Academic literature on the topic 'Reactive oxigen species (ROS)'
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Journal articles on the topic "Reactive oxigen species (ROS)"
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Romecin, P. A., J. E. Millán, A. B. Meseguer, M. C. Ortiz, F. Gragnolini, E. M. García, N. Atucha, and J. García-Estañn. "533 INCREASED PLATELET REACTIVE OXIGEN SPECIES (ROS) PRODUCTION IN EXPERIMENTAL CIRRHOSIS." Journal of Hepatology 52 (April 2010): S213—S214. http://dx.doi.org/10.1016/s0168-8278(10)60535-1.
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Sawayama, Yasushi, Yasushi Miyazaki, Chizuko Tsutsumi, Koji Ando, Kazutaka Kuriyama, and Masao Tomonaga. "Myeloperoxidase Increases Chemosensitivity of Leukemia Cells through the Generation of Reactive Oxigen and Nitrogen Species." Blood 108, no. 11 (November 16, 2006): 4506. http://dx.doi.org/10.1182/blood.v108.11.4506.4506.
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Abstract Myeloperoxidase (MPO) is a specific enzyme whose expression is restricted to the late stage of myeloid differentiation such as promyelocytes and more matured cells. In a pathological situation, however, morphologically immature blasts of acute myeloid leukemia (AML) express MPO at variety of percentages that has been utilized for the diagnosis of AML. On the other hand, the expression of MPO has been shown to have prognostic value for AML cases. Several groups including ours reported that the high percentage of MPO positive blasts at diagnosis was related to the favorable prognosis. Recently, we also found that the expression of the MPO gene in CD133 positive cells also related to the better prognosis of AML cases, suggesting the MPO in the very immature fraction, that is thought to contain leukemia stem cells, is related to the chemosensitivity of AML cells. These results made us hypothesize that MPO directly changes chemosensitivity of leukemia cells through its enzymatic activity. To test this hypothesis, we transfected wild type and enzymaticaly defective MPO (dMPO) cDNA into MPO-negative leukemia cells line, K562, generating K562-MPO and K562-dMPO. Control cells were K562-vector that were transfected with empty vector. The expression of MPO protein was shown in K562-MPO cells, but only precursor of MPO protein, apo-pro-MPO was expressed in K562-dMPO cells as expected. The enzymatic activity was shown only in K562-MPO cells. When these cells were treated with cytosine arabinoside (AraC), K562-MPO cells showed decreased proliferation by WST1 assay compared with wild type K562, K562-vector and K562-dMPO. The expression of Annexin V was increased in AraC-treated K562-MPO suggesting these cells died through apoptosis. Using flowcytometer or confocal microscopy with aminophenyl fluorescein (APF), reactive oxygen species (ROS) were detected in wild type K562 and K562-MPO cells after treatment with AraC. The amount of ROS shown by the intensity of APF-fluorescence increased more in K562-MPO compared with wild type K562 or K562-vector. The difference in the APF-fluorescence observed AraC-treated K562-vector and K562-MPO cells was strongly enhanced by the addition of hydrogen peroxide as a donor of ROS. However, this difference completely disappeared with the addition of N-acetyl cystein (NAC), an inhibitor of ROS, suggesting the involvement of MPO to generate ROS in K562-MPO cells. Although flowcytometer with DAF-2DA failed to detect the significant differences in the amount of reactive nitrogen species (RNS) among AraC-treated wild type K562, K562-vector and K562-MPO cells, immunoblotting against the nitrated tyrosine residue demonstrated the increased nitration of protein in K562-MPO cells compared with wild type or K562-vector. It was suggested that RNS was generated in K562-MPO treated with AraC. These results supported our working hypothesis that MPO in leukemia cells enhanced the sensitivity against chemotherapeutic agents through the generation of ROS and RNS.
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Butsanets, P., A. Baik, N. Shugaeva, and A. Shugaev. "EFFECT OF SALICYLIC ACID ON RESPIRATORY ACTIVITY AND REACTIVE OXIGEN SPECIES GENERATION IN PLANT MITOCHONDRIA." EurasianUnionScientists 2, no. 10(79) (November 20, 2020): 9–15. http://dx.doi.org/10.31618/esu.2413-9335.2020.2.79.1043.
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The aim of this work was to study the effect of a stress phytohormone, salicylic acid (SA), on respiration and generation of reactive oxygen species (ROS) in mitochondria isolated from the cotyledons of lupine seedlings (Lupinus angustifolius L.) and stored taproots of sugar beet (Beta vulgaris L.). Mitochondria were isolated by differential centrifugation, respiration of organelles was measured polarographically using a Clark-type oxygen electrode, and the formation of ROS (hydrogen peroxide) in mitochondria was determined using a fluorogenic dye 2,7-dichlorodihydrofluorescein diacetate (DCFDA). The results obtained showed that SA is capable of exerting a direct regulatory effect on the main parameters of the oxidative phosphorylation process (the rate of substrate oxidation, the value of respiratory control and the ADP/O coefficient), as well as on the formation of ROS. It was shown for the first time that the character of the SA action on mitochondrial metabolism depends not only on the phytohormone concentration, but also on the functional state of the organelles, which is determined by the specificity of the metabolism of tissues and organs from which they were isolated.
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Granato, Marisa, Maria Gilardini Montani, Camilla Angiolillo, Gabriella D’Orazi, Alberto Faggioni, and Mara Cirone. "Cytotoxic Drugs Activate KSHV Lytic Cycle in Latently Infected PEL Cells by Inducing a Moderate ROS Increase Controlled by HSF1, NRF2 and p62/SQSTM1." Viruses 11, no. 1 (December 24, 2018): 8. http://dx.doi.org/10.3390/v11010008.
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Previous studies have indicated that cytotoxic treatments may induce or not activate viral lytic cycle activation in cancer cells latently infected by Kaposi’s sarcoma-associated herpesvirus (KSHV). To investigate the molecular mechanisms responsible for such an effect, we compared two cytotoxic treatments able to induce the viral lytic cycle, named 12-O-tetradecanoylphorbol 13-acetate (TPA) (T) in combination with sodium butyrate (B) and bortezomib (BZ), with two cytotoxic treatments that did not activate this process, named metformin (MET) and quercetin (Q). Our results indicated that TB and bortezomib increased levels of oxygen reactive species (ROS) while metformin and quercetin reduced them. The finding that N-acetylcysteine (NAC), a reactive oxigen species (ROS) scavenger, counteracted K-bZIP expression induced by TB or bortezomib, confirmed that an ROS increase played a role in KSHV lytic cycle activation. Moreover, we found that TB and bortezomib up-regulated p62/Sequestosome1(p62/SQSTM1) protein, while metformin and quercetin down-regulated it. p62/SQSTM1 silencing or the inhibition of NF-E2-related factor 2 (NRF2) or Heat Shock Factor 1 (HSF1), that mediate p62/SQSTM1 transcription, also reduced KSHV lytic antigen expression induced by TB or bortezomib. Interestingly, such combination treatments further increased intracellular ROS and cytotoxicity induced by the single TB or bortezomib treatment, suggesting that NRF2, HSF1 and p62/SQSTM1 keep the ROS level under control, allowing primary effusion lymphoma (PEL) cells to continue to survive and KSHV to replicate.
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LEVY-PEREIRA, Nycolas, Ricardo Luiz Moro de SOUSA, Roberson SAKABE, Fernanda de Alexandre SEBASTIÃO, Elisabeth Criscuolo URBINATI, and Fabiana PILARSKI. "DIETARY MANNAN-OLIGOSACCHARIDE INCREASES REACTIVE OXIGEN SPECIES PRODUCTION BUT DECREASES SERUM LYSOZYME IN HIGH LEVELS OF INCLUSION FOR NILE TILAPIA." Boletim do Instituto de Pesca 46, no. 3 (December 16, 2020): 1–7. http://dx.doi.org/10.20950/1678-2305.2020.46.3.551.
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In the present experiment, the effects of mannan-oligosaccharide (MOS) on health and growth of Nile tilapia juveniles were investigated. In addition to the control treatment (without MOS),three levels of MOS were included in Nile tilapia diets (1, 8, and 15 g kg−1), and hematology, reactive oxygen species (ROS) production, lysozyme and productive parameters were analyzed. Fish blood was sampled at day zero (basal sample) and after 60 days of trial, and the productive parameters were evaluated at the end of the experiment. MOS feeding decreased the feed consumption (p = 0.0299) in fish fed with 1 and 8 g kg-1, but without any alteration in weight gain (WG) and feed conversion ratio (FCR). No changes were observed in the hematology due to MOS feeding after 60 days. However, the prebiotic caused changes in the innate immunity of fish, giving rise to ROS production in fish fed with 1 g kg-1 (p<0.0001) and decreasing the serum lysozyme activity of fish fed with 15 g kg-1 (p<0.0001). In conclusion, the authors recommend the inclusion of 1 g kg-1 for Nile tilapia juveniles feeding due to the positive effect in innate immune system.
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Dreyer, Maik, Anna Rabe, Eko Budiyanto, Klaus Friedel Ortega, Sharif Najafishirtari, Harun Tüysüz, and Malte Behrens. "Dynamics of Reactive Oxygen Species on Cobalt-Containing Spinel Oxides in Cyclic CO Oxidation." Catalysts 11, no. 11 (October 29, 2021): 1312. http://dx.doi.org/10.3390/catal11111312.
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Reactive oxygen species (ROS) are considered to be responsible for the high catalytic activity of transition metal oxides like Co3-xFexO4 in oxidation reactions, but the detailed influences of catalyst composition and morphology on the formation of these reactive oxygen species are not fully understood. In the presented study, Co3O4 spinels of different mesostructures, i.e., particle size, crystallinity, and specific surface area, are characterized by powder X-ray diffraction, scanning electron microscopy, and physisorption. The materials were tested in CO oxidation performed in consecutive runs and compared to a Co3-xFexO4 composition series with a similar mesostructure to study the effects of catalyst morphology and composition on ROS formation. In the first run, the CO conversion was observed to be dominated by the exposed surface area for the pure Co-spinels, while a negative effect of Fe content in the spinels was seen. In the following oxidation run, a U-shaped conversion curve was observed for materials with high surface area, which indicated the in situ formation of ROS on those materials that were responsible for the new activity at low temperature. This activation was not stable at the higher reaction temperature but was confirmed after temperature-programmed oxidation (TPO). However, no activation after the first run was observed for low-surface-area and highly crystalline materials, and the lowest surface-area material was not even activated after TPO. Among the catalyst series studied here, a correlation of small particle size and large surface area with the ability for ROS formation is presented, and the benefit of a nanoscaled catalyst is discussed. Despite the generally negative effect of Fe, the highest relative activation was observed at intermediate Fe contents suggesting that Fe may be involved in ROS formation.
