The inhibition of flavoproteins by phenoxaiodonium, a new iodonium analogue

Moulton, Paul J.; Martin, Hannah M.; Ainger, Adele; Cross, Andrew R.; Hoare, Catherine; Doel, Justin J.; Harrison, Roger; Eisenthal, Robert; Hancock, John T.

doi:10.1016/s0014-2999(00)00454-4

Cited by 17 publications

(12 citation statements)

References 25 publications

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“…1 A ), internalized GFP-SA remained fluorescent after ingestion by PMN treated with diphenylene iodonium (DPI) (Fig. 2 A ), a potent inhibitor of flavoproteins, including the phagocyte NADPH oxidase (17). Despite complete inhibition of NADPH oxidase activity, phagocytosis is normal in DPI-treated PMN (16, 18).…”

Section: Resultsmentioning

confidence: 99%

Neutrophil Bleaching of GFP-Expressing Staphylococci: Probing the Intraphagosomal Fate of Individual Bacteria

Schwartz

Leidal

Femling

et al. 2009

The Journal of Immunology

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Successful host defense against bacteria such as Staphylococcus aureus (SA) depends on a prompt response by circulating polymorphonuclear leukocytes (PMN). Stimulated PMN create in their phagosomes an environment inhospitable to most ingested bacteria. Granules that fuse with the phagosome deliver an array of catalytic and noncatalytic antimicrobial peptides, while activation of the NADPH oxidase at the phagosomal membrane generates reactive oxygen species within the phagosome, including hypochlorous acid (HOCl), formed by the oxidation of chloride by the granule protein myeloperoxidase in the presence of H2O2. In this study, we used SA-expressing cytosolic GFP to provide a novel probe of the fate of SA in human PMN. PMN bleaching of GFP in SA required phagocytosis, active myeloperoxidase, H2O2 from the NADPH oxidase, and chloride. Not all ingested SA were bleached, and the number of cocci within PMN-retaining fluorescent GFP closely correlated with the number of viable bacteria remaining intracellularly. The percent of intracellular fluorescent and viable SA increased at higher multiplicity of infection and when SA presented to PMN had been harvested from the stationary phase of growth. These studies demonstrate that the loss of GFP fluorescence in ingested SA provides a sensitive experimental probe for monitoring biochemical events within individual phagosomes and for identifying subpopulations of SA that resist intracellular PMN cytotoxicity. Defining the molecular basis of SA survival within PMN should provide important insights into bacterial and host properties that limit PMN antistaphylococcal action and thus contribute to the pathogenesis of staphylococcal infection.

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Section: Resultsmentioning

confidence: 99%

Neutrophil Bleaching of GFP-Expressing Staphylococci: Probing the Intraphagosomal Fate of Individual Bacteria

Schwartz

Leidal

Femling

et al. 2009

The Journal of Immunology

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“…In wounded tomato leaves, the accumulation of H 2 O 2 in bundle sheath cells is inhibited by DPI (Orozco‐Cárdenas and Ryan, 1999; Orozoco‐Cárdenas et al ., 2001). DPI is an inhibitor of NADPH oxidases and other flavoenzymes (Cross and Jones, 1986; Moulton et al ., 2000; O'Donnell et al ., 1993). This observation has led to the proposal that wound‐induced H 2 O 2 accumulation may be catalysed by a bundle sheath‐located NADPH oxidase (Orozoco‐Cárdenas et al ., 2001).…”

