Difference in Changes of Membrane Fluidity of Polymorphonuclear Leukocytes Stimulated With Phorbol Myristate Acetate and Formyl-Methionyl-Leucyl-Phenylalanine: Role of Excited Oxygen Species

1990 ◽  
Vol 47 (2) ◽  
pp. 105-110 ◽  
Author(s):  
Midori Masuda ◽  
Yutaka Komiyama ◽  
Takashi Murakami ◽  
Kenjiro Murata ◽  
Masafumi Hasui ◽  
...  
Keyword(s):  
Membrane Fluidity ◽  
Phorbol Myristate Acetate ◽  
Polymorphonuclear Leukocytes ◽  
Oxygen Species ◽  
Myristate Acetate ◽  
Excited Oxygen

scholarly journals Angiotensin Type 1a Receptor Signaling Is Not Necessary for the Production of Reactive Oxygen Species in Polymorphonuclear Leukocytes

2012 ◽  
Vol 2012 ◽  
pp. 1-5
Author(s):  
Fumiko Yamato ◽  
Junji Takaya ◽  
Shoji Tsuji ◽  
Masafumi Hasui ◽  
Kazunari Kaneko
Keyword(s):  
Hydrogen Peroxide ◽  
Polymorphonuclear Leukocytes ◽  
No Production ◽  
Polymorphonuclear Leucocytes ◽  
Oxygen Species ◽  
Ang Ii ◽  
Wild Type ◽  
Myristate Acetate ◽  
At1a Receptor

Background. Although angiotensin II (Ang II) has inflammatory effects, little is known about its role in polymorphonuclear leucocytes (PMLs). To elucidate the role of Ang II in PMLs ROS production, we examined hydrogen peroxide (H2O2), one of the ROS, and NO production in AT1a receptor knockout (AT1KO) mice. Methods and Results. PMLs were analyzed from Ang II type 1a receptor knockout mice (AT1KO) and C57BL/6 wild type mice. Using flow cytometry, we studied hydrogen peroxide (H2O2) production from PMLs after Staphylococcus aureus phagocytosis or phorbol myristate acetate (PMA) stimulation. Nitric oxide (NO) production in the AT1KO was low at basal and after phagocytosis. In the AT1KO, basal H2O2 production was low. After PMA or phagocytosis stimulation, however, H2O2 production was comparable to wild type mice. Next we studied the H2O2 production in C57BL/6 mice exposed to Ang II or saline. H2O2 production stimulated by PMA or phagocytosis did not differ between the two groups. Conclusions. AT1a pathway is not necessary for PMLs H2O2 production but for NO production. There was a compensatory pathway for H2O2 production other than the AT1a receptor.

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.

scholarly journals Quinones and hydroxyquinones as generators and quenchers of singlet molecular oxygen

1997 ◽  
Vol 75 (4) ◽  
pp. 423-428 ◽  
Author(s):  
Isela Gutiérrez ◽  
Sonia G. Bertolotti ◽  
M.A. Biasutti ◽  
Arnaldo T. Soltermann ◽  
Norman A. García
Keyword(s):  
Oxygen Species ◽  
Type Ii ◽  
Carbonyl Groups ◽  
Quenching Mechanism ◽  
Singlet Molecular Oxygen ◽  
Dye Sensitized ◽  
Quenching Process ◽  
First Time ◽  
Excited Oxygen

The role of quinones and hydroxyquinones as sensitizers and as quenchers in Type II photooxygenations has been examined. The second aspect is discussed here, through a systematic study, for the first time in the open literature. Quinonic compounds are excellent generators of O2(1Δg) in aprotic solvents (excluding those quinones possessing substituents in positions adjacent to the carbonyl groups, in the case of anthraquinone derivatives). Benzoquinones, anthraquinones, and hydroxy derivatives are good O2(1Δg) quenchers upon dye-sensitized photoirradiation. The excited oxygen species is deactivated with rate constants in the range 106–107 M−1 s−1 depending on the solvent employed. The quenching process deactivates O2(1Δg) without further destruction of the quinone. The main interaction with O2(1Δg) is driven by the quinone moiety, in spite of the presence of potentially active nuclear substituents. The quenching mechanism could involve a reversible charge transfer intermediate, with the quinonic compound acting as an electron donor. Keywords: photooxidation, quenching, quinones, rose bengal, singlet oxygen.

scholarly journals Increased phagocytosis and production of reactive oxygen species by neutrophils during magnesium deficiency in rats and inhibition by high magnesium concentration

2002 ◽  
Vol 87 (2) ◽  
pp. 107-113 ◽  
Author(s):  
Françoise I. Bussière ◽  
Elyett Gueux ◽  
Edmond Rock ◽  
Jean-Pierre Girardeau ◽  
Arlette Tridon ◽  
...  
Keyword(s):  
Phorbol Myristate Acetate ◽  
Magnesium Deficiency ◽  
Control Diet ◽  
Magnesium Concentration ◽  
Polymorphonuclear Leucocytes ◽  
Myristate Acetate ◽  
Mg Deficiency ◽  
Opsonized Zymosan ◽  
Male Wistar Rats

Recent studies underline the importance of the immunoinflammatory processes in the pathology of Mg deficiency. Neutrophils possess a superoxide anion-generating NADPH oxidase and its inappropriate activation may result in tissue damage. The aim of the present study was to assess the effect of experimental Mg deficiency in the rat on polymorphonuclear leucocytes (PMN) activity and the role of increasing extracellular Mg. Weaning male Wistar rats were fed either a Mg-deficient or a control diet for 8 d. In Mg-deficient rats, the characteristic inflammatory response was accompanied by a marked increase in the number of PMN. Higher plasma interleukin 6 and NO concentrations and increased lipid peroxidation in the heart were found in Mg-deficient rats as compared with control rats. As shown by chemiluminescence studies, basal neutrophil activity from Mg-deficient rats was significantly elevated when compared with neutrophils from control rats. Moreover, the chemiluminescence of PMN from Mg-deficient rats was significantly higher than that of control rats following phorbol myristate acetate or opsonized zymosan activation. PMN from Mg-deficient rats also showed an increased activity of phagocytosis in comparison with neutrophils from control animals. Increasing extracellular Mg concentration in the incubating medium of PMN (0·8v.8·0 mM) decreased the chemiluminescence activity of PMN from control rats following opsonized zymosan activation. Chemiluminescence activities of PMN from Mg-deficient rats following phorbol myristate acetate or opsonized zymosan challenge were also decreased by high extracellular Mg concentration. From this work, it appears that PMN activation is an early consequence of Mg deficiency and that high extracellular Mg concentration inhibits free radicals generation.

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