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Iannuzzi, Anna Maria, Chiara Giacomelli, Marinella De Leo, Lara Russo, Fabiano Camangi, Nunziatina De Tommasi, Alessandra Braca, Claudia Martini, and Maria Letizia Trincavelli. "Cornus sanguinea Fruits: a Source of Antioxidant and Antisenescence Compounds Acting on Aged Human Dermal and Gingival Fibroblasts." Planta Medica 87, no. 10/11 (April 15, 2021): 879–91. http://dx.doi.org/10.1055/a-1471-6666.
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AbstractFive new compounds, a flavonol glycoside ( 1), a megastigmane ( 2), 2 cyclohexylethanoids ( 3, 4), and a phenylethanoid derivative ( 5), together with 15 known compounds ( 6– 20) including flavonoid glycosides, cyclohexylethanoids, and phenolic compounds, have been isolated from Cornus sanguinea drupes. All the structures have been determined by 1D and 2D NMR spectroscopic analysis and mass spectrometry data. The antioxidant capability of the most representative isolated compounds was evaluated in the hydrogen peroxide (H2O2)-induced premature cellular senescence model of human dermal and gingival fibroblasts. Several derivatives counteracted the increase of reactive oxigen species (ROS) production in both cellular models. Among the most promising, compounds 8, 14, and 20 were able to counteract cell senescence, decreasing the expression of p21 and p53. Furthermore, compound 14 decreased the expression of inflammatory cytokines (IL-6) in both cell models and counteracted the decrease of collagen expression induced by the H2O2 in dermal human fibroblasts. These data highlight the anti-aging properties of several isolated compounds from C. sanguinea drupes, supporting its possible use in the cure of skin or periodontitis lesions.
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Imelda, Eva, Rinaldi Idroes, Khairan Khairan, Rodiah Rahmawaty Lubis, Abdul Hawil Abas, Ade John Nursalim, Mohamad Rafi, and Trina Ekawati Tallei. "Natural Antioxidant Activities of Plants in Preventing Cataractogenesis." Antioxidants 11, no. 7 (June 28, 2022): 1285. http://dx.doi.org/10.3390/antiox11071285.
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A cataract is a condition that causes 17 million people to experience blindness and is the most significant cause of vision loss, around 47.9%. The formation of cataracts is linked to both the production of reactive oxygen species (ROS) and the reduction of endogenous antioxidants. ROS are highly reactive molecules produced by oxygen. Examples of ROS include peroxides, super-oxides, and hydroxyl radicals. ROS are produced in cellular responses to xenobiotics and bacterial invasion and during mitochondrial oxidative metabolism. Excessive ROS can trigger oxidative stress that initiates the progression of eye lens opacities. ROS and other free radicals are highly reactive molecules because their outer orbitals have one or more unpaired electrons and can be neutralized by electron-donating compounds, such as antioxidants. Examples of natural antioxidant compounds are vitamin C, vitamin E, and beta-carotene. Numerous studies have demonstrated that plants contain numerous antioxidant compounds that can be used as cataract preventatives or inhibitors. Natural antioxidant extracts for cataract therapy may be investigated further in light of these findings, which show that consuming a sufficient amount of antioxidant-rich plants is an excellent approach to cataract prevention. Several other natural compounds also prevent cataracts by inhibiting aldose reductase and preventing apoptosis of the eye lens.
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Altaf, Muhammad, Naike Casagrande, Elena Mariotto, Nadeem Baig, Abdel-Nasser Kawde, Giuseppe Corona, Roberto Larcher, et al. "Potent In Vitro and In Vivo Anticancer Activity of New Bipyridine and Bipyrimidine Gold (III) Dithiocarbamate Derivatives." Cancers 11, no. 4 (April 4, 2019): 474. http://dx.doi.org/10.3390/cancers11040474.
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We synthesized eight new bipyridine and bipyrimidine gold (III) dithiocarbamate-containing complexes (C1–C8) and tested them in a panel of human cancer cell lines. We used osteosarcoma (MG-63), lung (A549), prostate (PC3 and DU145), breast (MCF-7), ovarian (A2780 and A2780cis, cisplatin- and doxorubicin-resistant), and cervical (ME-180 and R-ME-180, cisplatin resistant) cancer cell lines. We found that C2, C3, C6, and C7 were more cytotoxic than cisplatin in all cell lines tested and overcame cisplatin and doxorubicin resistance in A2780cis and R-ME-180 cells. In the PC3 prostate cancer cell line, the gold (III) complex C6 ([Au2(BPM)(DMDTC)2]Cl4) induced apoptosis and double-stranded DNA breaks, modified cell cycle phases, increased Reactive Oxigen Species (ROS) generation, and reduced thioredoxin reductase and proteasome activities. It inhibited PC3 cell migration and was more cytotoxic against PC3 cells than normal human adipose-derived stromal cells. In mice bearing PC3 tumor xenografts, C6 reduced tumor growth by more than 70% without causing weight loss. Altogether, our results demonstrate the anticancer activity of these new gold (III) complexes and support the potential of C6 as a new agent for prostate cancer treatment.
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Misra, A. N., M. Misra, and R. Singh. "Nitric oxide ameliorates stress responses in plants." Plant, Soil and Environment 57, No. 3 (March 4, 2011): 95–100. http://dx.doi.org/10.17221/202/2010-pse.
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Nitric oxide (NO) is a gaseous diatomic molecule with a wide variety of physiological and pathological implications in plants. Presence of unpaired electron in its molecular orbital makes it highly reactive; it can react directly with metal complexes, radicals, DNA, proteins, lipids and other biomolecules. Nitric oxide (NO) and reactive oxygen species (ROS) are known to play essential role in a number of important plant physiological processes. This manuscript reviews the role of NO on these processes during various biotic and abiotic stresses.
Dissertations / Theses on the topic "Reactive oxigen species (ROS)"
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Ristic, Marko. "ROS/SUMO relationship in the chemotherapeutic treatment of Acute Myeloid Leukemia." Thesis, Montpellier, 2015. http://www.theses.fr/2015MONTT047.
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Les leucémies aiguë myéloïde (LAM) sont un groupe d’hémopathies malignes, dont le traitement est généralement composé de deux génotoxiques : la cytarabine (Ara-C) et la daunorubicine (DNR). Nous avons montré que l’Ara-C et la DNR induisent la déconjugaison rapide de SUMO (Small Ubiquitin-related Modifier) de ses protéines cibles. Cette deSUMOylation est dûe à l'inactivation des enzymes E1 et E2 de SUMOylation par les espèces réactives de l'oxygène (ROS) produites par l’Ara-C et la DNR et est impliquée dans l'activation de l'apoptose. En outre, cet axe ROS/SUMO est anergisé dans les LAM chimiorésistantes. Cependant, il peut être réactivé par des pro-oxydants ou par inhibition de la voie SUMO par l'acide anacardique. Pour identifier les protéines contrôlées par l’axe ROS/SUMO nous avons effectué une approche de spectrométrie de masse quantitative (SILAC). Parmi les 1000 protéines SUMOylées identifiées, la plupart des 114 protéines qui perdent leur SUMOylation lors du traitement sont impliquées dans la régulation de l'expression des gènes. De plus, un ChIP-Seq avec des anticorps anti SUMO-2 a permis de montrer que les génotoxiques, en particulier la DNR, induisent une diminution massive de la présence de protéines SUMOylées sur la chromatine. La recherche de motifs au sein des séquences fixant SUMO a permis d’identifier le motif de liaison de CTCF à l’ADN. De plus, CTCF a été trouvé dans la SILAC comme l’une des protéines déSUMOylées par les traitements. En utilisant des données publiques de Chip-Seq pour CTCF, nous avons identifié 55 gènes qui fixent à la fois CTCF et SUMO et dont l’expression est régulée par les traitements. Dans la dernière partie de ce travail, nous avons étudié le groupe de 19 protéines dont la SUMOylation augmente suite aux traitements génotoxiques. Parmi ces protéines, nous avons trouvé diverses protéines centromériques, y compris CENP-B et CENP-C. En utilisant le PLA (Proximity Ligation Assay) nous avons pu montrer que CENP-B et CENP-C colocalisent avec SUMO et yH2AX après traitement. Cela suggère que la SUMOylation des protéines centromériques se produit sur les sites de cassure et pourrait jouer un rôle dans la réparation des dommages de l'ADNAcute Myeloid Leukemias (AML) are a group a severe hematological malignancies, which treatment is generally composed of two genotoxics: Cytarabine (Ara-C) and Daunorubicin (DNR). We have shown that these drugs induce the rapid deconjugation of the Small Ubiquitin-related Modifier (SUMO) from its target protein. This is due to the inactivation of SUMO E1 and E2 enzymes by Reactive oxygen species (ROS). This deSUMOylation participated in the activation of specific genes and is involved the induction of apoptosis. In addition, this ROS/SUMO axis is anergized in chemoresistant AMLs. However, it can be reactivated by pro-oxidants or inhibition of the SUMO pathway with anacardic acid, an inhibitor of the SUMO E1. To identify which proteins are regulated by this ROS/SUMO axis, we performed a quantitative mass spectrometry approach. Among the 1000 identified SUMO targets, most of the 114 proteins, which SUMOylation decrease upon treatment, are involved in the regulation of gene expression. In addition, we showed by ChIP-Seq with SUMO-2 antibodies that genotoxics, in particular DNR, induce a massive decrease of the presence of SUMOylated proteins on the chromatin. Motif search analysis of the SUMO binding sequences in these genes identified CTCF binding motif. Interestingly, CTCF was found in the SILAC as deSUMOylated by the drugs. Using publicly available ChIP-Seq data for CTCF, we found 55 genes which are occupied by both SUMO-2 and CTCF and which expression is regulated by the drugs. In the last part of this work, we got interested in the 19 proteins that get up-SUMOylated upon treatment. Among them, we found centromeric proteins, including CENP-B and CENP-C. Using Proximity Ligation Assay, we could show that CENP-B and CENP-C colocalize with both SUMO and yH2AX upon DNR treatment. Altogether, this suggests that centromeric protein up-SUMOylation occurs at sites of DNA damage and might play a role in DNA damage repair
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Menazza, Sara. "Relationship between mitochondrial ROS formation and myofibrillar protein oxidation in contractile dysfunction." Doctoral thesis, Università degli studi di Padova, 2011. http://hdl.handle.net/11577/3421607.
