Academic literature on the topic 'Production de ROS'
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Journal articles on the topic "Production de ROS":
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Brand, M. "Mitochondrial ROS production." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 146, no. 4 (April 2007): S56—S57. http://dx.doi.org/10.1016/j.cbpa.2007.01.044.
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Hole, Paul S., Lorna Pearn, Amanda J. Tonks, Philip E. James, Alan K. Burnett, Richard L. Darley, and Alex Tonks. "Ras-induced reactive oxygen species promote growth factor–independent proliferation in human CD34+ hematopoietic progenitor cells." Blood 115, no. 6 (February 11, 2010): 1238–46. http://dx.doi.org/10.1182/blood-2009-06-222869.
Abstract:
Abstract Excessive production of reactive oxygen species (ROS) is a feature of human malignancy and is often triggered by activation of oncogenes such as activated Ras. ROS act as second messengers and can influence a variety of cellular process including growth factor responses and cell survival. We have examined the contribution of ROS production to the effects of N-RasG12D and H-RasG12V on normal human CD34+ progenitor cells. Activated Ras strongly up-regulated the production of both superoxide and hydrogen peroxide through the stimulation of NADPH oxidase (NOX) activity, without affecting the expression of endogenous antioxidants or the production of mitochondrially derived ROS. Activated Ras also promoted both the survival and the growth factor–independent proliferation of CD34+ cells. Using oxidase inhibitors and antioxidants, we found that excessive ROS production by these cells did not contribute to their enhanced survival; rather, ROS promoted their growth factor–independent proliferation. Although Ras-induced ROS production specifically activated the p38MAPK oxidative stress response, this failed to induce expression of the cell-cycle inhibitor, p16INK4A; instead, ROS promoted the expression of D cyclins. These data are the first to show that excessive ROS production in the context of oncogene activation can promote proliferative responses in normal human hematopoietic progenitor cells.
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Kobayashi, Y., X. Qi, and G. Chen. "MK2 Regulates Ras Oncogenesis through Stimulating ROS Production." Genes & Cancer 3, no. 7-8 (July 1, 2012): 521–30. http://dx.doi.org/10.1177/1947601912462718.
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Jia, Rui. "Probing the Production of Intracellular Vesicles Containing Reactive Oxygen and Nitrogen Species by Electrochemical Resistive-pulse Sensing." Electrochemical Society Interface 31, no. 4 (December 1, 2022): 43–44. http://dx.doi.org/10.1149/2.f07224if.
Abstract:
Reactive oxygen and nitrogen species (ROS/RNS) are known to play an essential role in cell signaling, disease development and progression. The production of ROS/RNS in living cells can be induced by diacylglycerol-lactone (DAG-lactone) through activation of protein kinase C, an important therapeutic target for cancer and other diseases. In a previous report, nano-electrochemistry was performed to evaluate the production of ROS/RNS inside a human breast cell (MCF-10A) treated with DAG-lactone. Simultaneously, the formation of large intracellular vacuoles was observed using a microscope. These results suggest a possibility that the ROS/RNS were stored in the intracellular vacuoles. The experiments carried out during this summer were aimed to elucidate the relationship between the intracellular production of vesicles and ROS/RNS.
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Pino, José A., Nelson Osses, Daniela Oyarzún, Jorge G. Farías, Ricardo D. Moreno, and Juan G. Reyes. "Differential effects of temperature on reactive oxygen/nitrogen species production in rat pachytene spermatocytes and round spermatids." REPRODUCTION 145, no. 2 (February 2013): 203–12. http://dx.doi.org/10.1530/rep-12-0330.
Abstract:
Reactive oxygen species (ROS) and reactive nitrogen species (RNS) like superoxide and nitric oxide are produced by testis and spermatogenic cells in response to heat stress. However, the magnitude and mechanisms of this production in spermatogenic cells have not been described. In this work, we evaluated ROS/RNS production, its pharmacology, mitochondrial oxidative metabolism, membrane potential and antioxidant capacity at different temperatures in isolated rat pachytene spermatocytes and round spermatids. Our results showed an increment in ROS/RNS production by pachytene spermatocytes when increasing the temperature to 40 °C. Instead, ROS/RNS production by round spermatids did not change at temperatures higher than 33 °C. ROS/RNS production was sensitive to NADPH oxidase inhibitor diphenylene iodonium or the mitochondrial complex I inhibitor rotenone. No additive effects were observed for these two compounds. Our results suggest an important mitochondrial ROS/RNS production in spermatogenic cells. Oligomycin-insensitive oxygen consumption (uncoupled oxygen consumption) increased with temperature and was significantly larger in round spermatids than pachytene spermatocytes, indicating a likely round spermatid mitochondrial uncoupling at high temperatures. A similar conclusion can be reached by measuring the mitochondrial membrane potential using rhodamine 123 fluorescence in permeabilized cells or JC-1 fluorescence in intact cells. The antioxidant capacity was higher in round spermatids than pachytene spermatocytes at 40 °C. Our results strongly suggest that at high temperatures (40 °C) pachytene spermatocytes are more susceptible to oxidative stress, but round spermatids are more protected because of a temperature-induced mitochondrial uncoupling together with a larger antioxidant capacity.
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N. Agbedanu, Prince, Troy B. Puga, Joshua Schafer, Pearce Harris, Gary Branum, and Nora Strasser. "Investigation of Reactive Oxygen Species production in Human Hepatocytes." Gastroenterology Pancreatology and Hepatobilary Disorders 6, no. 2 (January 12, 2022): 01–06. http://dx.doi.org/10.31579/2641-5194/058.
