Interaction between reactive oxygen species and nitric oxide in drought-induced abscisic acid synthesis in root tips of wheat seedlings

2001 ◽  
Vol 28 (10) ◽  
pp. 1055 ◽  
Author(s):  
Zhiguang Zhao ◽  
Guocang Chen ◽  
Chenglie Zhang
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Abscisic Acid ◽  
Reactive Oxygen ◽  
Acid Synthesis ◽  
Oxygen Species ◽  
Root Tips ◽  
Wheat Seedlings ◽  
Acid Accumulation ◽  
Oxide Synthase

Abscisic acid accumulation and oxidative stress are two common responses of plants to environmental stresses. However, little is known about their relationships. The purpose of this article is to investigate the effects of reactive oxygen species and nitric oxide on the plant hormone abscisic acid synthesis in root tips of wheat (Triticum aestivum L.) seedlings under drought stress. Detached root tips were subjected to drought stress by naturally evaporating until 20% of their fresh weights were lost. The activities of superoxide synthases and nitric oxide synthase (EC 1.14.13.39) increased after 20 min of treatment and abscisic acid began to accumulate 60 min later. The induction of abscisic acid by drought was strongly blocked by pretreating the root tips with reactive oxygen species eliminators tiron or ascorbate acid, and with nitric oxide synthase inhibitor Nω-nitro-L-arginine or nitric oxide eliminator 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl 3-oxide. Consistent with these results, reactive oxygen species generators diethyldithiocarbamic acid, xanthine–xanthine oxidase and triazole or nitric oxide donor sodium nitroprusside can also induce abscisic acid accumulation in root tips of wheat seedlings. While potentiated by reactive oxygen species, the effect of sodium nitroprusside on abscisic acid accumulation was blocked by 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl 3-oxide. Based on these results, we suggest that reactive oxygen species and nitric oxide play important roles in drought-induced abscisic acid synthesis in plant, they may be the signals through which the plant can ‘sense’ the drought condition.

Levodopa modulating effects of inducible nitric oxide synthase and reactive oxygen species in glioma cells

Life Sciences ◽  
2002 ◽  
Vol 72 (2) ◽  
pp. 185-198 ◽  
Author(s):  
Mark K Soliman ◽  
Elizabeth Mazzio ◽  
Karam F.A Soliman
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Glioma Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

scholarly journals Mutational disruption of the nitric oxide synthase/calmodulin interaction causes increased formation of reactive oxygen species

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Dean L. Kellogg ◽  
Bettie Sue S. Masters ◽  
Linda J. Roman
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Nitric Oxide Synthase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Oxide Synthase

Induction of inducible nitric oxide synthase increases the production of reactive oxygen species in RAW264.7 macrophages

2010 ◽  
Vol 30 (4) ◽  
pp. 233-241 ◽  
Author(s):  
Kai Zhao ◽  
Zhen Huang ◽  
Hongling Lu ◽  
Juefei Zhou ◽  
Taotao Wei
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Nitric Oxide Synthase ◽  
Reactive Oxygen ◽  
Inos Expression ◽  
Raw264.7 Cells ◽  
Ros Production ◽  
Oxygen Species ◽  
Raw264.7 Macrophages ◽  
Oxide Synthase

Macrophages produce a large volume of ROS (reactive oxygen species) through respiratory burst. However, the influence of iNOS [inducible NOS (nitric oxide synthase)] activation on ROS production remains unclear. In the present study, the kinetic generation of ROS in RAW264.7 murine macrophages was monitored by chemiluminescence. PMA induces a robust chemiluminescence in RAW264.7 cells, suggesting PKC (protein kinase C)-related assembly and activation of NOX (NADPH oxidase). The effects of iNOS induction on ROS production were examined. Induction of iNOS expression in RAW264.7 cells with LPS (lipopolysaccharide; 1 μg/ml) causes a significant increase in PMA-induced chemiluminescence, which could be enhanced by the NOS substrate, L-arginine, and could be abolished by the NOS inhibitor, L-NNA (NG-nitro-L-arginine). Further experiments reveal that induction of iNOS expression enhances the PMA-stimulated phosphorylation of the p47phox subunit of NOX, and promotes the relocalization of cytosolic p47phox and p67phox subunits to the membrane. Inhibition of PKCζ by its myristoylated pseudosubstrate significantly decreased the PMA-stimulated phosphorylation of the p47phox in LPS-pretreated cells, suggesting that PKCζ is involved in the iNOS-dependent assembly and activation of NOX. Taken together, the present study suggests that the induction of iNOS upregulates the PMA-induced assembly of NOX and leads to the enhanced production of ROS via a PKCζ-dependent mechanism.