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Oxidative stress has been related in numerous cardiovascular and muscular pathologies, but the causal relationship between ROS accumulation and contractile impairment is not clear yet. We hypothesized that upon oxidative stress myofibrillar proteins (MPs) are oxidized providing a relevant contribution to the decrease of contractile performance. The evidence provided in the present work demonstrates the key role of mitochondrial dysfunction in muscle injury. We demonstrated that ROS produced in mitochondria alter MPs causing contractile dysfunction in cardiac and skeletal muscle. These results demonstrated that MP oxidation is an important target of ROS. In addition, this study provides evidence that the MAO-dependent ROS accumulation is responsible for both oxidative modifications of MPs and cell death. In fact, inhibition of MAO protects dystrophic skeletal muscle by reducing ROS production and myofiber degeneration. These results demonstrate the pivotal role of mitochondria and suggest a therapeutic potential for MAO inhibition.Lo stress ossidativo è stato riconosciuto come uno dei meccanismi alla base di molte patologie cardiovascolari e muscolari, ma non è ancora stata chiarita quale possa essere la relazione tra l’elevato accumulo di ROS e la disfunzione contrattile. Noi abbiamo ipotizzato che in presenza di stress ossidativo le proteine miofibrillari (MPs) possano venire ossidate, contribuendo cosi al danno contrattile. I risultati ottenuti in questo lavoro dimostrano che la disfunzione mitocondriale svolge un ruolo chiave nel danno muscolare, sia nelle malattie cardiovascolari che nella distrofia muscolare. Abbiamo dimostrato che le ROS prodotte nel mitocondrio modificano le MPs causando una disfunzione contrattile. Questi risultati dimostrano che le ossidazioni alle MPs sono un importante bersaglio delle ROS. Inoltre questo studio mette in evidenza che le ROS prodotte dalla monoamino ossidasi (MAO) sono responsabili sia delle modifiche a carico delle MPs che della morte cellulare. Infatti l’inibizione farmaceutica della MAO protegge il fenotipo distrofico riducendo la produzione delle ROS e la degenerazione delle fibre muscolari. Questo dimostra il ruolo chiave dei mitocondri nella disfunzione contrattile, suggerendo un nuovo potenziale terapeutico per gli inibitori della MAO.
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Hirst, Suzanne Marie. "Anti-inflammatory Effects and Biodistribution of Cerium Oxide Nanoparticles." Thesis, Virginia Tech, 2010. http://hdl.handle.net/10919/76806.
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Cerium oxide nanoparticles have the unique ability to accept and donate electrons, making them powerful antioxidants. Their redox nature is due to oxygen defects in the lattice structure, which are more abundant at the nanoscale. Reactive oxygen species (ROS) are pro-oxidants whose presence is increased during periods of inflammation in the body. ROS damage tissues and cellular function by stripping electrons from proteins, lipids, and DNA. We investigated the ability of nanoceria to quench ROS in vitro and in vivo, and examined the biodistribution and biocompatibility of nanoceria in murine models. Nanoceria was internalized in vitro by macrophages, is non-toxic at the concentrations we investigated, and proteins, mRNA, and oxidative markers of ROS were abated with nanoceria pretreatment in immune stimulated cells as measured by western blot, real time RT PCR, and Greiss assay respectively. In vivo, nanoceria was deposited in the spleen and liver, with trace amounts in the lungs and kidneys as determined by ICP-MS. Using IVIS in vivo imaging, it appeared that nanoceria deposition occurred in lymph tissue. Histology grades show no overt pathology associated with nanoceria deposition, although white blood cell (WBC) counts were generally elevated with nanoceria treatment. Nanoceria suspect particles were seen in lysosomes from kidney samples of IV injected mice in HRTEM images. Lastly, IV nanoceria treatment appears to reduce markers of oxidative stress in mice treated with carbon tetrachloride (CCl4) to induce ROS production. Taken together, our data suggest that nanoceria treatment has the potential to reduce oxidative stress.Master of Science
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Wason, Melissa. "Cerium Oxide Nanoparticles Sensitize Pancreatic Cancer Cells to Radiation by Promoting Acidic pH, ROS, and JNK Dependent Apoptosis." Doctoral diss., University of Central Florida, 2013. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/6033.
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Side effects of radiation therapy (RT) remain the most challenging issue for pancreatic cancer treatment. In this report we determined whether and how cerium oxide nanoparticles (CONPs) sensitize pancreatic cancer cells to RT. CONP pretreatment enhanced radiation-induced reactive oxygen species (ROS) production preferentially in acidic cell-free solutions as well as acidic human pancreatic cancer cells. In acidic environments, CONPs favor the scavenging of superoxide radical over the hydroxyl peroxide resulting in accumulation of the latter whereas in neutral pH CONPs scavenge both. CONP treatment prior to RT markedly potentiated the cancer cell apoptosis both in culture and in tumors and the inhibition of the pancreatic tumor growth without harming the normal tissues or host mice. Mechanistically, CONPs were not able to significantly impact RT-induced DNA damage in cancer cells, thereby ruling out sensitization through increased mitotic catastrophe. However, JNK activation, which is known to be a key driver of RT-induced apoptosis, was significantly upregulated by co-treatment with CONPs and RT in pancreatic cancer cells in vitro and human pancreatic tumors in nude mice in vivo compared to CONPs or RT treatment alone. Further, CONP-driven increase in RT-induced JNK activation was associated with marked increases in Caspase 3/7 activation, indicative of apoptosis. We have shown CONPs increase ROS production in cancer cells; ROS has been shown to drive the oxidation of thioredoxin (TRX) 1 which results in the activation of Apoptosis Signaling Kinase (ASK) 1. The dramatic increase in ASK1 activation following the co-treatment of pancreatic cancer cells with CONPs followed by RT in vitro suggests that increased the c-Jun terminal kinase (JNK) activation is the result of increased TRX1 oxidation. The ability of CONPs to sensitize pancreatic cancer cells to RT was mitigated when the TRX1 oxidation was prevented by mutagenesis of a cysteine residue, or the JNK activation was blocked by an inhibitor,. Additionally, angiogenesis in pancreatic tumors treated with CONPs and RT was significantly reduced compared to other treatment options. Taken together, these data demonstrate an important role and mechanisms for CONPs in specifically killing cancer cells and provide novel insight into the utilization of CONPs as a radiosensitizer and therapeutic agent for pancreatic cancer.Ph.D.
Doctorate
Molecular Biology and Microbiology
Medicine
Biomedical Sciences
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Barreiro, Portela Esther. "Study of reactive oxygen species (ROS) and nitric oxide (NO) as molecular mediators of the sepsis-induced diaphragmatic contractile dysfunction : protective effect of heme oxygenases." Doctoral thesis, Universitat Pompeu Fabra, 2002. http://hdl.handle.net/10803/7066.
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Protein nitration is considered as a marker of reactive nitrogen species formation. Heme oxygenases (HOs) are important for the defence against oxidative stress. We evaluated the involvement of the neuronal (nNOS), the endothelial (eNOS), and the inducible (iNOS) in nitrotyrosine formation and localitzation, and both the expression and funcional significance (HO inhibition and contractility studies) of HOs in sepsis-induced muscle contractile dysfunction. Sepsis was elicited by injecting rats and transgenic mice deficient in either nNOS, eNOS, or iNOS isoforms with E.Coli lipolysaccharide (LPS). Nitrotyrosine formation and HO expressions were assessed by immunoblotting. Oxidative stress was assessed measuring protein oxidation, lipid peroxidation, and muscle glutathione. We conclude that protein tyrosine nitration occurs in normal muscles, and sepsis-mediated increase in nitrotyrosine formation is limited to the mitochondria and membrane muscle fractions. The iNOS isoform is mostly involved in nitrotyrosine formation. HOs protect normal and septic muscles from the deleterious effects of oxidants.En un model de sepsi de disfunció diafragmàtica, s´ha avaluat el paper de les sintetases de l'òxid nítric (NOS) en la formació i localitzacio de 3-nitrotirosina, i l´expressió i significat biològic de les hemo oxigenases (HOs) (inhibidor de les HOs i estudis de contractilitat) davant l' estrès oxidatiu. La sepsi s'induí mitjançant injecció de 20 mg/kg del lipolisacàrid (LPS) d´Escherichia Coli a rates, i a ratolins deficients en les NOS induïble (iNOS), neuronal (nNOS) i endotelial (eNOS). Les proteïnes nitrificades i les HOs es van detectar amb anticossos específics. L' estrès oxidatiu s' avaluà mitjançant l' oxidació proteica, la peroxidació lipídica i el glutation muscular. Concloem que hi han proteïnes nitrificades en el múscul normal i aquestes s'incrementen durant la sepsi en les fraccions mitocondrial i membranar. L'isoforma iNOS és majorment responsable de la formació de nitrotirosina. Les HOs protegirien el múscul normal i sèptic dels efectes deleteris dels oxidants.
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Viegas, Juliane Oliveira. "Cytotoxic potential of graphene oxide in human lung Adenocarcinoma cell line." Master's thesis, Universidade de Aveiro, 2016. http://hdl.handle.net/10773/22356.
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Mestrado em Biologia Molecular e CelularGraphene oxide (GO) is a compound with application in several fields, especially biomedicine and environment, due to its unique properties which confer excellent characteristics. Despite the nowadays wide application of nanomaterials, the lack of information regarding the risks to human health and the environment is still remaining. Consequently, the investigation about the toxicity of nanoparticles must be a priority. The lung is one of the main routes of entry for nanoparticles into the body, therefore, the aim of this study is to evaluate the cytotoxic potential of graphene oxide in lung, using as model the human carcinoma epithelial cell line (A549). The morphology and viability of A549 cells were evaluated after 24h of exposure to GO at concentrations from 10μg/ml to 200μg/ml. The uptake of GO and the production of reactive oxygen species were also investigated by flow cytometry. The results suggest that GO has no obvious toxicity to A549 cells when assessed by WST-8 assay, though the cell cycle showed a slightly alteration in the S and G2 phase at 50μg/mL with arrest at G2 phase. Also, GO showed an increasing in the ROS production at the lowest doses (10ug/mL and 37μg/mL). The intracellular uptake increased for the highest concentration. Together these results suggest that this form of GO shows biocompatibility for lung cells.
O óxido de grafeno (GO) é um composto com aplicação em diversas áreas, especialmente biomedicina e ambiente, devido as suas propriedades únicas que lhe conferem excelentes características. Apesar da atual ampla utilização de nanomateriais, a falta de informação sobre os riscos para a saúde humana e para o ambiente ainda permanece. Consequentemente, a investigação sobre a toxicidade das nanopartículas deve ser uma prioridade. Sendo o pulmão uma das principais vias de entrada das nanopartículas no organismo, o objetivo deste trabalho é avaliar o potencial citotóxico de óxido de grafeno no pulmão, usando com modelo uma linha celular epitelial de carcinoma do pulmão humano (A549). A morfologia e a viabilidade das células A549 foram avaliados após 24 horas de exposição a concentrações de GO entre 10μg/mL a 200μg/mL. A captação de GO e a produção de espécies reativas de oxigênio foram avaliadas por citometria de fluxo. Os resultados sugerem que GO não apresenta óbvia toxicidade para as células A549, quando avaliada pelo ensaio WST-8. No entanto, no ciclo celular observou-se uma ligeira alteração na fase S e na fase G2 em 50μg/mL, com paragem na fase G2. GO induziu também um aumento na produção de ROS em doses mais baixas (10μg/mL e 37μg/mL). A captação intracelular de GO aumentou para a dose mais elevada. Em conjunto, estes resultados sugerem que esta forma de GO apresenta biocompatibilidade para as células de pulmão.