Abstract:
1. Aim/Background: Reactive oxygen species (ROS) have been identified as compounds responsible for producing cellular damage. The purpose of this research is to examine if there is production of reactive oxygen species through free radical intermediates within human hepatocytes treated with morphine, bilirubin, or furosemide. The investigation examines the early stages of biotransformation by measuring the levels of reactive oxygen species produced inside of the treated hepatocytes within the first and second hours of treatment. The experiment was designed upon a case of a jaundiced (elevated bilirubin) infant who received morphine and furosemide and later died through unknown mechanisms. The experiment looks to examine if these drug compounds could contribute to cellular damage. This can help to further understand the potential interactions and complications of free radical intermediates produced during the phases of biotransformation. 2. Method: Previously cultured human hepatocytes were washed by centrifugation and re-suspended in 1x supplemental buffer to a concentration of 1x106 cells/mL and seeded in a dark clear bottom 96-well microplate at 100,000 stained cells/well. The cells were treated with either furosemide, morphine, bilirubin, a Tert-Butyl hydro peroxide (TBHP) positive control, or left as a background. Reactive oxygen generated in the presence of these agents were quantified by fluorescence excitation/emission measurement at 495nm/529nm. Fluorescence was measured at one and two hours. ROS generated convert 2',7'-dichlorodihydrofluorescein diacetate to 2',7'-dichlorodihydrofluorescein within the cells, which fluoresces. The fluorescence intensity detected is equivalent to the level of ROS generated. Wells that were untreated were used as blanks and subtracted from background and TBPH. 3. Results: Furosemide and Morphine did not produce statistically significant levels of ROS (p >0.05) above the background in both hours 1 and 2 of biotransformation and ROS measurement (Figure 1). Although Bilirubin did not produce statistically significant (p >0.05) levels of ROS above the background (Figure 2) during the first hour, it did produce statistically significant levels in the second hour of biotransformation. Each compound’s level of ROS was reduced during the second hour, signaling the removal of intermediate ROS metabolites (Figure 2). The production of ROS in each compound signifies that there is biotransformation to an intermediate that produces ROS. 4. Conclusion: The production of ROS above the background by each of the compounds shows there is an intermediate free radical compound that is produced during the biotransformation of each compound [21]. In this study, although furosemide and morphine did not produce statistically significant levels of ROS in both hours of biotransformation, bilirubin did produce significant levels of ROS in the second hour of biotransformation. This finding is in line with previous studies that shows morphine to offer protective effects against ROS production [16, 17]; and bilirubin demonstrating deleterious production of ROS at high doses [18]. Further work must be done to examine the correlation between the levels of ROS and extent of hepatocellular damage.
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Ito, Seigo, Hiroyuki Nakashima, Takuya Ishikiriyama, Masahiro Nakashima, Akira Yamagata, Toshihiko Imakiire, Manabu Kinoshita, Shuhji Seki, Hiroo Kumagai, and Naoki Oshima. "Effects of a CCR2 antagonist on macrophages and Toll-like receptor 9 expression in a mouse model of diabetic nephropathy." American Journal of Physiology-Renal Physiology 321, no. 6 (December 1, 2021): F757—F770. http://dx.doi.org/10.1152/ajprenal.00191.2021.
Abstract:
We classified kidney macrophages (Mφs) into bone marrow-derived (BM-) macrophages expressing high CD11b and tissue-specific resident (Res-) macrophages expressing low CD11b. In diabetic nephropathy (DN) model mice, TLR9 expression and TNF-α production via TLR9 activation in BM-Mφs and ROS production in Res-Mφs were enhanced. Furthermore, CCR2 antagonist suppressed the kidney infiltration of BM-Mφs and their function and the ROS production by Res-Mφs, with concomitant TLR9 suppression. Our study presents a new therapeutic strategy for DN.
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Doering, Talisa, Justin Maire, Wing Yan Chan, Alexis Perez-Gonzalez, Luka Meyers, Rumi Sakamoto, Isini Buthgamuwa, Linda L. Blackall, and Madeleine J. H. van Oppen. "Comparing the Role of ROS and RNS in the Thermal Stress Response of Two Cnidarian Models, Exaiptasia diaphana and Galaxea fascicularis." Antioxidants 12, no. 5 (May 6, 2023): 1057. http://dx.doi.org/10.3390/antiox12051057.
Abstract:
Coral reefs are threatened by climate change, because it causes increasingly frequent and severe summer heatwaves, resulting in mass coral bleaching and mortality. Coral bleaching is believed to be driven by an excess production of reactive oxygen (ROS) and nitrogen species (RNS), yet their relative roles during thermal stress remain understudied. Here, we measured ROS and RNS net production, as well as activities of key enzymes involved in ROS scavenging (superoxide dismutase and catalase) and RNS synthesis (nitric oxide synthase) and linked these metrics to physiological measurements of cnidarian holobiont health during thermal stress. We did this for both an established cnidarian model, the sea anemone Exaiptasia diaphana, and an emerging scleractinian model, the coral Galaxea fascicularis, both from the Great Barrier Reef (GBR). Increased ROS production was observed during thermal stress in both species, but it was more apparent in G. fascicularis, which also showed higher levels of physiological stress. RNS did not change in thermally stressed G. fascicularis and decreased in E. diaphana. Our findings in combination with variable ROS levels in previous studies on GBR-sourced E. diaphana suggest G. fascicularis is a more suitable model to study the cellular mechanisms of coral bleaching.
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Wojtovich, Andrew P., and Thomas H. Foster. "Optogenetic control of ROS production." Redox Biology 2 (2014): 368–76. http://dx.doi.org/10.1016/j.redox.2014.01.019.
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Garama, Daniel J., Tiffany J. Harris, Christine L. White, Fernando J. Rossello, Maher Abdul-Hay, Daniel J. Gough, and David E. Levy. "A Synthetic Lethal Interaction between Glutathione Synthesis and Mitochondrial Reactive Oxygen Species Provides a Tumor-Specific Vulnerability Dependent on STAT3." Molecular and Cellular Biology 35, no. 21 (August 17, 2015): 3646–56. http://dx.doi.org/10.1128/mcb.00541-15.
Abstract:
Increased production of mitochondrion-derived reactive oxygen species (ROS) is characteristic of a metabolic shift observed during malignant transformation. While the exact sources and roles of ROS in tumorigenesis remain to be defined, it has become clear that maintaining redox balance is critical for cancer cell proliferation and survival and, as such, may represent a vulnerability that can be exploited therapeutically. STAT3, a latent cytosolic transcription factor activated by diverse cytokines and growth factors, has been shown to exhibit an additional, nontranscriptional function in mitochondria, including modulation of electron transport chain activity. In particular, malignant transformation by Ras oncogenes exploits mitochondrial STAT3 functions. We used mass spectrometry-based metabolomics profiling to explore the biochemical basis for the STAT3 dependence of Ras transformation. We identified the gamma-glutamyl cycle, the production of glutathione, and the regulation of ROS as a mitochondrion-STAT3-dependent pathway in Ras-transformed cells. Experimental inhibition of key enzymes in the glutathione cycle resulted in the depletion of glutathione, accumulation of ROS, oxidative DNA damage, and cell death in an oncogenic Ras- and mitochondrial STAT3-dependent manner. These data uncover a synthetic lethal interaction involving glutathione production and mitochondrial ROS regulation in Ras-transformed cells that is governed by mitochondrial STAT3 and might be exploited therapeutically.
Dissertations / Theses on the topic "Production de ROS":
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Bergman, Malin, and Emma Flodin. "Dagens Polis- Ros eller Ris? : En kvalitativ studie om polisers upplevelser av myndighetens omorganisation." Thesis, Högskolan i Halmstad, Akademin för hälsa och välfärd, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:hh:diva-40038.
