Regulation of S-thiolation and S-nitrosylation in the thiol/nitric oxide system by radical scavengers

Koshiishi, Ichiro; Takajo, Tokuko; Tsuchida, Kazunori

doi:10.1016/j.niox.2006.12.002

Cited by 16 publications

(18 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, Gonzales et al (Gonzalez et al, 2008) studied the acute effect of tempol on the ionotropic state of the rat isolated heart. The addition of 100 μM tempol did not affect contractility but tempol did prevent the increased contractility caused by a modest concentration of a NO donor (Paolocci et al, 2000; Espey et al, 2002; Schrammel et al, 2003; Koshiishi et al, 2007) yet did not prevent the increased contractility with higher concentrations of NO (Gonzalez et al, 2008). …”

Section: Major Organ Effects Of Tempolmentioning

confidence: 92%

Effects of tempol and redox-cycling nitroxides in models of oxidative stress

Wilcox

2010

Pharmacology & Therapeutics

417

344

View full text Add to dashboard Cite

Tempol is a redox cycling nitroxide that promotes the metabolism of many reactive oxygen species (ROS) and improves nitric oxide bioavailability. It has been studied extensively in animal models of oxidative stress. Tempol has been shown to preserve mitochondria against oxidative damage and improve tissue oxygenation. Tempol improved insulin responsiveness in models of diabetes mellitus and improved the dyslipidemia, reduced the weight gain and prevented diastolic dysfunction and heart failure in fat-fed models of the metabolic syndrome. Tempol protected many organs, including the heart and brain, from ischemia/reperfusion damage. Tempol prevented podocyte damage, glomerulosclerosis, proteinuria and progressive loss of renal function in models of salt and mineralocorticosteroid excess. It reduced brain or spinal cord damage after ischemia or trauma and exerted a spinal analgesic action. Tempol improved survival in several models of shock. It protected normal cells from radiation while maintaining radiation sensitivity of tumor cells. Its paradoxical pro-oxidant action in tumor cells accounted for a reduction in spontaneous tumor formation. Tempol was effective in some models of neurodegeneration. Thus, tempol has been effective in preventing several of the adverse consequences of oxidative stress and inflammation that underlie radiation damage and many of the diseases associated with aging. Indeed, tempol given from birth prolonged the life span of normal mice. However, presently tempol has been used only in human subjects as a topical agent to prevent radiation-induced alopecia.

show abstract

Section: Major Organ Effects Of Tempolmentioning

confidence: 92%

Effects of tempol and redox-cycling nitroxides in models of oxidative stress

Wilcox

2010

Pharmacology & Therapeutics

417

344

View full text Add to dashboard Cite

show abstract

“…low [GSNO]/[NO] ratio) should provide conditions for low GSSG formation rate. [Note that previous studies [22, 39, 40, 65] have often used lower [NO]/[GSH] ratios and reaction is followed for several minutes]. Interference from Reaction 8 will occur at low [NO]/[GSH] ratios and will be documented with a decrease in GSNO formation rate as GSH concentration increases (Fig.…”

Section: Discussionmentioning

confidence: 98%

“…An important observation in previous studies [22, 39, 40, 65] is the significant generation of GSSG. Reactants and active intermediates may be utilized for the generation of GSSG and this utilization can affect GSNO formation rate.…”

Section: Discussionmentioning

confidence: 99%

“…This allows for significant increase in GSNO formation through mechanism 1(N 2 O 3 based nitrosation scheme) when mechanism 2 ( • NO 2 based nitrosation scheme) is inhibited. Thus, there is conflicting evidence for the effect of thiyl radical scavenging on GSNO formation with some studies reporting a decrease [8, 39] while others an increase [22, 65]. However, as pointed outin [22], cross talk between the two pathways makes difficult the interpretation of the results and to conclusively determine which is the dominant mechanism.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Glutathiyl radical as an intermediate in glutathione nitrosation

Madrasi

Joshi

Gadkari

et al. 2012

Free Radical Biology and Medicine

View full text Add to dashboard Cite

Nitrosation of thiols is thought to be mediated by Dinitrogen Trioxide (N2O3) or by Nitrogen Dioxide radical (•NO2). A kinetic study of Glutathione (GSH) nitrosation by NO donors in aerated buffered solutions was undertaken. S-nitrosoglutathione (GSNO) formation was assessed spectrophotometrically and by chemiluminescence. Results suggest an increase in the rate of GSNO formation with an increase in GSH with a half-maximum constant EC50 that depends on NO concentration. Our observed increase in EC50 with NO concentration suggests a significant contribution of •NO2 mediated nitrosation with the glutathiyl radical as an intermediate in the production of GSNO.

show abstract

“…Increases in cellular ROS and RNS production lead to decreases in the intracellular reduced glutathione (GSH) pool, thereby attenuating GSH-mediated trans- or denitrosylation and stabilizing SNO formation [44]. The stability of SNO is favored by low ambient oxygen, whereas with increasing oxygen S-thiolation is promoted [45,46]. The intermediate thiyl radical may be involved in the decomposition of SNO [47].…”

Section: No Based Signalingmentioning

confidence: 99%

Regulation of cardiovascular cellular processes by S-nitrosylation

Schulman

Hare

2012

Biochimica et Biophysica Acta (BBA) - General Subjects

View full text Add to dashboard Cite

Background Nitric oxide (NO), a highly versatile signaling molecule, exerts a broad range of regulatory influences in the cardiovascular system that extends from vasodilation to myocardial contractility, angiogenesis, inflammation, and energy metabolism. Considerable attention has been paid to deciphering the mechanisms for such diversity in signaling. S-nitrosylation of cysteine thiols is a major signaling pathway through which NO exerts its actions. An emerging concept of NO pathophysiology is that the interplay between NO and reactive oxygen species (ROS), the nitroso/redox balance, is an important regulator of cardiovascular homeostasis. Scope Of Review ROS react with NO, limit its bioavailability, and compete with NO for binding to the same thiol in effector molecules. The interplay between NO and ROS appears to be tightly regulated and spatially confined based on the co-localization of specific NO synthase (NOS) isoforms and oxidative enzymes in unique subcellular compartments. NOS isoforms are also in close contact with denitrosylases, leading to crucial regulation of S-nitrosylation. Major Conclusions Nitroso/redox balance is an emerging regulatory pathway for multiple cells and tissues, including the cardiovascular system. Studies using relevant knockout models, isoform specific NOS inhibitors, and both in vitro and in vivo methods have provided novel insights into NO- and ROS-based signaling interactions responsible for numerous cardiovascular disorders. General Significance An integrated view of the role of nitroso/redox balance in cardiovascular pathophysiology has significant therapeutic implications. This is highlighted by human studies where pharmacologic manipulation of oxidative and nitrosative pathways exerted salutary effects in patients with advanced heart failure. This article is part of a Special Issue entitled Regulation of Cellular Processes by S-nitrosylation.

show abstract

Regulation of S-thiolation and S-nitrosylation in the thiol/nitric oxide system by radical scavengers

Cited by 16 publications

References 25 publications

Effects of tempol and redox-cycling nitroxides in models of oxidative stress

Effects of tempol and redox-cycling nitroxides in models of oxidative stress

Glutathiyl radical as an intermediate in glutathione nitrosation

Regulation of cardiovascular cellular processes by S-nitrosylation

Contact Info

Product

Resources

About