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Garlid, Anders Olav. "Mitochondrial Reactive Oxygen Species (ROS): Which ROS is Responsible for Cardioprotective Signaling?" PDXScholar, 2014. https://pdxscholar.library.pdx.edu/open_access_etds/1641.
Full textAbstract:
Mitochondria are the major effectors of cardioprotection by procedures that open the mitochondrial ATP-sensitive potassium channel (mitoKATP), including ischemic and pharmacological preconditioning. MitoKATP opening leads to increased reactive oxygen species (ROS), which then activate a mitoKATP-associated PKCε, which phosphorylates mitoKATP and leaves it in a persistent open state (Costa, ADT and Garlid, KD. Am J Physiol 295, H874-82, 2008). Superoxide (O2•-), hydrogen peroxide (H2O2), and hydroxyl radical (HO•) have each been proposed as the signaling ROS but the identity of the ROS responsible for this feedback effect is not known. Superoxide was excluded in earlier work on the basis that it does not activate PKCε and does not induce mitoKATP opening.To further examine the identity of the signaling ROS, respiring rat heart mitochondria were preincubated with ATP and diazoxide to induce the phosphorylation-dependent open state, together with agents that may interrupt feedback activation of mitoKATP by ROS scavenging or by blocking ROS transformations. Swelling assays of the preincubated mitochondria revealed that dimethylsulfoxide (DMSO), dimethylformamide (DMF), deferoxamine, trolox, and bromoenol lactone (BEL) each blocked the ROS-dependent open state but catalase did not interfere with this step. The lack of a catalase effect and the inhibitory effects of agents acting downstream of HO• excludes H2O2 as the endogenous signaling ROS and focuses attention on HO•. In support of the hypothesis that HO• is required, we also found that HO•-scavenging by DMF blocked cardioprotection by both ischemic preconditioning and diazoxide in the Langendorff perfused rat heart. HO• itself cannot act as a signaling molecule, because its lifetime is too short and it reacts immediately with nearest neighbor phospholipids and proteins. Therefore, these findings point to a product of phospholipid peroxidation, such as hydroperoxy-fatty acids. Indeed, this hypothesis was supported by the finding that hydroperoxylinoleic acid (LAOOH) opens the ATP-inhibited mitoKATP in isolated mitochondria. This effect was blocked by the specific PKCε inhibitor peptide εV1-2, showing that LAOOH activates the mitoKATP-associated PKCε. During ischemia, catabolism of mitochondrial phospholipids is accelerated, causing accumulation of plasmalogens and free fatty acids (FA) in the heart by the action of calcium independent phospholipases A2 (iPLA2). We first assessed the role of FAs and hydroxy FAs on mitoKATP opening and cardioprotection. Swelling assays of isolated rat heart mitochondria showed that naturally formed free FAs inhibit mitoKATP opening and that they are more potent inhibitors of the pharmacological open state of mitoKATP than the phosphorylation-dependent open state. That is, sustained mitoKATP opening induced by the phosphorylation-dependent feedback loop is more resistant to FA inhibition than direct mitoKATP opening by a potassium channel opener. Moreover, rat hearts perfused with micromolar concentrations of FA were resistant to cardioprotection by diazoxide or ischemic preconditioning. Racemic bromoenol lactone (BEL), a selective inhibitor of iPLA2, confers protection to otherwise untreated Langendorff perfused hearts by preventing ischemic FA release. To bring this story full circle, BEL blocks protection afforded by preconditioning and postconditioning by preventing the iPLA2-mediated release of FAOOH generated in the conditioned heart. HO• resulting from mitoKATP opening oxidizes polyunsaturated fatty acid components of the membrane phospholipids, resulting in a peroxidized side chain. FAOOH must be released in order to act on the mitochondrial PKCε, and this is achieved by the action of iPLA2. iPLA2 is essential for most modes of cardioprotection because it catalyzes the release of FAOOH. This fully supports the hypothesis that the second messenger of cardioprotective ROS-mediated signaling is hydroperoxy fatty acid (FAOOH), a downstream oxidation product of HO•.
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Vaidyanathan, V. V. "Oxidative Stress In The Brain: Effects Of Hydroperoxides And Nitric Oxide On Glyceraldehyde 3-Phosphate Dehydrogenase And Phosphoinositide Cycle Enzymes." Thesis, Indian Institute of Science, 1994. http://hdl.handle.net/2005/142.
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In the aerobic cell, oxygen can be converted into a series of reactive metabolites, together called as "reactive oxygen species" (ROS). This large group include both radical and non-radical species such as superoxide anion (02"), hydroxyl radical ("0H), H202, nitric oxide (N0') and lipid hydroperoxides (LOOH). ROS are generated in very small amounts at all stages of aerobic life, and probably have a role in cellular regulation. However, their formation in excess leads to toxicity and damage to tissues. This situation, called 'oxidative stress', is responsible, atleast in part, to the pathophysioiogy of a number of disease states such as inflammation, arthritis, cancer, ageing, ischemia-reperfusion and several neurodegenerative disorders.
Compared to other organs in the animal body, brain tissue is more vulnerable to oxidative stress. This is due to three major reasons; (1) brain has a high oxygen consumption (2) high content of polyunsaturated fatty acids and iron, that can promote lipid peroxidation, and (3) low levels of antioxidant enzymes such as catalase and glutathione peroxidase. The inability of neurons to regenerate also contributes to exacerbate an oxidant damage in the brain.
The main objective of this investigation was to identify biochemical systems in the brain that are susceptible to ROS, on the following two issues:
1. What are the targets for the action of H2O2 and NO in the glycolytic cycle, the major route for the oxidation of glucose in brain?
2. What are the targets for the action of polyunsaturated fatty acids and their oxidative metabolites among the enzymes of phosphoinositide cycle (PI cycle), the ubiquitous signal transduction event in the brain?
Using sheep brain cytosol , it was found that among the various glycolytic enzymes, only glyceraldehyde 3-phosphate dehydrogenase (GAPD) was inhibited by H2O2. The enzyme was purified to homogeneity from sheep brain and its inactivation with H202 was studied in detail. Commercial preparations of rabbit skeletal muscle GAPD was also used in this study. An unusual requirement of glutathione for the complete inactivtion of the enzyme by H2O2 was observed. The H2O2-inactivated GAPD was partially reactivated by prolonged treatment with thiol compounds. Using CD-spectral analysis, a significant change was found in the secondary structure in H2O2-treated GAPD.
GAPD was inactivated by NO only in presence of high concentrations of DTT and after prolonged incubation. The N0-inactivated GAPD was partially reactivated by treatment with thiol compounds. A new activity, namely ADP-ribosylation (ADPR) emerged in the NO-treated mammalian, but not in yeast. GAPD, ADPR activity could be generated in GAPD through NO-independent treatments such as incubation with NADPH and aerobic dialysis. During NADPH treatment no loss of dehydrogenase activity occurred. Thus, it was concluded that loss of dehydrogenase activity and emergence of ADPR in NO-treated GAPD were not correlated but coincidental, and that NO treatment yielded small amounts of modified-GAPD that had ADPR activity.
In the brain, onset of ischemia is characterized by a significant elevation in free fatty acid (FFA) levels, predominantly, arachidonic acid (AA). It is suggested that AA can be oxidised to its metabolites like prostaglandins and 15-hydroperoxy arachidonic acid (15-HPETE) and some of these might exert toxic effects during reperfusion. Using whole membranes or tissue slices prepared from rat brain, effects of polyunsaturated fatty acids and their oxidative metabolites on five enzymes of PI cycle namely PI synthase, PI and PIP kinases, agonist-stimulated PLC and DG kinase was studied. Hydroperoxides of linoleic- and arachidonic acids inactivated PI synthase selectively among the PI cycle enzymes. Interestingly, AA selectively stimulated DG kinase in neural membranes. Docasahexaenoic acid (DHA) a highly unsaturated fatty acid found in the brain, also stimulated DG kinase activity while saturated, mono-and di-unsaturated fatty acids were ineffective. It was concluded that AA and DHA have a role in modulating neural DG kinase.
The data presented in the thesis indicate that ROS have selective targets in cells and the consequent protein modifications can be used to modulate cellular functions under normal and oxidative stress conditions.
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Al-Nu'airat, Jomana. "Implications of reactive oxygen species (ROS) in initiating chemical reactions." Thesis, Al-Nu'airat, Jomana (2018) Implications of reactive oxygen species (ROS) in initiating chemical reactions. PhD thesis, Murdoch University, 2018. https://researchrepository.murdoch.edu.au/id/eprint/42916/.
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This thesis presents a series of scientific studies exploring the initiation of various chemical reactions with reactive oxygen species (ROS), mainly singlet oxygen. These studies have revealed new mechanistic insights in environmental, industrial and biological systems, have described the associated set of reactions, have illustrated the detection of new radicals i.e., environmentally persistent free radicals (EPFR), and have provided a new insight explaining the spontaneous fire in coal mines. Comprehensive experimental and quantum-mechanical calculations afforded the investigation of oxidation reactions of singlet oxygen with wastewater organic contaminants, for example, the photodegradation of Phenol and Aniline in water. Detailed experimental studies on modelled surrogates, i.e., Anisole, resolved the fundamentals of thermal interaction of coal with iron oxide Fe2O3 nanoparticles. Along the same line of interest, enhancing the combustion efficiency of fuel constitutes a mainstream strategy in the pursuit of meeting the ever-increasing energy demand. Therefore, this thesis also provides a comprehensive mechanistic and thermo-kinetic accounts underpinning the reaction of fuel surrogates, namely Toluene, with singlet oxygen in the internal combustion (IC) engines. Finally, this work extends insights into biological systems, mapping the Alloxan-Glutathione redox cycle to expose the formation of ROS, species that eventually cause necrosis of the pancreatic insulin-producing beta cells and prompt the insulin-dependent diabetes mellitus (IDDM).
The methodology involve customised LED-photoreactors, thermal packed-bed reactor, and various reaction product-monitoring systems, e.g., Fourier transform infrared spectroscopy (FTIR) to quantitate the ignition temperatures of fuel surrogates, in-situ electron paramagnetic resonance (EPR) to elucidate the formation of environmentally-persistent free radicals (EPFR) as well as intermediate radical species, diffuse reflectance infrared Fourier transform spectroscopy (DRIFTS) to monitor the chemisorption of organic substrates on the nanoparticles, X-ray diffraction for particles characterisation, as well as broad-scan UV-Vis spectroscopy and high-performance liquid chromatography (HPLC) to identify and quantify the intermediate and product species in solutions.