Abstract:
Organisationsförändringar kan medföra risker som innefattar oro, stress och konflikter inom verksamheten. Det är inte ovanligt att ledningen förväntar sig att verksamheten ska fungera som den alltid gjort samtidigt som genomförandearbetet läggs på medarbetarna. Risken finns att en organisationsförändring kan ge konsekvenser som innebär att folk säger upp sig. Denna kandidatuppsats syftar till att ta reda på hur omorganisationen av polismyndigheten som genomfördes den 1 Januari 2015 upplevs av poliser i den ingripande verksamheten. Vi vill skapa förståelse för hur polisens arbete har påverkats i och med organisationsförändringen. Det som gör vår studie unik och egen är att den på ett nyanserat sätt belyser nya aspekter av omorganisationen ur en sociologisk synvinkel, med fokus på polisernas egna känslor och upplevelser. Teorierna vi valt att utgå ifrån behandlar organisationsförändring ur ett strukturellt perspektiv men även på individnivå. Organisationsmodellerna Lean Production, Den byråkratiska organisationsformen och Organisationsförändringsteorin har vi valt att tillämpa för att skapa förståelse för hur poliserna upplever omorganisationens verksamhetsidé i praktiken. Vi har även använt oss av teorierna Alienation och Erkännande för att få en djupare förståelse för hur poliserna upplever att omorganisationen har påverkat deras arbete och arbetsvillkor. Vår sociologiska analys kommer grunda sig i samtliga teorier, vetenskapliga artiklar och den empiriska sammanställningen genom en utförlig diskussion i förhållande till varandra. Vi har använt oss av ett kvalitativt tillvägagångssätt där den empiriska datan samlades in genom semistrukturerade intervjuer. Den insamlade empirin tillsammans med med våra teoretiska utgångspunkter lade grunden för vår analys samt avslutande reflektioner och slutsatser. Slutsatsen vi kunde dra utifrån polisernas upplevelser av omorganisationen är att det var brist på kommunikation och information under reformens genomförande, vilket i sin tur skapade motstånd och friktioner i relation till polisernas försämrade arbetsvillkor.Unsuccessful organizational changes can imply risks that include anxiety, stress and conflicts within the agency. While the management expects the agency to function as it always has, it is not uncommon for the implementation work to be imposed on the employees. Therefore, there is a risk that organizational changes can have consequences that results in people resigning. This bachelor's thesis aims to examine how the reorganization of the Swedish police which implemented on January 1, 2015 is experienced by cops in Intervention activities. Furthermore, we also intended to create an understanding for how police work has been affected by this particular organizational change. What makes our study unique is that it in a nuanced way highlights new aspects of the reorganization from a sociological approach directed on the police officers own emotions and experiences related to the organizational change. The theories we have chosen to start from deal with organizational change from a structural perspective, but also at the individual level. The organizational models Lean Production, The Bureaucratic organizational form and The organizational change theory we have chosen to apply to create an understanding of how the police experience the reorganization's business idea in practice. We have also used the theories Alienation and The struggle to Recognition to gain a deeper understanding of how the police experience that the reorganization has affected their work and working conditions. Our sociological analysis will be based on all theories, scientific articles and the empirical compilation through a detailed discussion in relation to each other. Our study had been based on a qualitative approach through which we collected the empirical data by semi-structured interviews. The collected empirics, associated with our theoretical basis, formed the foundation for our analysis as well as our concluding reflections and conclusions. The most comprehensive conclusion we can compose from the police officers personal experiences of the reorganization, is that there was a deficient communication and information related to the reform that constituted resistance and frictions within the agency.
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Eduafo, Augusta K. "Mechanisms of Hyperglycemia-Induced ROS Production in Osmotically Swollen Glial Cells." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1433185840.
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Bell, Amy. "The response of the mitochondrial proteome and ROS production to ageing and dietary restriction." Thesis, University of Newcastle upon Tyne, 2016. http://hdl.handle.net/10443/3179.
Abstract:
The free radical theory of ageing proposes ageing is the result of macromolecules, damaged by free radicals, accumulating in cells over time. Mitochondria are critical to this theory as they are the primary source of the free radical superoxide. This thesis aims to understand the effect of age and dietary restriction (DR) with regard to mitochondrial protein abundance and superoxide generation. Superoxide production and protein composition was studied from multiple ages in isolated mitochondria from both ad libitum (AL) and DR mice. Superoxide production was assessed by measuring hydrogen peroxide release from multiple electron transport chain (ETC) sites. Mass spectrometry was used to determine the mitochondrial protein composition from mouse liver tissue. Older mice have increased hydrogen peroxide release from ETC complexes I and III. DR has decreased complex I hydrogen peroxide release in brain, skeletal muscle and liver mitochondria analysed at 15 and 24 months old. DR doesn’t prevent but delays the age associated hydrogen peroxide release. Hydrogen peroxide release at the same survival point is not significantly different between AL and DR mice. The liver mitochondrial proteome is affected by age and DR. Fatty acid metabolism protein abundance increases with age whereas amino acid metabolism protein abundance decreased. Superoxide clearance protein abundance is increased in older and DR liver mitochondria. Catalase had increased abundance in DR mitochondria at 15 and 24 months than at 3 or 36 months old. In conclusion hydrogen peroxide release, superoxide clearance protein abundance and fatty acid metabolism protein abundance are increased with ageing. The age associated increase in hydrogen peroxide release is delayed in DR mitochondria possibly due to increased abundance of catalase.
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Messenger, David James. "Impact of UV light on the plant cell wall, methane emissions and ROS production." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/4347.