Intracellular generation of reactive oxygen species in endothelial cells exposed to anoxia-reoxygenation

1997 ◽  
Vol 272 (5) ◽  
pp. L897-L902 ◽  
Author(s):  
J. J. Zulueta ◽  
R. Sawhney ◽  
F. S. Yu ◽  
C. C. Cote ◽  
P. M. Hassoun
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Intracellular Ros ◽  
Ros Formation ◽  
Oxide Synthase

Reactive oxygen species (ROS) play an important role in the pathogenesis of ischemia-reperfusion injury. Extracellular H2O2 generation from bovine pulmonary artery endothelial cells (EC) is known to increase in response to anoxia-reoxygenation (A-R). To determine potential sources of intracellular ROS formation in EC in response to A-R, a fluorometric assay based on the oxidation of 2',7'-dichlorofluorescin was used. Intracellular ROS production declined 40% during 6 h of anoxia (P < 0.05). After A-R, the rates of intracellular ROS formation increased to 148 +/- 9% (P < 0.001) that of normoxic EC (100 +/- 3%). In EC exposed to A-R, allopurinol and NG-methyl-L-arginine (L-NMMA), inhibitors of xanthine oxidase (XO) and nitric oxide synthase (NOS), respectively, reduced intracellular ROS formation by 25 +/- 1% (P < 0.001) and 36 +/- 4% (P < 0.01). Furthermore, at low doses (i.e., 20 microM), deferoxamine and diethylenetriaminepentaacetic acid (DTPA) significantly inhibited intracellular ROS formation. However, at 100 microM, only deferoxamine caused further reduction in DCF fluorescence. In summary, EC respond to A-R by generating increased amounts of XO- and NOS-derived intracellular ROS. The inhibition, to a similar extent, caused by allopurinol and L-NMMA, as well as the effect of deferoxamine and DTPA suggest that the ROS detected is peroxynitrite. Based on these findings and previous work, we conclude that EC generate ROS in response to A-R from at least two different sources: a plasma membrane-bound NADPH oxidase-like enzyme that releases H2O2 extracellularly and XO, which generates intracellular O2-, which in turn may react with nitric oxide to form peroxynitrite.

scholarly journals Upregulation of Endothelial and Inducible Nitric Oxide Synthase Expression by Reactive Oxygen Species

2008 ◽  
Vol 21 (1) ◽  
pp. 28-34 ◽  
Author(s):  
J. Zhen ◽  
H. Lu ◽  
X. Q. Wang ◽  
N. D. Vaziri ◽  
X. J. Zhou
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Reactive oxygen species enhances the induction of inducible nitric oxide synthase by sphingomyelinase in RAW264.7 cells

1998 ◽  
Vol 1393 (1) ◽  
pp. 203-210 ◽  
Author(s):  
Yutaka Hatanaka ◽  
Junichi Fujii ◽  
Tatsushi Fukutomi ◽  
Toshiya Watanabe ◽  
Wenyi Che ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Reactive Oxygen ◽  
Raw264.7 Cells ◽  
Oxygen Species ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

scholarly journals Up-regulation of the peroxiredoxin-6 related metabolism of reactive oxygen species in skeletal muscle of mice lacking neuronal nitric oxide synthase

2009 ◽  
Vol 587 (3) ◽  
pp. 655-668 ◽  
Author(s):  
Luis Da Silva-Azevedo ◽  
Sebastian Jähne ◽  
Christian Hoffmann ◽  
Daniel Stalder ◽  
Manfred Heller ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Nitric Oxide Synthase ◽  
Reactive Oxygen ◽  
Neuronal Nitric Oxide Synthase ◽  
Oxygen Species ◽  
Peroxiredoxin 6 ◽  
Oxide Synthase

scholarly journals Insulin-Induced Generation of Reactive Oxygen Species and Uncoupling of Nitric Oxide Synthase Underlie the Cerebrovascular Insulin Resistance in Obese Rats

2012 ◽  
Vol 32 (5) ◽  
pp. 792-804 ◽  
Author(s):  
Prasad VG Katakam ◽  
James A Snipes ◽  
Mesia M Steed ◽  
David W Busija
Keyword(s):  
Nitric Oxide ◽  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Nitric Oxide Synthase ◽  
Cerebral Arteries ◽  
Reactive Oxygen ◽  
Ros Generation ◽  
Oxygen Species ◽  
Fluorescence Studies ◽  
Oxide Synthase

Hyperinsulinemia accompanying insulin resistance (IR) is an independent risk factor for stroke. The objective is to examine the cerebrovascular actions of insulin in Zucker obese (ZO) rats with IR and Zucker lean (ZL) control rats. Diameter measurements of cerebral arteries showed diminished insulin-induced vasodilation in ZO compared with ZL. Endothelial denudation revealed vasoconstriction to insulin that was greater in ZO compared with ZL. Nonspecific inhibition of nitric oxide synthase (NOS) paradoxically improved vasodilation in ZO. Scavenging of reactive oxygen species (ROS), supplementation of tetrahydrobiopterin (BH4) precursor, and inhibition of neuronal NOS or NADPH oxidase or cyclooxygenase (COX) improved insulin-induced vasodilation in ZO. Immunoblot experiments revealed that insulin-induced phosphorylation of Akt, endothelial NOS, and expression of GTP cyclohydrolase-I (GTP-CH) were diminished, but phosphorylation of PKC and ERK was enhanced in ZO arteries. Fluorescence studies showed increased ROS in ZO arteries in response to insulin that was sensitive to NOS inhibition and BH4 supplementation. Thus, a vicious cycle of abnormal insulin-induced ROS generation instigating NOS uncoupling leading to further ROS production underlies the cerebrovascular IR in ZO rats. In addition, decreased bioavailability and impaired synthesis of BH4 by GTP-CH induced by insulin promoted NOS uncoupling.

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