Results obtained in this thesis elucidate, for the very first time, the formation of para-semibenzoquinone anion (PSBQ) supporting the reaction pathway leading to the formation of para-benzoquinone during the reaction of phenol (and aniline) with singlet oxygen. These results have practical application to quantify the degradation of organic pollutants in wastewater. Investigations regarding combustion applications shows that the presence of singlet oxygen considerably lowers the activation energy of the initiation channels of aromatic hydrocarbons (e.g., in IC engines), resulting in an energetically improved combustion process, the relative reactivity of singlet oxygen, based on the reaction rate constants, follows the order of OH > H > CH3 > 1O2 > HO2 > 3O2. Furthermore, the chemisorption of anisole on α-Fe2O3 surfaces has been elucidated to follow a direct dissociation of the O–CH3 (and OCH2–H), leading to the formation of surface-bound phenoxy radicals and gaseous species at temperatures as low as 25 °C. This insight applies to free-radical chain reactions that induce spontaneous fires of coal, as low-ranked coal comprises ferric oxide nanoparticles, and equally, to coexistence of aromatic fuels with thermodynamically reactive Fe2O3 surface, e.g., in fly ash, at the cooled-down tail of combustion stacks. Results from alloxan-glutathione redox cycle clarified, for the first time, the direct synchronised generation of dialuric acid radical (DA˙) and glutathione radical (GS˙), assigning the nature of the mysterious “compound 305” to the DA˙- GS˙ complex. These results explain the alloxan-induced diabetes on precise molecular bases.
This thesis provides new perspectives on opportunities in understanding the influence of ROS, mainly singlet oxygen (1O2) and superoxide (O2−) in germane chemical reactions. Such attempts will advance the existing ROS-related technologies, and improve the fundamental theories in supports of environmental management and application decisions.
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Todd, Adam. "The role and inhibition of reactive oxygen species (ROS) in psoriasis." Thesis, University of Sunderland, 2009. http://sure.sunderland.ac.uk/3699/.
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Psoriasis is a chronic inflammatory skin disorder that affects around two percent of the population. There are many treatments available for the management of psoriasis including topical therapy, systemic agents and phototherapy. Despite the number of treatments available, however, there are still problems in the management of psoriasis. It is suggested here that the thioredoxin enzyme system may play a role in the pathology of psoriasis. Using specific molecular modelling techniques, a lead compound, RDP00060, was identified as a potential inhibitor of thioredoxin reductase, a key enzyme in the thioredoxin system. In vitro RDP00060 showed moderate inhibitory activity against the thioredoxin enzyme system with an IC50 value of 1.4 mM. RDP00060 also showed powerful activity in an MTT assay using a human papilloma virus immortalized keratinocyte (HPV-16) cell line. To increase the inhibitory activity towards thioredoxin reductase, molecular modelling techniques were used to identify analogues of RDP00060 with a high binding affinity for thioredoxin reductase. Several novel compounds were then synthesized, characterized and evaluated for inhibitory activity towards the thioredoxin system. One of the compounds, N-(3,4-bis-(toluene-4- sulfonylamino)phenyl)-2-furamide (33f) showed good inhibitory activity against the thioredoxin enzyme with an IC50 value of 37 μM. It is anticipated that N-(3,4- bis-(toluene-4-sulfonylamino)phenyl)-2-furamide (33f) binds to thioredoxin reductase irreversibly through a 1,4-conjugate addition mechanism. This compound also showed powerful activity in the MTT assay using an HPV-16 immortalized keratinocyte cell line. Further testing revealed that N-(3,4-bis-(toluene-4-sulfonylamino)phenyl)-2- furamide (33f) also showed apoptotic and antiproliferative properties in human Tcells. As a result of this work, N-(3,4-bis-(toluene-4-sulfonylamino)phenyl)-2- furamide (33f) has been selected for further investigation as a potential antipsoriatic agent.
Books on the topic "Reactive oxigen species (ROS)"
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Musonda, Alam Clement. Quercetin as a modulator of xenobiotic metabolism and reactive oxygen species (ROS) in human hepG2 cells. Birmingham: University of Birmingham, 1998.
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Nakamura, Tomohiro, and Stuart A. Lipton. Neurodegenerative Diseases as Protein Misfolding Disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190233563.003.0002.
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Neurodegenerative diseases (NDDs) often represent disorders of protein folding. Rather than large aggregates, recent evidence suggests that soluble oligomers of misfolded proteins are the most neurotoxic species. Emerging evidence points to small, soluble oligomers of misfolded proteins as the cause of synaptic dysfunction and loss, the major pathological correlate to disease progression in many NDDs including Alzheimer’s disease. The protein quality control machinery of the cell, which includes molecular chaperones as found in the endoplasmic reticulum (ER), the ubiquitin-proteasome system (UPS), and various forms of autophagy, can counterbalance the accumulation of misfolded proteins to some extent. Their ability to eliminate the neurotoxic effects of misfolded proteins, however, declines with age. A plausible explanation for the age-dependent deterioration of the quality control machinery involves compromise of these systems by excessive generation of reactive oxygen species (ROS), such as superoxide anion (O2-), and reactive nitrogen species (RNS), such as nitric oxide (NO). The resulting redox stress contributes to the accumulation of misfolded proteins. Here, we focus on aberrantly increased generation of NO-related species since this process appears to accelerate the manifestation of key neuropathological features, including protein misfolding. We review the chemical mechanisms of posttranslational modification by RNS such as protein S-nitrosylation of critical cysteine thiol groups and nitration of tyrosine residues, showing how they contribute to the pathogenesis of NDDs.
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Filip, Cristiana, and Elena Albu, eds. Reactive Oxygen Species (ROS) in Living Cells. InTech, 2018. http://dx.doi.org/10.5772/intechopen.69697.
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Zilliox, Lindsay, and James W. Russell. Diabetic and Prediabetic Neuropathy. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0115.
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Impaired glucose regulation (IGR) constitutes a spectrum of impaired glucose and metabolic regulation that can result in neuropathy. Several different pathways of injury in the diabetic peripheral nervous system that include metabolic dysregulation induced by metabolic syndrome induce oxidative stress, failure of nitric oxide regulation, and dysfunction of certain key signaling pathways. Oxidative stress can directly injure both dorsal route ganglion neurons and axons. Modulation of the nitric oxide system may have detrimental effects on endothelial function and neuronal survival. Reactive oxidative species can alter mitochondrial function, protein and DNA structure, interfere with signaling pathways, and deplete antioxidant defenses. Advanced glycelation end (AGE) products and formation of ROS are activated by and in turn regulate key signal transduction pathways.
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TG 495: Ros (Reactive Oxygen Species) Assay for Photoreactivity. OECD, 2019. http://dx.doi.org/10.1787/915e00ac-en.
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Singh, Vijay Pratap, Sheo Mohan Prasad, Durgesh K. Tripathi, Samiksha Singh, and Devendra K. Chauhan. Reactive Oxygen Species in Plants: Boon or Bane - Revisiting the Role of ROS. Wiley & Sons, Limited, John, 2017.
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Reactive Oxygen Species in Plants: Boon Or Bane - Revisiting the Role of ROS. Wiley, 2017.
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Singh, Vijay Pratap, Sheo Mohan Prasad, Durgesh Kumar Tripathi, Devendra Kumar Chauhan, and Samiksha Singh. Reactive Oxygen Species in Plants: Boon or Bane - Revisiting the Role of ROS. Wiley & Sons, Incorporated, John, 2017.
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Singh, Vijay Pratap, Sheo Mohan Prasad, Durgesh Kumar Tripathi, Devendra Kumar Chauhan, and Samiksha Singh. Reactive Oxygen Species in Plants: Boon or Bane - Revisiting the Role of ROS. Wiley & Sons, Incorporated, John, 2017.
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Reactive Oxygen Species (ROS), Nanoparticles, and Endoplasmic Reticulum (ER) Stress-Induced Cell Death Mechanisms. Elsevier, 2020. http://dx.doi.org/10.1016/c2019-0-04102-7.
Full textBook chapters on the topic "Reactive oxigen species (ROS)"
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Mehlhorn, Heinz. "Reactive Oxygen Species (ROS)." In Encyclopedia of Parasitology, 2314–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_4262.
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Mehlhorn, Heinz. "Reactive Oxygen Species (ROS)." In Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_4262-1.
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Kemp, Melissa L. "Reactive Oxygen Species (ROS)." In Encyclopedia of Systems Biology, 1817. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-9863-7_1263.
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Martemyanov, Kirill A., Pooja Parameswaran, Irene Aligianis, Mark Handley, Marga Gual-Soler, Tomohiko Taguchi, Jennifer L. Stow, et al. "ROS (Reactive Oxygen Species)." In Encyclopedia of Signaling Molecules, 1691. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101203.
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Tauler Riera, Pedro, Maurizio Volterrani, Ferdinando Iellamo, Francesco Fallo, Andrea Ermolao, William J. Kraemer, Nicholas A. Ratamess, Avery Faigenbaum, Andrew Philp, and Keith Baar. "Reactive Oxygen Species (ROS)." In Encyclopedia of Exercise Medicine in Health and Disease, 749. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2942.
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Gooch, Jan W. "Reactive Oxygen Species (ROS)." In Encyclopedic Dictionary of Polymers, 919. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14648.
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Agarwal, Ashok, Sajal Gupta, and Rakesh Sharma. "Reactive Oxygen Species (ROS) Measurement." In Andrological Evaluation of Male Infertility, 155–63. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-26797-5_21.
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Pham, Jasmine, and Radhika Desikan. "ROS Signalling in Stomata." In Reactive Oxygen Species in Plant Signaling, 55–71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00390-5_4.
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de Lamirande, Eve, and Claude Gagnon. "Reactive Oxygen Species (ROS) and Reproduction." In Free Radicals in Diagnostic Medicine, 185–97. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-1833-4_14.
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Wen, Tao, Jianbo Liu, Weiwei He, and Aiyun Yang. "Nanomaterials and Reactive Oxygen Species (ROS)." In Nanotechnology in Regenerative Medicine and Drug Delivery Therapy, 361–87. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5386-8_8.
Full textConference papers on the topic "Reactive oxigen species (ROS)"
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Elshiekh, Duaa Ibnomer, Hadeel Hendawi, Aya Goul, Dina Awartan, Isra Marei, Christopher Triggle, and Haissam Abou Saleh. "Effect of Hyperglycemia on eNOS function in EPCs." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0215.