Abstract:
This study presents the first attempt to combine the fields of ultraviolet (UV) photobiology, plant cell wall biochemistry, aerobic methane production and reactive oxygen species (ROS) mechanisms to investigate the effect of UV radiation on vegetation foliage. Following reports of a 17% increase in decomposition rates in oak (Quercus robur) due to increased UV, which were later ascribed to changes in cell wall carbohydrate extractability, this study investigated the effects of decreased UV levels on ash (Fraxinus excelsior), a fast-growing deciduous tree species. A field experiment was set up in Surrey, UK, with ash seedlings growing under polytunnels made of plastics chosen for the selective transmission of either all UV wavelengths, UV-A only, or no UV. In a subsequent field decomposition experiment on end-of-season leaves, a significant increase of 10% in decomposition rate was found after one year due to removal of UV-B. However, no significant changes in cell wall composition were found, and a sequential extraction of carbohydrate with different extractants suggested no effects of the UV treatments on cell wall structure. Meanwhile, the first observations of aerobic production of methane from vegetation were reported. Pectin, a key cell wall polysaccharide, was identified as a putative source of methane, but no mechanism was suggested for this production. This study therefore tested the effect of UV irradiation on methane emissions from pectin. A linear response of methane emissions against UV irradiation was found. UV-irradiation of de-esterified pectin produced no methane, demonstrating esters (probably methyl esters) to be the source of the observed methane. Addition of ROS-scavengers significantly decreased emissions from pectin, while addition of ROS without UV produced large quantities of methane. Therefore, this study proposes that UV light is generating ROS which are then attacking methyl esters to create methane. The study also demonstrates that this mechanism has the potential to generate several types of methyl halides. These findings may have implications for the global methane budget. In an attempt to demonstrate ROS generation in vivo by UV irradiation, radio-labelling techniques were developed to detect the presence of oxo groups, a product of carbohydrate attack by ROS. Using NaB3H4, the polysaccharides of ash leaflets from the field experiment were radio-labelled, but did not show any significant decrease in oxo groups due to UV treatments. However, UV-irradiation of lettuce leaves showed a significant increase in radio-labelling, suggesting increased UV irradiation caused an increase in the production of ROS. The study shows that the use of this radio-labelling technique has the potential to detect changes in ROS production due to changes in UV levels and could be used to demonstrate a link between ROS levels and methane emissions.
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Emami-Shahri, Nia. "The voltage-gated proton channel HVCN1 modulates mitochondrial ROS production and inflammatory response in macrophages." Thesis, Queen Mary, University of London, 2014. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8036.
Abstract:
It is clear that the voltage-gated proton channel HVCN1 plays an essential role in a range of cell types, in particular immune cells. Previous published work has confirmed the existence of proton channels in both murine and human macrophages. However, the role of HVCN1 in macrophages has not been investigated. Given that the current literature on voltage-gated proton channels in immune cells has found HVCN1 to be involved in several cellular processes (such as the respiratory burst and signalling events) it is important to establish its functional role in macrophages, which are a crucial constituent of the immune system. The aim of my thesis was to investigate the function of voltage-gated proton channels in macrophages with the use of mice with a disrupting mutation within the Hvcn1 gene, which results in HVCN1 loss. In particular, I wanted to address how Hvcn1-/- macrophages responded to LPS activation. I hypothesised that HVCN1 regulates the respiratory burst of macrophages and that it potentially modulates mitochondrial ROS production, and in doing so, may affect several functional aspects of macrophage biology.
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Silva, Cátia Liliana Marques da. "Dissecting the role of Profilin-1 in microglial cell function: the impact on ROS production." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/15607.
Abstract:
Mestrado em Biologia Molecular e CelularMicroglial cells are the resident immune cells of central nervous system (CNS) and the major players in neuroinflammation. These cells are also responsible for surveilling the neuronal microenvironment, and upon injury to the CNS they change their morphology and molecular profile and become activated. Activated status is associated with microglia proliferation, migration to injury foci, increased phagocytic capacity, production and release of reactive oxygen species (ROS), cytokines (pro- or anti-inflammatory) and reactive nitrogen species. Microglia activation is crucial for tissue repair in the healthy brain. However, their chronic activation or deregulation might contribute for the pathophysiology of neurodegenerative diseases. A better understanding of the mechanisms underlying microglial cell activation is important for defining targets and develop appropriate therapeutic strategies to control the chronic activation of microglia. It has been observed an increase in profilin (Pfn) mRNA in microglial cells in the rat hippocampus after unilateral ablation of its major extrinsic input, the entorhinal cortex. This observation suggested that Pfn might be involved in microglia activation. Pfn1 is an actin binding protein that controls assembly and disassembly of actin filaments and is important for several cellular processes, including, motility, cell proliferation and survival. Here, we studied the role of Pfn1 in microglial cell function. For that, we used primary cortical microglial cell cultures and microglial cell lines in which we knocked down Pfn1 expression and assessed the activation status of microglia, based on classical activation markers, such as: phagocytosis, glutamate release, reactive oxygen species (ROS), pro- and anti-inflammatory cytokines. We demonstrated that Pfn1 (i) is more active in hypoxia-challenged microglia, (ii) modulates microglia pro- and anti-inflammatory signatures and (iii) plays a critical role in ROS generation in microglia. Altogether, we conclude that Pfn1 is a key protein for microglia homeostasis, playing an essential role in their activation, regardless the polarization into a pro or anti-inflammatory signature.
As células da microglia são células imunes residentes no sistema nervoso central (SNC) e desempenham um papel importante em processos neuroinflamatórios. Estas células são responsáveis por monitorizar o parênquima neuronal, sendo capazes de responder rapidamente a danos no SNC. Após ativação, a microglia altera a sua morfologia e o seu perfil de expressão de proteínas. O processo de ativação induz a proliferação, migração para a foco da lesão, aumento da capacidade fagocítica, bem como produção e libertação de espécies reativas de oxigénio (EROs), espécies reativas de azoto e citocinas (pro- e anti-inflamatórias). A ativação da microglia é essencial para a reparação de tecidos e a manutenção da homeostasia do SNC. No entanto, a ativação crónica ou a sua desregulação podem contribuir para a patofisiologia de doenças neurodegenerativas. Assim sendo, o estudo dos mecanismos subjacentes à ativação das células da microglia é importante para ajudar a definir e desenvolver estratégias terapêuticas apropriadas para prevenir a sua ativação crónica. Um estudo anterior reportou o aumento dos níveis de RNAm da profilina (Pfn) em células da microglia no hipocampus de ratos após lesão unilateral no córtex entorrinal, sugerindo que a Pfn poderá estar envolvida no processo de ativação da microglia. A Pfn1 é uma proteína de ligação à actina que regula a polimerização do citoesqueleto de actina, sendo importante em diversos processos celulares, incluindo motilidade, proliferação e sobrevivência. Neste trabalho, nós estudamos o papel da Pfn1 na função da microglia. Para tal, utilizamos linhas celulares e células primárias de microglias corticais de rato nas quais reduzimos a expressão da Pfn1 e avaliamos o seu estado de ativação com base em marcadores clássicos de ativação, tais como: fagocitose, libertação de glutamato, produção e libertação de EROs e citocinas pro- e anti-inflamatórias. Nós demonstramos que a Pfn1 (i) se encontra mais ativa após estímulo da microglia por hipoxia, (ii) modula as assinaturas pro- e anti-inflamatória da microglia e (iii) desempenha um papel importante na produção de EROs pela microglia. Nesse estudo concluímos que a Pfn1 é uma proteína importante para o funcionamento da microglia, desempenhando um papel essencial na ativação da microglia, independentemente da polarização pró ou anti-inflamatória.
