Further investigations regarding the toxicity of sodium nitroprusside.

Butler, Anthony R.; Glidewell, C.; McGinnis, Joseph; Bisset, W.I.K.

doi:10.1093/clinchem/33.4.490

Cited by 26 publications

(5 citation statements)

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“…86 This is a surprising reaction as the formation constants of cyanoferrates are very high; e.g., β 6 for hexacyanoferrate(II) is 10 36 . Butler et al 87 examined this claim with a nonintrusive analytical procedure using 90% 13 C-labeled nitroprusside. This species has a very distinct 13 C NMR spectrum which remained unchanged over several hours after mixing with whole blood.…”

Section: Sodium Nitroprussidementioning

confidence: 99%

Non-Heme Iron Nitrosyls in Biology

2002

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Section: Sodium Nitroprussidementioning

confidence: 99%

Non-Heme Iron Nitrosyls in Biology

2002

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“…To overcome this aspect, several NO-related therapeutics have emerged over the past few decades, such as nitrosamines [2], organic nitrates [3], and N-diazeniumdiolates [4]. However, these compounds induce undesirable effects, such as tolerance and hypotension, and are often considered as oxidative stress enhancers in an environment rich in oxygen and/or radical species, where they may favour the formation of peroxynitrite ions (ONOO -), a reactive nitrogen species (RNS) producing deleterious protein nitration [5,6,7,8]. Other NO coumpounds, such as S-nitrosothiols may represent safer alternatives [9,10].…”

Section: Introductionmentioning

confidence: 99%

Oxidative stress enhances and modulates protein S-nitrosation in smooth muscle cells exposed to S-nitrosoglutathione

Belcastro

Fries

et al. 2017

Nitric Oxide

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Among S-nitrosothiols showing reversible binding between NO and -SH group, S-nitrosoglutathione (GSNO) represents potential therapeutics to treat cardiovascular diseases (CVD) associated with reduced nitric oxide (NO) availability. It also induces S-nitrosation of proteins, responsible for the main endogenous storage form of NO. Although oxidative stress parallels CVD development, little is known on the ability of GSNO to restore NO supply and storage in vascular tissues under oxidative stress conditions. Aortic rat smooth muscle cells (SMC) were stressed in vitro with a free radical generator (2,2'-azobis(2-amidinopropane) dihydrochloride, AAPH). The cellular thiol redox status was reflected through levels of reduced glutathione and protein sulfhydryl (SH) groups. The ability of GSNO to deliver NO to SMC and to induce protein S-nitrosation (investigated via mass spectrometry, MS), as well as the implication of two redox enzymes involved in GSNO metabolism (activity of gamma-glutamyltransferase, GGT, and expression of protein disulfide isomerase, PDI) were evaluated. Oxidative stress decreased both intracellular glutathione and protein -SH groups (53% and 32% respectively) and caused a 3.5-fold decrease of GGT activity, while PDI expression at the plasma membrane was 1.7-fold increased without any effect on extracellular GSNO catabolism. Addition of GSNO (50 μM) increased protein -SH groups and protein S-nitrosation (50%). Mass spectrometry analysis revealed a higher number of S-nitrosated proteins under oxidative stress (83 proteins, vs 68 in basal conditions) including a higher number of cytoskeletal proteins (15, vs 9 in basal conditions) related with cell contraction, morphogenesis and movement. Furthermore, proteins belonging to additional protein classes (cell adhesion, transfer/carrier, and transporter proteins) were S-nitrosated under oxidative stress. In conclusion, higher levels of GSNO-dependent S-nitrosation of proteins from the cytoskeleton and the contractile machinery were identified under oxidative stress conditions. The findings may prompt the identification of suitable biomarkers for the appraisal of GSNO bioactivity in the CVD treatment.

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“…Considering the existing medications and aiming at the improvement of clinical applications for treatment of vascular diseases, this system is advantageous because of the possibility of the controlled release of NO to specific biological targets 4 , 8 , 10 , 12 .Therefore, the present study aimed to investigate the effect of the Ru tetra-amines trans -[Ru II (NH 3 ) 4 (Py)(NO)] 3+ (PyNO), trans -[Ru II (Cl)(NO)(Cyclan)](PF 6 ) 2 (CyNO), and trans -[Ru II (NH 3 ) 4 (4-acPy)(NO)] 3+ (4-acPyNO) on the vascular response.…”

Section: Introductionmentioning

confidence: 99%

Vascular Response of Ruthenium Tetraamines in Aortic Ring from Normotensive Rats

Conceição-Vertamatti¹,

Ramos²,

Calandreli³

et al. 2014

Arquivos Brasileiros De Cardiologia

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BackgroundRuthenium (Ru) tetraamines are being increasingly used as nitric oxide (NO) carriers. In this context, pharmacological studies have become highly relevant to better understand the mechanism of action involved.ObjectiveTo evaluate the vascular response of the tetraamines trans-[RuII(NH3)4(Py)(NO)]3+, trans-[RuII(Cl)(NO) (cyclan)](PF6)2, and trans-[RuII(NH3)4(4-acPy)(NO)]3+.MethodsAortic rings were contracted with noradrenaline (10−6 M). After voltage stabilization, a single concentration (10−6 M) of the compounds was added to the assay medium. The responses were recorded during 120 min. Vascular integrity was assessed functionally using acetylcholine at 10−6 M and sodium nitroprusside at 10−6 M as well as by histological examination.ResultsHistological analysis confirmed the presence or absence of endothelial cells in those tissues. All tetraamine complexes altered the contractile response induced by norepinephrine, resulting in increased tone followed by relaxation. In rings with endothelium, the inhibition of endothelial NO caused a reduction of the contractile effect caused by pyridine NO. No significant responses were observed in rings with endothelium after treatment with cyclan NO. In contrast, in rings without endothelium, the inhibition of guanylate cyclase significantly reduced the contractile response caused by the pyridine NO and cyclan NO complexes, and both complexes caused a relaxing effect.ConclusionThe results indicate that the vascular effect of the evaluated complexes involved a decrease in the vascular tone induced by norepinephrine (10−6 M) at the end of the incubation period in aortic rings with and without endothelium, indicating the slow release of NO from these complexes and suggesting that the ligands promoted chemical stability to the molecule. Moreover, we demonstrated that the association of Ru with NO is more stable when the ligands pyridine and cyclan are used in the formulation of the compound.

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Further investigations regarding the toxicity of sodium nitroprusside.

Cited by 26 publications

References 0 publications

Non-Heme Iron Nitrosyls in Biology

Non-Heme Iron Nitrosyls in Biology

Oxidative stress enhances and modulates protein S-nitrosation in smooth muscle cells exposed to S-nitrosoglutathione

Vascular Response of Ruthenium Tetraamines in Aortic Ring from Normotensive Rats

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