Role of arachidonic acid metabolites and reactive oxygen species in glomerular immune-inflammatory process

1987 ◽  
Vol 9 (4) ◽  
Author(s):  
Raymond Ardaillou ◽  
Laurent Baud ◽  
Jos�e Sraer
Keyword(s):  
Reactive Oxygen Species ◽  
Arachidonic Acid ◽  
Inflammatory Process ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Arachidonic Acid Metabolites ◽  
Acid Metabolites

scholarly journals Reactive oxygen species mediate arachidonic acid-induced dilation in porcine coronary microvessels

2003 ◽  
Vol 285 (6) ◽  
pp. H2309-H2315 ◽  
Author(s):  
Christine L. Oltman ◽  
Neal L. Kane ◽  
Francis J. Miller ◽  
Arthur A. Spector ◽  
Neal L. Weintraub ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Arachidonic Acid ◽  
Coronary Arteries ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cox Inhibitors ◽  
Ros Scavenger ◽  
Krebs Buffer

Reactive oxygen species (ROS) have been proposed to mediate vasodilation in the microcirculation. We investigated the role of ROS in arachidonic acid (AA)-induced coronary microvascular dilation. Porcine epicardial coronary arterioles (110 ± 4 μm diameter) were mounted onto pipettes in oxygenated Krebs buffer. Vessels were incubated with vehicle or 1 mM Tiron (a nonselective ROS scavenger), 250 U/ml polyethylene-glycolated (PEG)-superoxide dismutase (SOD; an [Formula: see text] scavenger), 250 U/ml PEG-catalase (a H2O2 scavenger), or the cyclooxygenase (COX) inhibitors indomethacin (10 μM) or diclofenac (10 μM) for 30 min. After endothelin constriction (30–60% of resting diameter), cumulative concentrations of AA (10–10–10–5 M) were added and internal diameters measured by video microscopy. AA (10–7 M) produced 37 ± 6% dilation, which was eliminated by the administration of indomethacin (4 ± 7%, P < 0.05) or diclofenac (–8 ± 8%, P < 0.05), as well as by Tiron (–4 ± 5%, P < 0.05), PEG-SOD (–10 ± 6%, P < 0.05), or PEG-catalase (1 ± 4%, P < 0.05). Incubation of small coronary arteries with [3H]AA resulted in the formation of prostaglandins, which was blocked by indomethacin. In separate studies in microvessels, AA induced concentration-dependent increases in fluorescence of the oxidant-sensitive probe dichlorodihydrofluorescein diacetate, which was inhibited by pretreatment with indomethacin or by SOD + catalase. We conclude that in porcine coronary microvessels, COX-derived ROS contribute to AA-induced vasodilation.

scholarly journals Involvement of cytosolic phospholipase A2, and the subsequent release of arachidonic acid, in signalling by Rac for the generation of intracellular reactive oxygen species in Rat-2 fibroblasts

2000 ◽  
Vol 348 (3) ◽  
pp. 525-530 ◽  
Author(s):  
Chang-Hoon WOO ◽  
Zee-Won LEE ◽  
Byung-Chul KIM ◽  
Kwon-Soo HA ◽  
Jae-Hong KIM
Keyword(s):  
Reactive Oxygen Species ◽  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Active Form ◽  
Reactive Oxygen ◽  
Cytosolic Phospholipase A2 ◽  
Signalling Pathway ◽  
Oxygen Species ◽  
Cytosolic Phospholipase

Although there have been a number of recent studies on the role of Rac in the generation of reactive oxygen species (ROS), details of the signalling pathway remain unclear. In the present study we analysed the extent to which the activation of cytosolic phospholipase A2 and the resultant release of arachidonic acid (AA) are involved in the Rac-mediated generation of ROS. Transfection of Rat-2 cells with RacV12, a constitutively active form of Rac1, induced elevated levels of ROS, as reflected by increased H2O2-sensitive fluorescence of 2ʹ,7ʹ-dichlorofluorescein. These effects could be blocked by inhibiting phospholipase A2 or 5-lipoxygenase but not by inhibiting cyclo-oxygenase. The application of exogenous AA increased levels of ROS but the effect was dependent on the further metabolism of AA to leukotrienes C4/D4/E4 by 5-lipoxygenase. Indeed, the exogenous application of a mixture of leukotrienes C4/D4/E4 elicited transient elevations in the levels of ROS that were blocked by catalase. These findings indicate that phospholipase A2 and subsequent AA metabolism by 5-lipoxygenase act as downstream mediators in a Rac signalling pathway leading to the generation of ROS.

Role of mitochondrial complexes I and II, reactive oxygen species and arachidonic acid metabolism in deoxycholate-induced apoptosis

2002 ◽  
Vol 177 (2) ◽  
pp. 129-144 ◽  
Author(s):  
Delon Washo-Stultz ◽  
Cara L Crowley-Weber ◽  
Katerina Dvorakova ◽  
Carol Bernstein ◽  
Harris Bernstein ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Reactive Oxygen ◽  
Arachidonic Acid Metabolism ◽  
Oxygen Species ◽  
Mitochondrial Complexes ◽  
Induced Apoptosis
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