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Trein, Marcia Rodrigues. "Síntese e atividade anti-Trichomonas vaginalis de chalconas." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2017. http://hdl.handle.net/10183/164467.
Abstract:
Tricomoníase é a doença sexualmente transmissível não-viral mais comum no mundo e pode gerar sérias consequências na saúde reprodutiva, câncer e transmissão e aquisição do HIV. Por esta razão, esta infecção resulta em um pesado fardo para os sistemas de saúde pública. O único tratamento aprovado para esta infecção, que consiste nos 5-nitromidazois metronidazol e tinidazol, apresenta efeitos adversos e há uma subestimada taxa de resistência da infecção, atualmente considerada uma doença negligenciada, a estes fármacos. Portanto, há uma necessidade urgente de novas alternativas terapêuticas para a tricomoníase. Chalconas são uma família de moléculas que apresenta várias aplicações biológicas, como atividade contra diversos patógenos, incluindo protozoários patogênicos. Este trabalho apresenta o potencial anti-Trichomonas vaginalis de derivados de chalcona sintetizados e seus efeitos sobre os trofozoítos. Os valores de IC50 dos compostos mais ativos variaram de 27,5 a 76,4 μM, e as moléculas 4’-hidroxichalcona e 3’-aminochalcona apresentaram os valores mais baixos (27,5 e 28,9 μM). Estes dois compostos foram citotóxicos contra a linhagem de células epiteliais vaginais HMVII, consequentemente apresentaram baixos Índices de Seletividade; contudo, ao se utilizar larvas de Galleria mellonella, como modelo de toxicidade in vivo, não foi observada diminuição da viabilidade após o tratamento. As moléculas também não provocaram hemólise em eritrócitos humanos em 1 e 24 horas. Os compostos não induziram significativa produção de espécies reativas de oxigênio (EROs) nos trofozoítos. Neutrófilos humanos apresentaram aumento na produção de EROs quando coincubados com trofozoítos tratados com os compostos. Os resultados indicam que as chalconas são uma família de moléculas com potencial atividade contra T. vaginalis.Trichomoniasis is the most common non-viral sexually transmitted disease worldwide and can lead to serious consequences in reproductive health, cancer and HIV acquisition. For this reason, this infection results in a heavy burden for public health systems. Current approved treatment, which consists in 5-nitromidazole drugs, metronidazole and tinidazole, present adverse effects and there is underestimate drug resistance data on this parasitic infection, currently considered a neglected disease. Therefore, there is an urgent need for new alternatives for trichomoniasis treatment. Chalcones are a family of molecules that present various biological applications, such as activity against many pathogenic organisms including protozoan pathogens. This study presents the anti-Trichomonas vaginalis potential of synthetized chalcone derivatives and their effects on the trophozoites. IC50 values of the most active compounds ranged from 27.5 to 76.4 μM, and 4’-hydroxychalcone and 3’- aminochalcone presented the lowest values of IC50 (27.5 and 28.9 μM). These two compounds showed cytotoxicity against HMVII vaginal epithelial cells, thus presenting a low Selectivyty Index; however, when Galleria mellonella larvae were used as model for in vivo toxicity no significant decrease in viability after treatment was observed. The chalcones also did not induce hemolysis in human erythrocytes The compounds did not induce significant reactive oxygen species (ROS) production in the trophozoites. Human neutrophils have increased ROS production when exposed to treated trophozoites. Results indicate that chalcones are a family of molecules with potential activity against T. vaginalis.
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Lee, Flaherty Renée. "Stress hormone signalling contributes to tumourigenesis through the production of ROS/RNS, induction of DNA damage and interference with chemotherapy in breast cancer." Thesis, University of Brighton, 2017. https://research.brighton.ac.uk/en/studentTheses/28861765-5215-4dc1-b4c0-f1f8b794d924.
Abstract:
Breast cancer affects 1 in 8 women in the UK, and breast cancer patients often report increased levels of psychological stress. Psychological stress results in an increase in the circulating levels of the stress hormones glucocorticoids and catecholamines. Currently, few molecular mechanisms exist linking the actions of stress hormones and breast cancer progression. However, it has recently been suggested that stress hormones can promote DNA damage through the generation of reactive oxygen/nitrogen species (ROS/RNS). This research aims to explore the effect of stress hormone signalling on breast cancer progression and response to treatment. The generation of ROS/RNS and induction of DNA damage was measured in breast cancer cell lines. Pharmacological inhibition of the glucocorticoid receptor (GR) and inducible nitric oxide synthase (iNOS) was used to negate the effects of stress hormone exposure. Psychological stress, using restraint stress, was induced in a syngeneic mouse model of breast cancer, alongside in vivo inhibition of NOS. DNA damage and repair process were examined in response to the glucocorticoid cortisol in an endocrine therapy resistant cell line, and the effect of exposure to the exogenous glucocorticoid dexamethasone on the efficacy of chemotherapy in breast cancer cells was also explored. Stress hormones were shown to induce the generation of ROS/RNS and promote DNA damage. Specifically, exposure to cortisol produced an increase in nitric oxide (NO) through an iNOSmediated pathway. Inhibition of both the GR and iNOS reduced cortisol-induced DNA damage. In a mouse model of breast cancer, inhibition of NOS significantly reduced primary tumour volume, angiogenic signalling in the primary tumour and metastatic spread in stressed mice. Cortisol increased ROS/RNS and DNA damage in endocrine therapy resistant breast cancer cells compared to parental cells, and deregulated DNA repair processes. The cytotoxic effect of chemotherapy agents was reduced in response to co-treatment with the glucocorticoid dexamethasone, through upregulation of the antioxidant response. In conclusion, this research demonstrates that stress hormones impact tumourigenic progression in breast cancer through the induction of DNA damage, mediated by the release of NO. This data also shows that endocrine resistant breast cancer cells are more responsive to the actions of glucocorticoids on DNA damage and repair. Furthermore, exogenous glucocorticoids can impair the efficacy of chemotherapies, through the generation of ROS/RNS. The role of psychological stress should therefore be considered in the treatment of breast cancer patients, and stress hormone receptor signalling could provide potential therapeutic targets for the treatment of breast cancers.
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Johansson, Hampus. "Nox2/4 inhibition in NB69 during ischemia/reperfusion : Inhibition of ROS-production using M4, M107, and M114." Thesis, Högskolan i Skövde, Institutionen för hälsa och lärande, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-17941.