Section: Discussionmentioning

confidence: 99%

Induction of ASCORBATE PEROXIDASE 2 expression in wounded Arabidopsis leaves does not involve known wound‐signalling pathways but is associated with changes in photosynthesis

et al. 2004

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Both laboratories equally participated in this work. SummaryASCORBATE PEROXIDASE 2 (APX2) encodes a key enzyme of the antioxidant network. In excess lightstressed Arabidopsis leaves, photosynthetic electron transport (PET), hydrogen peroxide (H 2 O 2 ) and abscisic acid (ABA) regulate APX2 expression. Wounded leaves showed low induction of APX2 expression, and when exposed to excess light, APX2 expression was increased synergistically. Signalling pathways dependent upon jasmonic acid (JA), chitosan and ABA were not involved in the wound-induced expression of APX2, but were shown to require PET and were preceded by a depressed rate of CO 2 ®xation. This led to an accumulation of H 2 O 2 in veinal tissue. Diphenyl iodonium (DPI), which has been shown previously to be a potent inhibitor of H 2 O 2 accumulation in the veins of wounded leaves, prevented induction of APX2 expression probably by inhibition of PET. Thus, the weak induction of APX2 expression in wounded leaves may require H 2 O 2 and PET only. As in other environmental stresses, wounding of leaves resulted in decreased photosynthesis leading to increased reactive oxygen species (ROS) production. This may signal the induction of many`wound-responsive' genes not regulated by JA-dependent or other known JA-independent pathways.

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“…Although several investigators used DPI as an inhibitor of NAD(P)H oxidase (Murata et al 2001;Kwak et al 2006;BeVagna and Lutzu 2007;Zhang et al 2007), being a Xavoprotein inhibitor, DPI may also aVect NOS (Moulton et al 2000). However, the prevention by DPI of not only stomatal closure (Table 1) but also the ROS (Fig.…”

Section: Kinetics Of Xuorescence Changes: Ros Precedes Nomentioning

confidence: 99%

Nitric oxide production occurs downstream of reactive oxygen species in guard cells during stomatal closure induced by chitosan in abaxial epidermis of Pisum sativum

Srivastava

Gonugunta

Puli

et al. 2008

Planta

140

100

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The effects of chitosan (beta-1,4 linked glucosamine, a fungal elicitor), on the patterns of stomatal movement and signaling components were studied. cPTIO (NO scavenger), sodium tungstate (nitrate reductase inhibitor) or L: -NAME (NO synthase inhibitor) restricted the chitosan induced stomatal closure, demonstrating that NO is an essential factor. Similarly, catalase (H(2)O(2) scavenger) or DPI [NAD(P)H oxidase inhibitor] and BAPTA-AM or BAPTA (calcium chelators) prevented chitosan induced stomatal closure, suggesting that reactive oxygen species (ROS) and calcium were involved during such response. Monitoring the NO and ROS production in guard cells by fluorescent probes (DAF-2DA and H(2)DCFDA) indicated that on exposure to chitosan, the levels of NO rose after only 10 min, while those of ROS increased already by 5 min. cPTIO or sodium tungstate or L: -NAME prevented the rise in NO levels but did not restrict the ROS production. In contrast, catalase or DPI restricted the chitosan-induced production of both ROS and NO in guard cells. The calcium chelators, BAPTA-AM or BAPTA, did not have a significant effect on the chitosan induced rise in NO or ROS. We propose that the production of NO is an important signaling component and participates downstream of ROS production. The effects of chitosan strike a marked similarity with those of ABA or MJ on guard cells and indicate the convergence of their signal transduction pathways leading to stomatal closure.

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The inhibition of flavoproteins by phenoxaiodonium, a new iodonium analogue

Cited by 17 publications

References 25 publications

Neutrophil Bleaching of GFP-Expressing Staphylococci: Probing the Intraphagosomal Fate of Individual Bacteria

Neutrophil Bleaching of GFP-Expressing Staphylococci: Probing the Intraphagosomal Fate of Individual Bacteria

Induction of ASCORBATE PEROXIDASE 2 expression in wounded Arabidopsis leaves does not involve known wound‐signalling pathways but is associated with changes in photosynthesis

Nitric oxide production occurs downstream of reactive oxygen species in guard cells during stomatal closure induced by chitosan in abaxial epidermis of Pisum sativum

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