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Type 2 diabetes mullites (T2DM) results in different cardiovascular complications. The main cause of these complications is endothelial dysfunction, which affects the endothelium physiologically and pathologically. The chronic hyperglycemia introduced by T2DM impacts the pivotal enzyme endothelial nitric oxide synthase (eNOS) in terms of phosphorylation and dimerization, which initiates oxidative stress and reduces the bioavailability of the vasodilator nitric oxide. To overcome endothelial dysfunction, endothelial progenitor cells (EPCs) contribute to vascular repair due to their regenerative characteristics. The effects of hyperglycemia on EPCs are understudied. Thus, this study aims to investigate the effects of hyperglycemia on the eNOS/Akt signaling pathway and reactive oxygen species (ROS) formation. Cells were treated with normal glucose (NG, 5.5mM) and high glucose (HG, 25mM) media for 3 & 6 days, and the effect on eNOS and Akt phosphorylation were assessed using western blot. ROS was assessed using CellROX stain following 1 and 3 days of treatment. Results showed that both acute and chronic hyperglycemia showed a trend towards decrease in phosphorylation of eNOS and Akt. In addition, ROS formation was increased following 24hr compared to NG. Further investigations are needed to enhance the capability of BOECs to serve as therapeutic tools in T2DM.
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Yu, Miao, and Alisa Morss Clyne. "Dextran and PEG Coating Reduced Nanoparticle Toxicity to Cells." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80819.
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Iron oxide nanoparticles are of interest for drug delivery, since they can be targeted using a magnetic field. However, prior to using nanoparticles in vivo, they must be shown as relatively non-toxic to cells. We and others have shown that bare iron oxide nanoparticles are readily taken up by cells, where they catalyze production of highly toxic reactive oxygen species (ROS). This oxidative stress disrupts the cell cytoskeleton and alters cell mechanics. [1] Iron oxide nanoparticles under current development for in vivo biomedical applications are often coated with a polysaccharide (eg. dextran) or a polymer (eg. polyethylene glycol, PEG). Both the size and the surface coating of nanoparticle may play an important role in cell toxicity.
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Podder, Soumik, and Sunipa Roy. "Reactive Oxygen Species (ROS) Sensing- A Nanoscale Transistorized Approach." In 2022 IEEE International Conference of Electron Devices Society Kolkata Chapter (EDKCON). IEEE, 2022. http://dx.doi.org/10.1109/edkcon56221.2022.10032914.
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Yu, J. Q., L. K. Chin, Y. Fu, T. Yu, K. Q. Luo, and A. Q. Liu. "Pulsatile shear stress and high glucose concentrations induced reactive oxigen species production in endothelial cells." In TRANSDUCERS 2011 - 2011 16th International Solid-State Sensors, Actuators and Microsystems Conference. IEEE, 2011. http://dx.doi.org/10.1109/transducers.2011.5969310.
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Suyono, Handi, and Guritno Suryokusumo. "Hyperbaric Oxygen (HBO) Heals Cell Through Reactive Oxygen Species (ROS)." In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007334001230127.
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Norina, Svetlana B. "MAGNETOPHORETIC AND OPTICAL STUDY OF ANISOTROPIC MAGNETIC PROPERTIES OF BIOMICROPARTICLES CONTAINING REACTIVE OXIGEN SPECIES OR FERRITIN." In European Conference on Biomedical Optics. Washington, D.C.: OSA, 2003. http://dx.doi.org/10.1364/ecbo.2003.5143_126.
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Veronica, Gisca, Komariah, and Ln Gabriella Clara Maria. "Microencapsulation of Lemongrass Leaves Effect on Reactive Oxygen Species (ROS) Fibroblasts." In 2021 IEEE International Conference on Health, Instrumentation & Measurement, and Natural Sciences (InHeNce). IEEE, 2021. http://dx.doi.org/10.1109/inhence52833.2021.9537219.
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Khaing Oo, Maung Kyaw, Maria Gomez, Hongjun Wang, and Henry Du. "Enhanced Generation of Reactive Oxygen Species Using Gold Nanoparticles Conjugated With Protoporphyrin IX." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13115.
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Reactive oxygen species (ROS) is a vital trigger for photodynamic therapy (PDT) of cancer. We report the production of elevated ROS using gold nanoparticles (GNP) (20–100 nm in diameter) conjugated with Protophorphyrin IX (PpIX). The amount of ROS formation increases with the size of the GNP due to enhanced electromagnetic field resulting from localized surface plasmonic resonance.
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Sun, Qingrui, and Tongsheng Chen. "Reactive oxygen species (ROS) is not a promotor of taxol-induced cytoplasmic vacuolization." In SPIE BiOS: Biomedical Optics, edited by Wei R. Chen. SPIE, 2009. http://dx.doi.org/10.1117/12.807256.
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Johnson, Arnold, and Amy Barton-Pai. "Lipoteichoic Acid (LTA) Causes Reactive Oxygen Species (ROS) dependent Lung Endothelial Barrier Dysfunction." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3441.
Full textReports on the topic "Reactive oxigen species (ROS)"
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Asenath-Smith, Emily, Emma Ambrogi, Eftihia Barnes, and Jonathon Brame. CuO enhances the photocatalytic activity of Fe₂O₃ through synergistic reactive oxygen species interactions. Engineer Research and Development Center (U.S.), September 2021. http://dx.doi.org/10.21079/11681/42131.
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Iron oxide (α-Fe₂O₃, hematite) colloids were synthesized under hydrothermal conditions and investigated as catalysts for the photodegradation of an organic dye under broad-spectrum illumination. To enhance photocatalytic performance, Fe₂O₃ was combined with other transition-metal oxide (TMO) colloids (e.g., CuO and ZnO), which are sensitive to different regions of the solar spectrum (far visible and ultraviolet, respectively), using a ternary blending approach for compositional mixtures. For a variety of ZnO/Fe₂O₃/CuO mole ratios, the pseudo-first-order rate constant for methyl orange degradation was at least double the sum of the individual Fe₂O₃ and CuO rate constants, indicating there is an underlying synergy governing the photocatalysis reaction with these combinations of TMOs. A full compositional study was carried out to map the interactions between the three TMOs. Additional experiments probed the identity and role of reactive oxygen species and elucidated the mechanism by which CuO enhanced Fe₂O₃ photodegradation while ZnO did not. The increased photocatalytic performance of Fe2O3 in the presence of CuO was associated with hydroxyl radical ROS, consistent with heterogeneous photo-Fenton mechanisms, which are not accessible by ZnO. These results imply that low-cost photocatalytic materials can be engineered for high performance under solar illumination by selective pairing of TMOs with compatible ROS.
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Droby, Samir, Michael Wisniewski, Ron Porat, and Dumitru Macarisin. Role of Reactive Oxygen Species (ROS) in Tritrophic Interactions in Postharvest Biocontrol Systems. United States Department of Agriculture, December 2012. http://dx.doi.org/10.32747/2012.7594390.bard.
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To elucidate the role of ROS in the tri-trophic interactions in postharvest biocontrol systems a detailed molecular and biochemical investigation was undertaken. The application of the yeast biocontrol agent Metschnikowia fructicola, microarray analysis was performed on grapefruit surface wounds using an Affymetrix Citrus GeneChip. the data indicated that 1007 putative unigenes showed significant expression changes following wounding and yeast application relative to wounded controls. The expression of the genes encoding Respiratory burst oxidase (Rbo), mitogen-activated protein kinase (MAPK) and mitogen-activated protein kinase kinase (MAPKK), G-proteins, chitinase (CHI), phenylalanine ammonia-lyase (PAL), chalcone synthase (CHS) and 4-coumarate-CoA ligase (4CL). In contrast, three genes, peroxidase (POD), superoxide dismutase (SOD) and catalase (CAT), were down-regulated in grapefruit peel tissue treated with yeast cells. The yeast antagonists, Metschnikowia fructicola (strain 277) and Candida oleophila (strain 182) generate relatively high levels of super oxide anion (O2−) following its interaction with wounded fruit surface. Using laser scanning confocal microscopy we observed that the application of M. fructicola and C. oleophila into citrus and apple fruit wounds correlated with an increase in H2O2 accumulation in host tissue. The present data, together with our earlier discovery of the importance of H₂O₂ production in the defense response of citrus flavedo to postharvest pathogens, indicate that the yeast-induced oxidative response in fruit exocarp may be associated with the ability of specific yeast species to serve as biocontrol agents for the management of postharvest diseases. Effect of ROS on yeast cells was also studied. Pretreatment of the yeast, Candida oleophila, with 5 mM H₂O₂ for 30 min (sublethal) increased yeast tolerance to subsequent lethal levels of oxidative stress (50 mM H₂O₂), high temperature (40 °C), and low pH (pH 4). Suppression subtractive hybridization analysis was used to identify genes expressed in yeast in response to sublethal oxidative stress. Transcript levels were confirmed using semi quantitative reverse transcription-PCR. Seven antioxidant genes were up regulated. Pretreatment of the yeast antagonist Candida oleophila with glycine betaine (GB) increases oxidative stress tolerance in the microenvironment of apple wounds. ROS production is greater when yeast antagonists used as biocontrol agents are applied in the wounds. Compared to untreated control yeast cells, GB-treated cells recovered from the oxidative stress environment of apple wounds exhibited less accumulation of ROS and lower levels of oxidative damage to cellular proteins and lipids. Additionally, GB-treated yeast exhibited greater biocontrol activity against Penicillium expansum and Botrytis cinerea, and faster growth in wounds of apple fruits compared to untreated yeast. The expression of major antioxidant genes, including peroxisomal catalase, peroxiredoxin TSA1, and glutathione peroxidase was elevated in the yeast by GB treatment. A mild heat shock (HS) pretreatment (30 min at 40 1C) improved the tolerance of M. fructicola to subsequent high temperature (45 1C, 20–30 min) and oxidative stress (0.4 mol-¹) hydrogen peroxide, 20–60 min). HS-treated yeast cells showed less accumulation of reactive oxygen species (ROS) than non-treated cells in response to both stresses. Additionally, HS-treated yeast exhibited significantly greater (P≥0.0001) biocontrol activity against Penicillium expansum and a significantly faster (Po0.0001) growth rate in wounds of apple fruits stored at 25 1C compared with the performance of untreated yeast cells. Transcription of a trehalose-6-phosphate synthase gene (TPS1) was up regulated in response to HS and trehalose content also increased.
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Garlid, Anders. Mitochondrial Reactive Oxygen Species (ROS): Which ROS is Responsible for Cardioprotective Signaling? Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1640.
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Friedman, Haya, Chris Watkins, Susan Lurie, and Susheng Gan. Dark-induced Reactive Oxygen Species Accumulation and Inhibition by Gibberellins: Towards Inhibition of Postharvest Senescence. United States Department of Agriculture, December 2009. http://dx.doi.org/10.32747/2009.7613883.bard.