Abstract:
Cerebral stroke has become one of the leading causes of death and disability worldwide. During an ischemic stroke, oxygen and nutrient deprivation occurs, which combined lead to cell starvation, anoxia, and eventually cell death. However, when blood flow is restored, reperfusion damage occurs resulting in increased cell death through several mechanisms. One of the main reasons behind ischemia/reperfusion damage is oxidative stress due to elevated production of reactive oxygen species (ROS) during reperfusion. There are several proteins and processes that are thought to be involved in elevated oxidative stress and the formation of ROS during reperfusion, among which the NADPH oxidase (Nox) family is suggested to be the main contributor of ROS.To examine this hypothesis, in the present work, we inhibited activity of the Nox2 and Nox4 enzymes during ischemia/reperfusion with the Glucox Biotech AB (Sweden) inhibitors M4, M107, and M114 to evaluate whether reducing Nox activity could reduce the ischemia/reperfusion-induced cell death, hence be used as a potential stroke treatment, the cell viability was measured with MTS after ischemia/reperfusion induction and treatment with the Nox substances. We also examined the gene expression levels of the Nox enzymes Nox2 and Nox4 with qPCR after induced ischemia/reperfusion in the neuroblastoma cell line NB69.Our results showed a decrease in Nox4 gene expression after 1h ischemia/8h reperfusion and an increased expression after 1h ischemia/24h reperfusion in NB69 cells. Treatment with M114 resulted in increased cell viability after 2h ischemia/72h reperfusion. However, the toxic effect of ischemia/reperfusion-induced response was found to be inadequate, as indicated by extensive proliferation and lack of cell death. This unfavorable outcome is suggested to be excess of oxygen in medium, metabolization of L-glutamine, and effects of growth factors in the serum used in cell culture medium during the ischemic phase. Therefore, the cell culture protocol was modified to the use of PBS instead of glucose-free medium under serum-free condition during the ischemia. The altered ischemic conditions resulted in continuous reduction in cell viability at increasing ischemic time points with total cell death at 2h ischemia, suggesting applicable conditions for ischemia/reperfusion studies. Even though a conclusion could not be made about the inhibitors M4, M107, and M114 as the cell viability assay was performed under insufficient conditions; the Nox inhibitors shows high potential as future ischemic stroke treatments, which may help save lives and improve life quality for affected patients.
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Singhapol, Chatchawan. "Mitochondrial localisation of hTERT protects against nuclear DNA damage and mitochondrial ROS production after endogenous and exogenous stress." Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/2216.
Abstract:
Under oxidative stress condition, telomerase catalytic subunit can shuttle from the nucleus and localises within mitochondria. hTERT can improve mitochondrial functions and contribute to a decreased oxidative stress suggesting an entirely new function of telomerase in protecting mitochondria and cells under stress. However, there are still many questions about the mechanism and what factors influence the protective function of telomerase. In this study we investigated the kinetic exclusion of hTERT, the catalytic subunit of telomerase, in various cell lines under different oxidative stress conditions. We also used organelle specific hTERT localisation vectors to model hTERT localisation and investigated a correlation between hTERT location, nuclear DNA damage and ROS production. We found that cells excluded endogenous hTERT from the nucleus in a heterogeneous fashion independently of the cell types. Importantly, nuclear DNA damage showed a significant correlation with the localisation of hTERT. Cells where hTERT remained in the nucleus displayed high DNA damage while cells which excluded hTERT from the nucleus displayed no or very low DNA damage. Our results from specific hTERT localisation vectors specified that mitochondrial localisation of hTERT protects the nucleus from DNA damage and did not showed any sign of apoptosis induction while nuclear localisation of hTERT correlated with higher amounts of DNA damage and apoptosis. Moreover, mitochondrial localisation of hTERT decreased mitochondrial ROS generation levels directly after both endogenous and exogenous stress which we interpret as the reason for the prevention of nuclear DNA damage. Additionally, we analysed whether p53 status might influence the protective function of telomerase. Our results in an isogenic cell pair of glioblastoma cells showed that p53 status does not prominently influence the protective function of mitochondrial hTERT under low stress condition. However, nuclear hTERT of cells which contained inactive p53 displayed a significantly higher nuclear DNA damage than cells which contained an active p53 and this became more pronounced when stress levels were increased. We hypothesise that telomerase localisation might possibly interact with p53 when a cancer cell is under stress condition. However, the molecular mechanism for that is unknown. Our results demonstrate a novel link between mitochondrial localisation of hTERT, decrease of mitochondrial ROS generation and the protective capacity of hTERT to nuclear DNA from damage after stress treatments.
Books on the topic "Production de ROS":
1
Middaugh, Jeffrey A. A study of the metabolic adaptation provoked by decreased aconitase activity and increased ROS production as a consequence of aluminum stress in Pseudomonas fluorescens. Sudbury, Ont: Laurentian University, School of Graduate Studies, 2004.
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Whittier, Jack. Comparative performance analysis, commercial cut-flower rose production. Santa Fe, N.M: New Mexico Research and Development Institute, 1990.
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R, Layne Desmond, and Bassi Daniele, eds. The peach: Botany, production and uses. Wallingford, Oxfordshire, UK: CABI, 2008.
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Pemberton, H. B. Production of pot roses. Portland, Ore: Timber Press, 1997.
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Dikova, Peti︠a︡. Intervi︠u︡ s piesa: "Seks, narkotit︠s︡i i rok&rol" igrae se ot 1992 : istorii︠a︡ta na naĭ-dŭlgo igraniya spektakŭl v edin i sŭsht sŭstav v sveta. Sofii︠a︡: Iztok-Zapad, 2020.
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Krajewski, Lee J. Operations management: Strategy and analysis. 3rd ed. Reading, Mass: Addison-Wesley Pub. Co., 1993.
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Krajewski, Lee J. Operations management: Strategy and analysis. Reading, Mass: Addison-Wesley, 1987.
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(Firm), Caroselli Design. Rodster street rods: Step-by-step assembly manual for the award-winning street rods you build on a modern production vehicle. El Segundo, CA: Caroselli Design, 2003.
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Chisick, Harvey. The production, distribution and readership of a conservative journal of the early French Revolution: The Ami du roi of the abbé Royou. Philadelphia: American Philosophical Society, 1992.
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Kronja, Ivana. Estetika avangardnog i eksperimentalnog filma: Telo, rod i identitet : Evropa - SAD - Srbija. Beograd: Filmski centar Srbije, 2020.
Book chapters on the topic "Production de ROS":
1
Starkov, Anatoly A. "Measurement of Mitochondrial ROS Production." In Methods in Molecular Biology, 245–55. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-756-3_16.
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Kar, Rup Kumar. "ROS Signaling: Relevance with Site of Production and Metabolism of ROS." In Reactive Oxygen Species and Oxidative Damage in Plants Under Stress, 115–25. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20421-5_5.
