scholarly journals Organochlorine Insecticides Induce NADPH Oxidase-Dependent Reactive Oxygen Species in Human Monocytic Cells via Phospholipase A2/Arachidonic Acid

2015 ◽  
Vol 28 (4) ◽  
pp. 570-584 ◽  
Author(s):  
Lee C. Mangum ◽  
Abdolsamad Borazjani ◽  
John V. Stokes ◽  
Anberitha T. Matthews ◽  
Jung Hwa Lee ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Arachidonic Acid ◽  
Nadph Oxidase ◽  
Phospholipase A2 ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Monocytic Cells ◽  
Organochlorine Insecticides

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.

scholarly journals Role of NADPH Oxidase-Mediated Reactive Oxygen Species in Podocyte Injury

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Shan Chen ◽  
Xian-Fang Meng ◽  
Chun Zhang
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Epithelial To Mesenchymal Transition ◽  
Kidney Diseases ◽  
Treatment Strategies ◽  
Reactive Oxygen ◽  
Glomerular Sclerosis ◽  
Oxygen Species ◽  
Podocyte Injury ◽  
Mesenchymal Transition

Proteinuria is an independent risk factor for end-stage renal disease (ESRD) (Shankland, 2006). Recent studies highlighted the mechanisms of podocyte injury and implications for potential treatment strategies in proteinuric kidney diseases (Zhang et al., 2012). Reactive oxygen species (ROS) are cellular signals which are closely associated with the development and progression of glomerular sclerosis. NADPH oxidase is a district enzymatic source of cellular ROS production and prominently expressed in podocytes (Zhang et al., 2010). In the last decade, it has become evident that NADPH oxidase-derived ROS overproduction is a key trigger of podocyte injury, such as renin-angiotensin-aldosterone system activation (Whaley-Connell et al., 2006), epithelial-to-mesenchymal transition (Zhang et al., 2011), and inflammatory priming (Abais et al., 2013). This review focuses on the mechanism of NADPH oxidase-mediated ROS in podocyte injury under different pathophysiological conditions. In addition, we also reviewed the therapeutic perspectives of NADPH oxidase in kidney diseases related to podocyte injury.

Reactive oxygen species produced via plasma membrane NADPH oxidase regulate anthocyanin synthesis in apple peel

Planta ◽  
2014 ◽  
Vol 240 (5) ◽  
pp. 1023-1035 ◽  
Author(s):  
Jiangli Zhang ◽  
Changsheng Chen ◽  
Di Zhang ◽  
Houhua Li ◽  
Pengmin Li ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Plasma Membrane ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Anthocyanin Synthesis ◽  
Oxygen Species ◽  
Apple Peel

scholarly journals Arachidonic acid- and prostaglandin E2-induced cerebral vasodilation is mediated by carbon monoxide, independent of reactive oxygen species in piglets

2011 ◽  
Vol 301 (6) ◽  
pp. H2482-H2487 ◽  
Author(s):  
Alie Kanu ◽  
Charles W. Leffler
Keyword(s):  
Reactive Oxygen Species ◽  
Carbon Monoxide ◽  
Arachidonic Acid ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Artificial Cerebrospinal Fluid ◽  
Newborn Pigs ◽  
Cerebral Vasodilation ◽  
Prostacyclin Analog ◽  
Cerebral Vascular

Arachidonic acid (AA) and prostaglandin (PG) E2 stimulate carbon monoxide (CO) production, and AA metabolism is known to be associated with the generation of reactive oxygen species (ROS). This study was conducted to address the hypothesis that CO and/or ROS mediate cerebrovascular dilation in newborn pigs. Experiments were performed on anesthetized newborn pigs with closed cranial windows. Different concentrations of AA (10−8-10−6 M), PGE2 (10−8-10−6 M), iloprost (10−8-10−6 M), and their vehicle (artificial cerebrospinal fluid) were given. Piglets with PGE2 and iloprost received indomethacin (5 mg/kg iv) to inhibit cyclooxygenase. AA, PGE2, and iloprost caused concentration-dependent increases in pial arteriolar diameter. The effects of both AA and PGE2 in producing cerebral vascular dilation and associated CO production were blocked by the heme oxygenase inhibitor chromium mesoporphyrin (2 × 10−5 M), but not by the prostacyclin analog, iloprost. ROS inhibitor tempol (SOD mimetic) (1 × 10−5 M) and the H2O2 scavenger catalase (1,000 U/ml) also do not block these vasodilator effects of AA and PGE2. Heme-l-lysinate-induced cerebrovascular dilation and CO production was blocked by chromium mesoporphyrin. Hypoxanthine plus xanthine oxidase, a combination that is known to generate ROS, caused pial arteriolar dilation and CO production that was inhibited by tempol and catalase. These data suggest that AA- and PGE2-induced cerebral vascular dilation is mediated by CO, independent of ROS.

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