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Dark-induced senescence could pose a major problem in export of various crops including cuttings. The assumption of this work was that ROS which is increased at a specific organelle can serve as a signal for activation of cell senescence program. Hormones which reduce senescence in several crops like gibberellic acid (GA) and possibly cytokinin (CK) may reduce senescence by inhibiting this signal. In this study we worked on Pelargonium cuttings as well as Arabidopsis rosette. In Pelargonium the increase in ROS occurred concomitantly with increase in two SAGs, and the increase persisted in isolated chloroplasts. In Arabidopsis we used two recentlydeveloped technologies to examine these hypotheses; one is a transcriptome approach which, on one hand, enabled to monitor expression of genes within the antioxidants network, and on the other hand, determine organelle-specific ROS-related transcriptome footprint. This last approach was further developed to an assay (so called ROSmeter) for determination of the ROS-footprint resulting from defined ROS stresses. The second approach involved the monitoring of changes in the redox poise in different organelles by measuring fluorescence ratio of redox-sensitive GFP (roGFP) directed to plastids, mitochondria, peroxisome and cytoplasm. By using the roGFP we determined that the mitochondria environment is oxidized as early as the first day under darkness, and this is followed by oxidation of the peroxisome on the second day and the cytoplast on the third day. The plastids became less oxidized at the first day of darkness and this was followed by a gradual increase in oxidation. The results with the ROS-related transcriptome footprint showed early changes in ROS-related transcriptome footprint emanating from mitochondria and peroxisomes. Taken together these results suggest that the first ROS-related change occurred in mitochondria and peroxisomes. The analysis of antioxidative gene’s network did not yield any clear results about the changes occurring in antioxidative status during extended darkness. Nevertheless, there is a reduction in expression of many of the plastids antioxidative related genes. This may explain a later increase in the oxidation poise of the plastids, occurring concomitantly with increase in cell death. Gibberellic acid (GA) prevented senescence in Pelargonium leaves; however, in Arabidopsis it did not prevent chlorophyll degradation, but prevented upregulation of SAGs (Apendix Fig. 1). Gibberellic acid prevented in Pelargonium the increase in ROS in chloroplast, and we suggested that this prevents the destruction of the chloroplasts and hence, the tissue remains green. In Arabidopsis, reduction in endogenous GA and BA are probably not causing dark-induced senescence, nevertheless, these materials have some effect at preventing senescence. Neither GA nor CK had any effect on transcriptome footprint related to ROS in the various organelles, however while GA reduced expression of few general ROS-related genes, BA mainly prevented the decrease in chloroplasts genes. Taken together, GA and BA act by different pathways to inhibit senescence and GA might act via ROS reduction. Therefore, application of both hormones may act synergistically to prevent darkinduced senescence of various crops.
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Horwitz, Benjamin, and Nicole M. Donofrio. Identifying unique and overlapping roles of reactive oxygen species in rice blast and Southern corn leaf blight. United States Department of Agriculture, January 2017. http://dx.doi.org/10.32747/2017.7604290.bard.
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Plants and their fungal pathogens both produce reactive oxygen species (ROS). CytotoxicROS act both as stressors and signals in the plant-fungal interaction. In biotrophs, a compatible interaction generates little ROS, but is followed by disease. An incompatible interaction results in a strong oxidative burst by the host, limiting infection. Necrotrophs, in contrast, thrive on dead and dying cells in an oxidant-rich local environment. Rice blast, Magnaportheoryzae, a hemibiotroph, occurs worldwide on rice and related hosts and can decimate enough rice each year to feed sixty million people. Cochliobolusheterostrophus, a necrotroph, causes Southern corn leaf blight (SLB), responsible for a major epidemic in the 1970s. The objectives of our study of ROS signaling and response in these two cereal pathogens were: Confocal imaging of ROS production using genetically encoded redox sensor in two pathosystems over time. Forward genetic screening of HyPer sensor lines in two pathosystems for fungal genes involved in altered ROSphenotypes. RNA-seq for discovery of genes involved in ROS-related stress and signaling in two pathosystems. Revisions to the research plan: Library construction in SLB was limited by low transformation efficiency, compounded by a protoplasting enzyme being unavailable during most of year 3. Thus Objective 2 for SLB re-focused to construction of sensor lines carrying deletion mutations in known or candidate genes involved in ROS response. Imaging on rice proved extremely challenging, so mutant screening and imaging were done with a barley-infecting line, already from the first year. In this project, ROS imaging at unprecedented time and spatial resolution was achieved, using genetically-encoded ratio sensors in both pathogens. This technology is currently in use for a large library of rice blast mutants in the ROS sensor background, and Southern corn leaf blight mutants in final stages of construction. The imaging methods developed here to follow the redox state of plant pathogens in the host tissue should be applicable to fungal pathogens in general. Upon completion of mutant construction for SCLB we hope to achieve our goal of comparison between intracellular ROS status and response in hemibiotroph and necrotroph cereal pathogens.
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Miller, Gad, and Jeffrey F. Harper. Pollen fertility and the role of ROS and Ca signaling in heat stress tolerance. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7598150.bard.
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The long-term goal of this research is to understand how pollen cope with stress, and identify genes that can be manipulated in crop plants to improve reproductive success during heat stress. The specific aims were to: 1) Compare heat stress dependent changes in gene expression between wild type pollen, and mutants in which pollen are heat sensitive (cngc16) or heat tolerant (apx2-1). 2) Compare cngc16 and apx2 mutants for differences in heat-stress triggered changes in ROS, cNMP, and Ca²⁺ transients. 3) Expand a mutant screen for pollen with increased or decreased thermo-tolerance. These aims were designed to provide novel and fundamental advances to our understanding of stress tolerance in pollen reproductive development, and enable research aimed at improving crop plants to be more productive under conditions of heat stress. Background: Each year crop yields are severely impacted by a variety of stress conditions, including heat, cold, drought, hypoxia, and salt. Reproductive development in flowering plants is highly sensitive to hot or cold temperatures, with even a single hot day or cold night sometimes being fatal to reproductive success. In many plants, pollen tube development and fertilization is often the weakest link. Current speculation about global climate change is that most agricultural regions will experience more extreme environmental fluctuations. With the human food supply largely dependent on seeds, it is critical that we consider ways to improve stress tolerance during fertilization. The heat stress response (HSR) has been intensively studied in vegetative tissues, but is poorly understood during reproductive development. A general paradigm is that HS is accompanied by increased production of reactive oxygen species (ROS) and induction of ROS-scavenging enzymes to protect cells from excess oxidative damage. The activation of the HSR has been linked to cytosolic Ca²⁺ signals, and transcriptional and translational responses, including the increased expression of heat shock proteins (HSPs) and antioxidative pathways. The focus of the proposed research was on two mutations, which have been discovered in a collaboration between the Harper and Miller labs, that either increase or decrease reproductive stress tolerance in a model plant, Arabidopsis thaliana (i.e., cngc16--cyclic nucleotide gated channel 16, apx2-1--ascorbate peroxidase 2,). Major conclusions, solutions, achievements. Using RNA-seq technology, the expression profiles of cngc16 and apx2 pollen grains were independently compared to wild type under favourable conditions and following HS. In comparison to a wild type HSR, there were 2,776 differences in the transcriptome response in cngc16 pollen, consistent with a model in which this heat-sensitive mutant fails to enact or maintain a normal wild-type HSR. In a comparison with apx2 pollen, there were 900 differences in the HSR. Some portion of these 900 differences might contribute to an improved HSR in apx2 pollen. Twenty-seven and 42 transcription factor changes, in cngc16 and apx2-1, respectively, were identified that could provide unique contributions to a pollen HSR. While we found that the functional HS-dependent reprogramming of the pollen transcriptome requires specific activity of CNGC16, we identified in apx2 specific activation of flavonol-biosynthesis pathway and auxin signalling that support a role in pollen thermotolerance. Results from this study have identified metabolic pathways and candidate genes of potential use in improving HS tolerance in pollen. Additionally, we developed new FACS-based methodology that can quantify the stress response for individual pollen in a high-throughput fashion. This technology is being adapted for biological screening of crop plant’s pollen to identify novel thermotolerance traits. Implications, both scientific and agricultural. This study has provided a reference data on the pollen HSR from a model plant, and supports a model that the HSR in pollen has many differences compared to vegetative cells. This provides an important foundation for understanding and improving the pollen HSR, and therefor contributes to the long-term goal of improving productivity in crop plants subjected to temperature stress conditions. A specific hypothesis that has emerged from this study is that pollen thermotolerance can be improved by increasing flavonol accumulation before or during a stress response. Efforts to test this hypothesis have been initiated, and if successful have the potential for application with major seed crops such as maize and rice.
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Prusky, Dov, Noel T. Keen, and Stanley Freeman. Elicitation of Preformed Antifungal Compounds by Non-Pathogenic Fungus Mutants and their Use for the Prevention of Postharvest Decay in Avocado Fruits. United States Department of Agriculture, January 1996. http://dx.doi.org/10.32747/1996.7570573.bard.
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C. gloeosporioides attacks unripe avocado fruits in the orchard. Germinated spores produce appressoria that germinate and breach the cuticle, but the resultant subcuticular hyphae become quiescent and do not develop further until fruit is harvested and ripens. Resistance of unripe avocado to attach by C. gloeosporioides is correlated with the presence of fungitoxic concentrations of the preformed antifungal compound, 1-acetoxy-2-hydroxy-4-oxoheneicosa-12, 15 diene in the pericarp of unripe fruits. The objective of this proposal was to study the signal transduction process by which elicitors induce resistance in avocado. It was found that abiotic elicitors, infection of avocado fruit with C. gloeosporioides or treatment of avocado cell suspension with cell-wall elicitor induced a significant production of reactive oxygen species (ROS). Ripe and unripe fruit tissue differ with regard to the ROS production. The unripe, resistant fruit are physiologically able to react and to produce high levels of ROS and increased activity of H+ATPase that can enhance the phenylpropanoid pathway ad regulate the levels of the antifungal compound-diene, inhibit fungal development, resulting in its quiescence. Interestingly, it was also found that growth regulators like cytokinin could do activation of the mechanism of resistance. Postharvest treatments of cytokinins strongly activated the phenylpropanoid pathway and induce resistance. We have developed non-pathogenic strains of C. gloeosporioides by Random Enzyme Mediated Integration and selected a hygromycin resistance, non-pathogenic strain Cg-142 out of 3500 transformants. This non-pathogenic isolate activates H+ATPase and induces resistance against Colletotrichum attack. As a basis for studying the importance of PL in pathogenicity, we have carried out heterologous expression of pel from C. gloeosporioides in the non-pathogenic C. magna and determine the significant increase in pathogenicity of the non-pathogenic strain. Based on these results we can state that pectate lyase is an important pathogenicity factor of C. gloeosporioides and found that fungal pathogenicity is affected not by pel but by PL secretion. Our results suggest that PH regulates the secretion of pectate lyase, and support its importance as a pathogenicity factor during the attack of avocado fruit by C. gloeosporioides . This implicates that if these findings are of universal importance in fungi, control of disease development could be done by regulation of secretion of pathogenicity factors.
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Horwitz, Benjamin A., and Barbara Gillian Turgeon. Fungal Iron Acquisition, Oxidative Stress and Virulence in the Cochliobolus-maize Interaction. United States Department of Agriculture, March 2012. http://dx.doi.org/10.32747/2012.7709885.bard.