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Starkov, Anatoly A. "Measuring Mitochondrial Reactive Oxygen Species (ROS) Production." In Systems Biology of Free Radicals and Antioxidants, 265–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-30018-9_8.
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Allaban, Anas Abou, Devin Bonnie, Emerson Knapp, Prajakta Gokhale, and Thomas Moulard. "Developing Production-Grade Applications with ROS 2." In Studies in Computational Intelligence, 3–54. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-75472-3_1.
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Yu, Liping, Brian D. Fink, and William I. Sivitz. "Simultaneous Quantification of Mitochondrial ATP and ROS Production." In Methods in Molecular Biology, 149–59. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2257-4_14.
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Pasqualotto, Fábio Firmbach, and Eleonora Bedin Pasqualotto. "Recreational Drugs and ROS Production in Mammalian Spermatozoa." In Studies on Men's Health and Fertility, 417–31. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-776-7_19.
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Konno, Tasuku, Cécile Crapart, and Edward Avezov. "H2O2/ROS Production, Consumption, and Transport across Organelles." In Peroxiporins, 54–87. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9781003160649-6.
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Milton, Rosemary H., and Andrey Y. Abramov. "Ischemia-Reperfusion Induces ROS Production from Three Distinct Sources." In Oxidative Neural Injury, 97–108. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-342-8_6.
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Sachdev, Swati, Shamim Akhtar Ansari, and Mohammad Israil Ansari. "ROS Production and Function at Plasma Membrane and Apoplast." In Reactive Oxygen Species in Plants, 125–42. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-9884-3_8.
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Li, Yida, Han Li, Liuyang Wang, and Man Zhang. "Autonomous Crop Image Acquisition System Based on ROS System." In Sensing Technologies for Field and In-House Crop Production, 53–76. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-7927-1_4.
Conference papers on the topic "Production de ROS":
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Moulard, Thomas. "Is ROS 2 ready for production? A look at ROS 2 reliability, performance and security improvements." In ROSCon2019FR. Mountain View, CA: Open Robotics, 2019. http://dx.doi.org/10.36288/roscon2019fr-900309.
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Moulard, Thomas. "Is ROS 2 ready for production? A look at ROS 2 reliability, performance and security improvements." In ROSCon2019FR. Mountain View, CA: Open Robotics, 2019. http://dx.doi.org/10.36288/roscon2019fr-900853.
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Kimmig, L. M., P. Woods, A. Y. Meliton, K. Sun, R. B. Hamanaka, and G. M. Mutlu. "LPS Does Not Induce Mitochondrial ROS Production in Alveolar Macrophages." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5566.
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Mittal, M., M. Roth, XQ Gu, R. Schermuly, H. Ghofrani, W. Seeger, F. Grimminger, G. Haddad, and N. Weissmann. "Role of NADPH Oxidase Derived ROS Production in Regulation of Kv Channels." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5124.
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Osborn, Heather L., Alan J. Ryan, Ana-Monica Racila, Shubha Murthy, and A. B. Carter. "Rac1 Mediates ROS Production Via Interaction With Cytochrome C In The Mitochondria." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2537.
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Yi, X., F. Liu, L. Schweitzer, F. Baghnavi, J. Seufert, and G. Päth. "Knockdown of Etv5 enhances ROS production and impairs viability in pancreatic beta cells." In Diabetes Kongress 2021 – 55. Jahrestagung der DDG. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1727367.
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Ferguson, Brent W., Xinsheng Gao, Maciej Zelazowski, Sabine Lange, Martin C. Abba, Richard D. Wood, and C. Marcelo Aldaz. "Abstract 5183: Loss of WWOX induces ANGPTL4 and ROS production in breast cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-5183.
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Waypa, GB, JD Marks, and PT Schumacker. "Hypoxia Increases ROS Signaling in the Cytosol and Mitochondrial Intermembrane Space, While It Decreases ROS Production in the Mitochondrial Matrix: Relationship to HPV." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6255.
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Ji, Yubin, Zhongyuan Qu, Xiang Zou, and Chenfeng Ji. "Effects of Juglone on ROS Production and Mitochondrial Transmembrane Potential in SGC-7901 Cells." In 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5517683.
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Fontana, Diletta, Mario Mauri, Antonio Niro, Luca Massimino, Mayla Bertagna, Giovanni Zambrotta, Mario Bossi, et al. "Abstract 3385: ETNK1 mutations promote ROS production and DNA damage through increased mitochondrial activity." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3385.
Reports on the topic "Production de ROS":
1
Paul, Satashree. Oxidative Stress: A Cause of Male Infertility. Science Repository OÜ, October 2020. http://dx.doi.org/10.31487/sr.blog.10.
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Prusky, Dov, Martin Dickman, and Robert Fluhr. Effect of pH Modulation and ROS Production by Postharvest Pathogens on Postharvest Disease Development. United States Department of Agriculture, July 2012. http://dx.doi.org/10.32747/2012.7613876.bard.
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Horwitz, Benjamin, and Barbara Gillian Turgeon. Secondary Metabolites, Stress, and Signaling: Roles and Regulation of Peptides Produced by Non-ribosomal Peptide Synthetases. United States Department of Agriculture, 2005. http://dx.doi.org/10.32747/2005.7696522.bard.
Abstract:
Fungal pathogens of plants produce a diverse array of small molecules. Often referred to as secondary metabolites because they were thought to be dispensable for basic functions, they may indeed have central roles as signals for the fungal cell, and in interactions with the host. We have identified more than a dozen genes encoding nonribosomal peptide synthetases (NPS) in Cochliobolusheterostrophus, the agent of southern corn leaf blight. The aim of this project was to identify roles of these genes in stress responses and signaling. The first objective was to test a complete collection of C. heterostrophus nonribosomal peptide synthetase (NRPS)-encoding gene deletion mutant and wildtype (WT) strains for sensitivity to various agents of oxidative (ROS) and nitrosative (RNOS) stress, in vitro. The second objective and next step in this part of the project was to study the relevance of sensitivity to ROS and RNOS in the host pathogen interaction, by measuring the production of ROS and RNOS in planta, when plants are inoculated with wild type and mutant strains. A third objective was to study expression of any genes shown to be involved in sensitivity to ROS or RNOS, in vitro and in planta. Another objective was to determine if any of the genes involved in oxidative or nitrosative stress responses are regulated by components of signal transduction pathways (STP) that we have identified and to determine where mechanisms overlap. Study of the collection of nps mutants identified phenotypes relevant for virulence, development and oxidative stress resistance for two of the genes, NPS2 and NPS6. Mutants in genes related to RNOS stress have no virulence phenotypes, while some of those related to ROS stress have reduced virulence as well as developmental phenotypes, so we focused primarily on ROS stress pathways. Furthermore, the identification of NPS2 and NPS6 as encoding for NRPS responsible for siderophore biosynthesis lent a new focus to the project, regulation by Fe. We have not yet developed good methods to image ROS in planta and work in this direction is continuing. We found that NPS6 expression is repressed by Fe, responding over the physiological Fe concentration range. Studying our collection of mutants, we found that conserved MAPK and G protein signal transduction pathways are dispensable for Fe regulation of NPS6, and initiated work to identify other pathways. The transcription factor SreA is one candidate, and is responsible for part, but not all, of the control of NPS6 expression. The results of this project show that the pathogen contends with oxidative stress through several signaling pathways. Loss of the siderophore produced by Nps6 makes the fungus sensitive to oxidative stress, and decreases virulence, suggesting a central role of the ability to sequester and take up extracellular iron in the host-pathogen interaction. Siderophores, and manipulation of Fe levels, could be targets for new strategies to deal with fungal pathogens of maize and other plants.
