Arachidonic acid reactive oxygen species

The formation of nitric oxide in microsomes results in the inhibition of microsomal reductase activity. It has been found that the inhibitory effect of nitric oxide mainly depend on the interaction with cytochrome P-450. NO reversibly reacts with P-450 isoforms to form the P-450-NO complex, but at the same time it irreversibly inactivates the cytochrome P-450 via the modification of its thiol residues [64]. Incubation of microsomes with nitric oxide causes the inhibition of 20-HETE formation from arachidonic acid [65], the generation of reactive oxygen species [66], and the release of catalytically active iron from ferritin [67],... [Pg.771]

Mitochondria, nitric oxide synthase and arachidonic acid metabolism are sources of reactive oxygen species during ischemia—reperfusion injury 568... [Pg.559]

Nitric oxide and peroxynitrite contribute to oxidative damage 569 Production of eicosanoids from polyunsaturated fatty acids such as arachidonic acid may generate reactive oxygen species 570 Brain antioxidant defenses modify ischemia-reperfusion injury 570 Reactive oxygen species may modify both the excitotoxic and the apoptotic components of ischemic brain damage 570... [Pg.559]

Mitochondria, nitric oxide synthase and arachidonic acid metabolism are sources of reactive oxygen species during ischemia-reperfusion injury. ROS generation during ischemia-reperfusion may come from several sources, including NOS activity, mitochondrial electron transport, multiple steps in the metabolism of arachidonic... [Pg.568]

D. Washo-Stultz, C. L. Crowley-Weber, K. Dvorakova, C. Bernstein, H. Bernstein, K. Kunke, C. N. Waltmire, H. Garewal and C. M. Payne, Role of mitochondrial complexes I and II, reactive oxygen species and arachidonic acid metabolism in deoxycholate-induced apoptosis. Cancer Lett., 2002, 177(2), 129. [Pg.63]

Neuroinflammation emerges as a driving force in chronic neurodegenerative processes like Alzheimer s (AD) or Parkinson s disease (PD). Neuroinflammatoiy mediators such as cytokines, reactive oxygen species and molecules of the arachidonic acid pathway are generated and released by microglia, astrocytes and neurons upon stimulation and activation. In general, enhanced release of these substances has been considered to be detrimental. [Pg.20]

Dehmlow, C., Murawski, N., de Groot, H. Scavenging of reactive oxygen species and inhibition of arachidonic acid metaboUsm by silibinin in human cells. Life Sci. 1996 58 1591-1600... [Pg.887]

FGF, PDGF, BDNF Arachidonic Acid Metabolites Prostaglandin E2, leukotrienes Platelet activating factors Reactive Oxygen Species... [Pg.96]

Mitochondria are the site of ROS production during ischemia. Arachidonic acid, eNOS, NADPH oxidase and xanthine oxidase are sources of reactive oxygen species at reperfusion. Cytochrome P450 monooxygenases (CYPs) have also been implicated. CYP catalyzes arachidonic acid oxidation to a variety of biologically active eicosanoids and generates reactive oxygen species.1 3... [Pg.37]

The production of reactive oxygen species e.g. superoxides is implicated in the biosynthesis of prostaglandins from arachidonic acid during tissue inflammation. Oxygen can be reduced to superoxide by plasma membrane bound NADPH-oxidase in rabbit and human cell neutrophils. The tsitsixenicins inhibited (> 80% at a concentration of approximately 30 pM) the production of superoxide in isolated rabbit neutrophils with only 94 retaining this level of activity on ten-fold dilution. The results observed with rabbit neutrophils cannot usually be directly extrapolated to human neutrophils and only 93 and 94 exhibited moderate activity when the assay was repeated using the latter neutrophils [91]-... [Pg.90]

Fig. 2.5 Diagram showing effect of oxidative and nitrosative stress on neuronal injury. Plasma membrane (PM) Af-methyl-D-aspartate receptor (NMDA-R) glutamate (Glu) phosphatidylcholine (PtdCho) lyso-phosphatidylcholine (lyso-PtdCho) cytosolic phospholipase A2 (CPLA2) secretory phosphohpase A2 (SPLA2) cyclooxygenase (COX-2) arachidonic acid (ARA) reactive oxygen species (ROS) nuclear factor kappaB (NF-kB) nuclear factor kappaB response element (NF-kB-RE) inhibitory subunit of NFkB (IkB) inducible nitric oxide synthase (iNOS) perox-ynitrite (ONOO ) Superoxide ( O2) matrix metalloproteinases (MMPs) vascular cell adhesion molecule-1 (VCAM-1) poly(ADP-ribose) polymerase (PARP) nicotinamide (Nam) nicotineunide adenine dinucleotide (NAD) positive sign (+) represents upregulation...

Fig. 5.4 Interactions among dynorphin, gluteimate, and Idnin receptors in spinal cord injury. Dinorphin (D) glutamate (Glu) arginine (Arg) nitric oxide synthase (NOS) nitric oxide (NO) superoxide (O2 ) peroxynitrite (ONOO ) phosphatidylcholine (PtdCho) cytosolic phosphoUpase A2 (CPLA2) arachidonic acid (ARA) phospholipase C (PLC) diacylglycerol (DAG) inositol 1,4,5-trisphosphate (InPs) endoplasmic reticulum (ER) platelet-activating factor (RAF) reactive oxygen species (ROS) and 4-hydroxynonenal (4-HNE)...

Prolonged seizure activity in animals results in increased production of reactive oxygen species via activation of phospholipase A2 (Dennis, 1994) and nitric oxide synthase (Lipton et al., 1996) leading to excess arachidonic acid and nitric oxide synthesis respectively. The resulting free radicals destroy cytoskeletons, nucleic acids, and membrane lipids (Hall et al., 1999). [Pg.118]

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