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Our project focused on genes for high affinity iron acquisition in Cochliobolus heterostrophus, a necrotrophic pathogen of maize, and their intertwined relationship to oxidative stress status and virulence of the fungus on the host. An intriguing question was why mutants lacking the nonribosomal peptide synthetase (NRPS) gene (NPS6) responsible for synthesis of the extracellular siderophore, coprogen, are sensitive to oxidative stress. Our overall objective was to understand the mechanistic connection between iron stress and oxidative stress as related to virulence of a plant pathogen to its host. The first objective was to examine the interface where small molecule peptide and reactive oxygen species (ROS) mechanisms overlap. The second objective was to determine if the molecular explanation for common function is common signal transduction pathways. These pathways, built around sensor kinases, response regulators, and transcription factors may link sequestering of iron, production of antioxidants, resistance to oxidative stress, and virulence. We tested these hypotheses by genetic manipulation of the pathogen, virulence assays on the host plant, and by following the expression of key fungal genes. An addition to the original program, made in the first year, was to develop, for fungi, a genetically encoded indicator of redox state based on the commercially available Gfp-based probe pHyper, designed for animal cell biology. We implemented several tools including a genetically encoded indicator of redox state, a procedure to grow iron-depleted plants, and constructed a number of new mutants in regulatory genes. Lack of the major Fe acquisition pathways results in an almost completely avirulent phenotype, showing how critical Fe acquisition is for the pathogen to cause disease. Mutants in conserved signaling pathways have normal ability to regulate NPS6 in response to Fe levels, as do mutants in Lae1 and Vel1, two master regulators of gene expression. Vel1 mutants are sensitive to oxidative stress, and the reason may be underexpression of a catalase gene. In nps6 mutants, CAT3 is also underexpressed, perhaps explaining the sensitivity to oxidative stress. We constructed a deletion mutant for the Fe sensor-regulator SreA and found that it is required for down regulation of NPS6 under Fe-replete conditions. Lack of SreA, though, did not make the fungus over-sensitive to ROS, though the mutant had a slow growth rate. This suggests that overproduction of siderophore under Fe-replete conditions is not very damaging. On the other hand, increasing Fe levels protected nps6 mutants from inhibition by ROS, implying that Fe-catalyzed Fenton reactions are not the main factor in its sensitivity to ROS. We have made some progress in understanding why siderophore mutants are sensitive to oxidative stress, and in doing so, defined some novel regulatory relationships. Catalase genes, which are not directly related to siderophore biosynthesis, are underexpressed in nps6 mutants, suggesting that the siderophore product (with or without bound Fe) may act as a signal. Siderophores, therefore, could be a target for intervention in the field, either by supplying an incorrect signal or blocking a signal normally provided during infection. We already know that nps6 mutants cause smaller lesions and have difficulty establishing invasive growth in the host. Lae1 and Vel1 are the first factors shown to regulate both super virulence conferred by T-toxin, and basic pathogenicity, due to unknown factors. The mutants are also altered in oxidative stress responses, key to success in the infection court, asexual and sexual development, essential for fungal dissemination in the field, aerial hyphal growth, and pigment biosynthesis, essential for survival in the field. Mutants in genes encoding NADPH oxidase (Nox) are compromised in development and virulence. Indeed the triple mutant, which should lack all Nox activity, was nearly avirulent. Again, gene expression experiments provided us with initial evidence that superoxide produced by the fungus may be most important as a signal. Blocking oxidant production by the pathogen may be a way to protect the plant host, in interactions with necrotrophs such as C. heterostrophus which seem to thrive in an oxidant environment.
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Pesis, Edna, Elizabeth J. Mitcham, Susan E. Ebeler, and Amnon Lers. Application of Pre-storage Short Anaerobiosis to Alleviate Superficial Scald and Bitter Pit in Granny Smith Apples. United States Department of Agriculture, January 2013. http://dx.doi.org/10.32747/2013.7593394.bard.
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There is increased demand for high quality fruit produced and marketed with reduced chemical inputs to minimize toxic effects on human health and the environment. Granny Smith (GS) apple quality is reduced by two major physiological disorders, superficial scald and bitter pit (BP). These disorders cause great loss to apple growers worldwide. Superficial scald is commonly controlled by chemical treatments, mainly the antioxidant diphenylamine (DPA) and/or the ethylene action inhibitor, 1-methylcyclopropene (1–MCP). Both chemicals are ineffective in controlling bitter pit incidence. We proposed to investigate the beneficial use of non-chemical, abiotic stress with low O2 (LO2) applied for 10d at 20°C on GS apple fruit. During the project we expanded the treatment to more apple cultivars, Golden Delicious (GD) and Starking Delicious (SD) and another pome fruit, the pear. Apple and pear have similar physiological disorders that develop during cold storage and we examined if the LO2 treatment would also be effective on pear. Application of 0.5% LO2 atmosphere for 10d at 20°C or 500ppb 1-MCP at 20°C prior to cold storage at 0°C, was effective in reducing superficial scald in GS apple. Moreover, LO2 pretreatment was also effective in reducing bitter pit (BP) development in California GS and Israeli GD and SD apples The BP symptoms in GS from California were much more prominent, so the effect of LO2 was more dramatic than the effect on the Israeli cvs. GD and SD, nevertheless the LO2 treatment showed the same trend in all cultivars in reducing BP. The LO2 and 1-MCP -treated fruit exhibited lower levels of ethylene, - farnesene and its oxidation product, 6-methyl-5-hepten-2-one (MHO), as determined by SPME/GC-MS analysis. In addition, LO2 pretreatment applied to California Bartlett or Israeli Spadona pears was effective in reducing superficial scald, senescent scald and internal breakdown after 4 m of cold storage at 0°C. For GS apple, low-temperature storage resulted in oxidative stress and chilling injury, caused by increased production of superoxide anions which in turn led to the generation of other dangerous reactive oxygen species (ROS). Using confocal laser-scanning microscopy and H2O2 measurements of apple peel, we observed ROS accumulation in control fruit, while negligible amounts were found in LO2 and 1-MCP treated fruit. Gene-expression levels of ROS-scavenging enzymes were induced by the various pretreatments: catalase was induced by LO2 treatment, whereas Mn superoxide dismutase was induced by 1-MCP treatment. We assume that LO2 and 1-MCP pretreated fruit remained healthier due to reduced production of ethylene and reactive oxygen substances, such as MHO, during cold storage. The LO2-treated apple exhibited greener peel and firmer fruit after 6 m of cold storage, and the fruit had high crispiness leading to high taste preference. In both pear cultivars, the LO2 treatment led to a reduction in internal breakdown and browning around the seed cavity. We tested the LO2 pre-storage treatment on a semi-commercial scale that would be applicable to a small organic grower by sealing the fruit within the plastic field bins. The treatment was most effective with a continuous flow of nitrogen through the bins; however, a single 6 hour flush of nitrogen was also fairly effective. In addition, we determined that it was very important to have the oxygen levels below 0.5% for approximately 10 days to achieve good scald control, not counting the time required to reduce the oxygen concentration. Our LO2 technology has been proven in this project to be effective in reducing several physiological disorders developed in pome fruit during cold storage. We hope that our non-chemical treatment which is friendly to the environment will be used in the near future for the organic apple and pear industry. The next step should be an analysis of the cost-benefits and commercial feasibility.
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Hansen, Peter J., Zvi Roth, and Jeremy J. Block. Improving oocyte competence in dairy cows exposed to heat stress. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598163.bard.
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Original Objectives. The overall goal is to develop methods to increase pregnancy rate in lactating dairy cows exposed to heat stress through methods that minimize damage to the oocyte and embryo caused by heat stress. Objectives were as follows: (1) examine the protective effects of melatonin on developmental competence of oocytes exposed to elevated temperature in vitro; (2) test whether melatonin feeding can improve developmental competence of oocytes in vivo and, if so, whether effects are limited to the summer or also occur in the absence of heat stress; and (3) evaluate the effectiveness of improving fertility by facilitating follicular turnover in the summer and winter. Revised Objectives. (1) Examine protective effects of melatonin and follicular fluid on developmental competence of oocytes exposed to elevated temperature in vitro; (2) examine the protective effects of melatonin on developmental competence of embryos exposed to elevated temperature in vitro; (3) evaluate effectiveness of improving fertility by administering human chorionicgonadotropin (hCG) to increase circulating concentrations of progesterone and evaluate whether response to hCG depends upon genotype for four mutations reported to be related to cow fertility; and (4) identify genes with allelic variants that increase resistance of embryos to heat shock. Background. The overall hypothesis is that pregnancy success is reduced by heat stress because of damage to the oocyte and cleavage-stage embryo mediated by reactive oxygen species (ROS), and that fertility can be improved by provision of antioxidants or by removing follicles containing oocytes damaged by heat stress. During the study, additional evidence from the literature indicated the potential importance of treatment with chorionicgonadotropin to increase fertility of heat- stressed cows and results from other studies in our laboratories implicated genotype as an important determinant of cow fertility. Thus, the project was expanded to evaluate hCG treatment and to identify whether fertility response to hCG depended upon single nucleotide polymorphisms (SNP) in genes implicated as important for cow fertility. We also evaluated whether a SNP in a gene important for cellular resistance to heat stress (HSPA1L, a member of the heat shock protein 70 family) is important for embryonic resistance to elevated temperature. Major conclusions, solutions & achievements. Results confirmed that elevated temperature increases ROS production by the oocyte and embryo and that melatonin decreases ROS. Melatonin reduced, but did not completely block, damaging effects of heat shock on the oocyte and had no effect on development of the embryo. Melatonin was protective to the oocyte at 0.1-1 μM, a concentration too high to be achieved in cows. It was concluded that melatonin is unlikely to be a useful molecule for increasing fertility of heat-stressed cows. Treatment with hCG at day 5 after breeding increased first-service pregnancy rate for primiparous cows but not for multiparous cows. Thus, hCG could be useful for increasing fertility in first-parity cows. The effectiveness of hCG depended upon genotype for a SNP in COQ9, a gene encoding for a mitochondrial-function protein. This result points the way to future efforts to use genetic information to identify populations of cows for which hormone treatments will be effective or ineffective. The SNP in HSPA1L was related to embryonic survival after heat shock. Perhaps, genetic selection for mutations that increase cellular resistance to heat shock could be employed to reduce effects of heat stress on fertility. Implications, both scientific and agricultural. This project has resulted in abandonment of one possible approach to improve fertility of the heat-stressed cow (melatonin therapy) while also leading to a method for improving fertility of primiparous cows exposed to heat stress (hCG treatment) that can be implemented on farms today. Genetic studies have pointed the way to using genetic information to 1) tailor hormonal treatments to cow populations likely to respond favorably and 2) select animals whose embryos have superior resistance to elevated body temperatures.