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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.
Abstract:
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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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.
Abstract:
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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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.
Abstract:
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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Dickman, Martin B., and Oded Yarden. Modulation of the Redox Climate and Phosphatase Signaling in a Necrotroph: an Axis for Inter- and Intra-cellular Communication that Regulates Development and Pathogenicity. United States Department of Agriculture, August 2011. http://dx.doi.org/10.32747/2011.7697112.bard.
Abstract:
The long-term goals of our research are to understand the regulation of sclerotial development and pathogenicity in S. sclerotiorum. The focus in this project is on the elucidation of the signaling events and environmental cues that contribute to broad pathogenic success of S. sclerotiorum. In this proposal, we have taken advantage of the recent conceptual (ROS/PPs signaling) and technical (genome sequence availability and gene inactivation possibilities) developments to address the following questions, as appear in our research goals stated below, specifically concerning the involvement of REDOX signaling and protein dephosphorylation in the regulation of hyphal/sclerotial development and pathogenicity of S. sclerotiorum. Our stated specific objectives were to progress our understanding of the following questions: (i) Which ROS species affect S. sclerotiorum development and pathogenicity? (ii) In what manner do PPs affect S. sclerotiorum development and pathogenicity? (iii) Are PPs affected by ROS production and does PP activity affect ROS production and SMK1? (iv) How does Sclerotinia modulate the redox environment in both host and pathogen? While addressing these questions, our main findings include the identification and characterization the NADPH oxidase (NOX) family in S. sclerotiorum. Silencing of Ssnox1 indicated a central role for this enzyme in both virulence and pathogenic (sclerotial) development, while inactivation of Ssnox2 resulted in limited sclerotial development but remained fully pathogenic. Interestingly, we found a consistent correlation with Ssnox1(involved with pathogenicity) and oxalate levels. This same observation was also noted with Sssod1. Thus, fungal enzymes involved in oxidative stress tolerance,when inactivated, also exhibit reduced OA levels. We have also shown that protein phosphatases (specifically PP2A and PTP1) are involved in morphogenesis and pathogenesis of S. sclerotiorum, demonstrating the regulatory role of these key proteins in the mentioned processes. While probing the redox environment and host-pathogen interactions we determined that oxalic acid is an elicitor of plant programmed cell death during S. sclerotiorum disease development and that oxalic acid suppresses host defense via manipulation of the host redox environment. During the course of this project we also contributed to the progress of understanding S. sclerotiorum function and the manipulation of this fungus by establishing an efficient gene replacement and direct hyphal transformation protocols in S. sclerotiorum. Lastly, both PIs were involved in thegenomic analysis of this necrotrophic fungal pathogen (along with Botrytis cinerea). Our results have been published in 11 papers (including joint papers and refereed reviews) and have set the basis for a continuum towards a better understanding and eventual control of this important pathogen (with implications to other fungal-host systems as well).
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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.
Abstract:
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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Droby, Samir, Tim R. Gottwald, Richard Stange, Efraim Lewinsohn, and T. Gregory McCollum. Characterization of the biochemical basis of host specificity of Penicillium digitatum and Penicillium italicum on citrus fruit. United States Department of Agriculture, May 2008. http://dx.doi.org/10.32747/2008.7587726.bard.
Abstract:
l. This research demonstrates that citrus fruit volatiles play an important role in host recognition by P. digitatum and P. italicum. 2. Volatiles derived from non-host fruits and vegetables (apple, pear, tomato, pepper, strawberry and avocado) had no effect on promotion of spore germination and growth of citrus pathogens. 3. Citrus volatiles have a specific stimulatory effect solely on P. digitatum and P. italicum. Non-citrus pathogens such as P. expansum and B. cinerea not affected orinhibited by the volatile materials. The specific stimulatory effect of fruit peelvolatiles on citrus pathogens and inhibitory effect on non-pathogens indicateimport ant role of volatile compounds in the host selectivity of citrus postharvestpathogens. 4. Comparative CG-MS quantification was per formed and identification of volatileconstituents of citrus commercial oils, peel extracts and the headspace of thewounded fruits was completed. Monoterpenehydrocarbons (limonene, a-pinene,sabinene, and myrcene) were the most abundant in all volatiles regardless of thesource. 5. Our results demonstrated stimulation of germination and germ tube growth in both P. digitatum and P. italicum by limonene, myrcene, a-pinene, and b-pinene). Limonenewas show n to be the most efficient in induction of germination and growth in bothpathogens. 6. P. digitatum spores placed on the surface of lemon fruit, adjacent to a wounded oil gland, were induced to germinate and grow, thus supporting all the in vitro results and demonstrating that the phenomenon of stimulation of germination and growth occurs on the fruit. 7. We established that P. digitatum is capable of biotransformation of limonene to a terpineol. a-terpinel was proved to be involved in induction of fungal sporulation process. 8. Chemotropism (directional growth) of P. digitatum towards the volatiles released from the oil glands on fruit surface was demonstrated. 9. Citrus germplasm screening work for fruit susceptibility/resistance for P. digitatum infection showed no definitive results regarding host range and susceptibility.Although the sour orange selections appear to show higher resistance to infection and decay development. 10. We demonstrated that P. expansum, non citrus pathogen, is capable of germinating in citrus fruit surface wounds, but it strongly induced host resistance mechanisms which restrict it growth and prevented decay development. The host (citrus fruit) reacted strongly by production of ROS. On the other hand, P. digitatum seems to actively suppress host natural resistance mechanisms possibly through inhibiting the production of ROS production.
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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.
Abstract:
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.