to evaluate IκB, NF-κB, JNK, p38, and STAT3 activation following treatments. Stimulation with ANG II (100 nM) significantly increased MMP-9 expression and activity, and also activated NF-κB, JNK, and p38 by 3.8-, 2.8- and 2.2-fold, respectively (P < 0.01). ANG II-induced MMP-9 expression was significantly reduced by 75 and 67%, respectively, by co-incubation of the cells with a selective inhibitor of protein kinase C (GF109203X, 5 µM) or of Rho kinase (Y-27632, 15 µM), but not with inhibitors of phosphoinositide 3-kinase (wortmannin, 200 nM), tyrosine kinases (genistein, 100 µM) or of reactive oxygen species (α-tocopherol, 100 µM). Thus, protein kinase C and Rho kinase are important components of the inflammatory signaling pathways activated by ANG II to increase MMP-9 expression in monocytic cells. Both signaling molecules may constitute potential targets for effective management of inflammation.
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Interactions among grapevine disease-causing fungi. The role of reactive oxygen species

Interactions among grapevine disease-causing fungi. The role of reactive oxygen species

radical accumulation, respectively. B. parva shows a superoxide production centred at the colony thal- lus, branching out to the border hyphae. The outer stretches of the colony produced a lighter and faint blue colour due to a lower mycelia density. This pro- duction appears to be more intense when challenged by other fungal species. E. lata seems to be a weaker superoxide producer, with the radical concentrated at the centre of the colony and a ring at the border hyphae. This pattern remains unchanged in the vicinity of other fungal species. P. viticola, on the other hand, shows an extremely high production of superoxide, which indicates a high NADPH oxidase activity (Bloomfi eld and Pears, 2003), when grown either alone and challenged with E. lata (Fig. 3F). Strangely enough, P. viticola seems to lose all its superoxide production capacity (including in the centre of the colony – Fig. 3E) when B. parva is nearby, suggesting a possible decrease in NADPH oxidase activity. Peroxide production was detected mainly at the border hyphae of all isolated fungal colonies (Fig. 4A, 4B, 4C). In addition, E. lata also presents a strong signal at the centre of the thallus. When challenged, B. parva, in the pairings B. parva / E. lata (Fig. 4D) and B. parva / P. viticola (Fig. 4E), specifi cally accumulated higher levels of peroxides at the confrontation zones, but in the pairing E. lata / P. viticola (Fig. 4F), fungal challenging did not affect the pattern of peroxide accumulation.
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Reactive oxygen species and angiotensin II signaling in vascular cells - implications in cardiovascular disease

Reactive oxygen species and angiotensin II signaling in vascular cells - implications in cardiovascular disease

(NFκB), which is activated by Ang II in vascular cells, is the prototype of redox- sensitive transcription factors. NFκB is se- questered in the cytoplasm in a complex with its inhibitor IκB. ROS influence NFκB activity by oxidative modification of cys- teine residues, by IκB degradation and by oxidative enhancement of upstream signal cascades (40). NFκB regulates transcription of many genes involved in vascular inflam- mation and growth, including interleukins, adhesion molecules and proto-oncogenes (41). Other Ang II-activated redox-sensitive transcription factors include activator pro- tein-1 (AP-1) and hypoxia-inducible factor-1 (HIF-1). AP-1 is a transcription factor com- plex formed by homo- or heterodimerization of members of the c-Jun and c-Fos families of proteins and influences vascular cell dif- ferentiation and growth. ROS regulate AP-1 activity through numerous mechanisms and targets, including the reversible S-glutathi-
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Paraquat-induced reactive oxygen species inhibit neutrophil apoptosis via a p38 MAPK/NF-κB-IL-6/TNF-α positive-feedback circuit.

Paraquat-induced reactive oxygen species inhibit neutrophil apoptosis via a p38 MAPK/NF-κB-IL-6/TNF-α positive-feedback circuit.

The nonselective contact herbicide paraquat (PQ) is a strong pneumotoxicant; it accumulates in the lung through a polyamine uptake system and can induce redox cycling, leading to oxidative stress-related damage [1,2]. Evidence has shown that reactive oxygen species (ROS) occupy a central role in PQ-induced acute lung injury (ALI). ROS production impairs tissue and cell function by inducing lipid peroxidation, protein damage, and DNA breakage [3]. In addition to direct ROS-induced pathology, the inflammation response that is secondary to PQ poisoning is also involved in disease pathogenesis. As intrinsic signal transduction molecules, ROS are important components in the complex modulation of neutrophil apoptosis [4,5]. Under normal circum- stances, rapid apoptosis is a neutrophilic characteristic. The average life span of neutrophil is 8-20 h in circulation [6]. Control of neutrophil apoptosis is essential to rapidly resolve inflammatory reactions [7]. Recent studies have shown that apoptosis contrib- utes to ALI pathogenesis, and neutrophil apoptosis in particular exacerbates the condition [8–11].
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J. Braz. Chem. Soc.  vol.21 número5

J. Braz. Chem. Soc. vol.21 número5

Proteins are vulnerable to oxidative stress; attack by reactive oxygen species causes oxidation and formation of carbonyl moieties, advanced oxidation protein products (AOPPs) and other undesired oxidation products. Resveratrol, a polyphenolic phytoalexin found abundantly in grapes and red-wine, is one of the most extensively studied natural products, with wide ranging biological activities including cardio-protective, neuro-protective, anti-aging, and anti-cancer. Most of the effects of these stilbenes are attributed to their antioxidant property. In the present study we have evaluated the role of resveratrol in the protection of plasma protein oxidation after induction of in vitro oxidative stress. Inducing oxidative stress by incubating with 10 -5 mol L -1
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Effect of hydrogen peroxide on thawed ovine sperm motility

Effect of hydrogen peroxide on thawed ovine sperm motility

Krzyzosiak J, Evenson D, Pitt C, Jost L, Molan P, Vishwanath R. 2000. Changes in susceptibility of bovine sperm to in situ DNA denaturation, during prolonged incubation at ambient temperature under conditions of exposure to reactive oxygen species and nuclease inhibitor. Reprod Fertil Dev, 12:251-261. Maia MS, Bicudo SD, Azevedo HC, Sicherle CC, Sousa DB, Rodello L. 2009. Motility and viability of ram sperm cryopreserved in a Tris-egg yolk extender supplemented with anti-oxidants. Small Rumin Res, 85:85-90.

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