Phorbol myristate acetate-induced lung injury: Involvement of reactive oxygen species

1992 ◽  
Vol 52 (7) ◽  
pp. 753-761 ◽  
Author(s):  
M. Okuda ◽  
H.-C. Lee ◽  
B. Chance ◽  
P. J. Cohent ◽  
C. Kumar
Keyword(s):  
Reactive Oxygen Species ◽  
Lung Injury ◽  
Phorbol Myristate Acetate ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Myristate Acetate

scholarly journals Platelet particle formation by anti–GPIIIa49-66 Ab, Ca2+ ionophore A23187, and phorbol myristate acetate is induced by reactive oxygen species and inhibited by dexamethasone blockade of platelet phospholipase A2, 12-lipoxygenase, and NADPH oxidase

Blood ◽  
2007 ◽  
Vol 110 (6) ◽  
pp. 1989-1996 ◽  
Author(s):  
Michael A. Nardi ◽  
Yelena Gor ◽  
Steven J. Feinmark ◽  
Fang Xu ◽  
Simon Karpatkin
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Phorbol Myristate Acetate ◽  
Reactive Oxygen ◽  
Autoimmune Disorder ◽  
Particle Formation ◽  
Ionophore A23187 ◽  
Oxygen Species ◽  
Myristate Acetate ◽  
12 Lipoxygenase

AbstractAn HIV antibody (Ab) against platelet integrin GPIIIa49-66 induces complement-independent platelet particle formation by the elaboration of reactive oxygen species (ROS) downstream of the activation of the platelet NADPH oxidase by the 12-lipoxygenase (12-LO) product 12(S)-HETE. To determine whether other inducers of platelet particle formation also function via the induction of ROS, we examined the effects of the Ca2+ ionophore A23187 and phorbol myristate acetate (PMA). Both agents induced oxidative platelet particle formation in an identical fashion as Ab, requiring Ca2+ flux and 12(S)-HETE production as well as intact NADPH oxidase and 12-LO pathways. Since HIV-ITP patients with this Ab correct their platelet counts with dexamethasone (Dex), we examined the role of this steroid in this unique autoimmune disorder. Dex at therapeutic concentrations inhibited Ab-, A23187-, or PMA-induced platelet particle formation by inhibiting platelet PLA2, 12-LO, and NADPH oxidase. The operational requirement of translocation of PLA2, 12-LO, and NADPH oxidase components (p67 phox) from cytosol to membrane for induction of ROS was both inhibited and partially reversed by Dex in platelets. We conclude that (1) platelet particle formation can be induced by the generation of ROS; and (2) platelet PLA2, 12-LO, NADPH oxidase, and cytosol membrane translocation, requirements for ROS production, are inhibited by Dex.

Modulating Luminol-Dependent Chemiluminescence Of Neutrophils By Flavones

1992 ◽  
Vol 47 (11-12) ◽  
pp. 889-892 ◽  
Author(s):  
W. Krol, J. Shani ◽  
Z. Czuba ◽  
S. Scheller
Keyword(s):  
Reactive Oxygen Species ◽  
Acetic Acid ◽  
Phorbol Myristate Acetate ◽  
Photon Emission ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Myristate Acetate ◽  
Structural Determinants

The effect of 14 flavones on luminol-dependent chemiluminescence of neutrophils was studied in vitro. Chemiluminescence was used in this study as an indicator for the production of a reactive oxygen species by neutrophils, stimulated by phorbol myristate acetate. While flavone- 8-acetic acid, and most of the compounds tested, inhibited chemiluminescence, flavone and its 5-hydroxy-7-methoxy derivatives enhanced it by up to 150%. The most active inhibitors of photon emission were the glycosides. These results indicate that lipophilicity and some structural determinants modulate the chemiluminescent capacity of neutrophils

scholarly journals High Concentrations of Reactive Oxygen Species in the BAL Fluid Are Correlated with Lung Injury in Rabbits after Hemorrhagic Shock and Resuscitation

2009 ◽  
Vol 219 (3) ◽  
pp. 193-199 ◽  
Author(s):  
Marios-Konstantinos Tasoulis ◽  
Olga Livaditi ◽  
Michalis Stamatakos ◽  
Charikleia Stefanaki ◽  
Pantelis Paneris ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Lung Injury ◽  
Hemorrhagic Shock ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
High Concentrations

scholarly journals Association of Toll-Like Receptor Signaling and Reactive Oxygen Species: A Potential Therapeutic Target for Posttrauma Acute Lung Injury

2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Meng Xiang ◽  
Janet Fan ◽  
Jie Fan
Keyword(s):  
Reactive Oxygen Species ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Therapeutic Target ◽  
Major Trauma ◽  
Pulmonary Inflammation ◽  
Reactive Oxygen ◽  
Oxygen Species

Acute lung injury (ALI) frequently occurs in traumatic patients and serves as an important component of systemic inflammatory response syndrome (SIRS). Hemorrhagic shock (HS) that results from major trauma promotes the development of SIRS and ALI by priming the innate immune system for an exaggerated inflammatory response. Recent studies have reported that the mechanism underlying the priming of pulmonary inflammation involves the complicated cross-talk between Toll-like receptors (TLRs) and interactions between neutrophils (PMNs) and alveolar macrophages (AMϕ) as well as endothelial cells (ECs), in which reactive oxygen species (ROS) are the key mediator. This paper summarizes some novel mechanisms underlying HS-primed lung inflammation focusing on the role of TLRs and ROS, and therefore suggests a new therapeutic target for posttrauma ALI.

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