The hypothesis of the main role of H2S in coupled sulphide-nitroso signalling pathway

Bertova, Anna; Čačányiová, Soňa; Kristek, Frantisek; Križanová, Oľga; Ondriaš, Karol; Tomaskova, Zuzana

doi:10.4149/gpb_2010_04_402

Cited by 22 publications

(24 citation statements)

References 42 publications

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“…We can assume that a similar mechanism is also valid for the inhibitory effects of CYS and GSH. This assumption is supported by our reported results that pre-treatment of serum albumin, Cys, NAC and lipids with H 2 S results in sulfur binding to these molecules, and these modified sulfur compounds release • NO from nitroso-compounds directly and/or through reliberated H 2 S (Bertova et al 2010). Our observation that 400 µmol/l Cys was not more efficient in decreasing GSNO decomposition than 200 µmol/l Cys (Fig.…”

Section: Effect Of Cys Nac Gsh Gssh and Met On H 2 S-induced Gsno supporting

confidence: 80%

“…These results support a hypothesis of a "coupled sulphidenitroso signalling pathway" (Bertova et al 2010). In spite of the fact that the steady-state free H 2 S concetrations in vivo are less than 20 nmol/l (Furne et al 2008), its storage forms, such as bound sulfane sulfur and acid-labile sulfide, may be critical in regulating H 2 S availability under different intracellular conditions (Ishigami et al 2009).…”

Section: Biological Significancesupporting

confidence: 70%

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Low molecular thiols, pH and O2 modulate H2S-induced S-nitrosoglutathione decomposition – •NO release

Grman

Misak²,

Jacob³

et al. 2014

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Abstract.We studied the involvement of O 2 , pH and low molecular thiols in H 2 S-induced decomposition of S-nitrosoglutathione (GSNO). The GSNO decomposition -• NO release was evaluated by UV-VIS spectroscopy and Griess assay. The H 2 S donor Na 2 S was used. O 2 slightly increased, but was not necessary for the H 2 S-induced GSNO decomposition. The rate of GSNO decomposition depended on pH; the maximum rate was observed at pH 7.4-8.0, and this decreased with lowering pH (6.4-4.5) as well as with increasing pH at 9.0-12.0. H 2 S-induced GSNO decomposition was slowed by the presence of other thiols, such as L-cysteine (Cys), N-acetyl-L-cysteine (NAC) and Lglutathione (GSH), but not in the presence of L-methionine (Met) or oxidized glutathione (GSSG). In sharp contrast, at pH 6.0, H 2 S-induced GSNO decomposition was negligible, yet the presence of Cys, NAC and GSH induced the H 2 S-driven GSNO decomposition (whilst Met and GSSG were inactive). In conclusion we postulate an involvement of low molecular thiols and pH in• NO signaling, by modulating the interactions of H 2 S with nitroso compounds, and hence in part they also appear to control H 2 S-triggered• NO release. The interaction of H 2 S and/or its derivatives with the thiol group may be responsible for the observed effects.

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Section: Effect Of Cys Nac Gsh Gssh and Met On H 2 S-induced Gsno supporting

confidence: 80%

Section: Biological Significancesupporting

confidence: 70%

Low molecular thiols, pH and O2 modulate H2S-induced S-nitrosoglutathione decomposition – •NO release

Grman

Misak²,

Jacob³

et al. 2014

gpb

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“…Experiments were carried out as previously described [8,9]. Briefly, preparations of thoracic aorta and arteria mesenterica superior (main branch) were prepared from male Wistar rats and mounted for recording of isometric tension changes in oxygenated (95% O2/5% CO2; 37°C) Krebsbicarbonate solution comprising (in mM) 118 NaCl, 5 KCl, 25 NaHCO3, 1.2 MgSO4, 1.2 KH2PO4, 2.5 CaCl2, 11 glucose, 0.032 CaNa2EDTA, pH 7.5.…”

Section: Measurement Of Rat Aorta Contractilitymentioning

confidence: 99%

“…Similarly, H2S can be stored in the form of sulfane sulfur and transported and released in response to a physiological stimulus [3]. A number of publications reported on the molecular interaction between H2S and NO or NO-donors [4][5][6][7][8][9][10][11][12][13][14], and H2S and NO were found to cooperatively regulate vascular tone by activating a neuroendocrine signaling pathway in which formation of nitroxyl (HNO) appears to play an important role [13]. Products of this H2S/NO interaction appear to have pronounced biological effects; however the nature of the reaction intermediates is currently unclear and many inconsistencies remain; for example, H2S donors were found to either potentiate or attenuate relaxation effect of NO donors in isolated aortic rings in vitro [15,16], or result in complete loss of vasodepressor activity in anesthetized rats [16].…”

Section: Introductionmentioning

confidence: 99%

The reaction products of sulfide and S-nitrosoglutathione are potent vasorelaxants

et al. 2015

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A B S T R A C TThe chemical interaction of sodium sulfide (Na2S) with the NO-donor S-nitrosoglutathione (GSNO) has been described to generate new reaction products, including polysulfides and nitrosopersulfide (SSNO -) via intermediacy of thionitrous acid (HSNO). The aim of the present work was to investigate the vascular effects of the longer-lived products of the Sulfide/GSNO interaction. Here we show that the products of this reaction relax precontracted isolated rings of rat thoracic aorta and mesenteric artery (but to a lesser degree rat uterus) with a >2-fold potency compared with the starting material, GSNO (50 nM), whereas Na2S and polysulfides have little effect at 1-5 μM. The onset of vasorelaxation of the reaction products was 7-10 times faster in aorta and mesenteric arteries compared with GSNO. Relaxation to GSNO (100-500 nM) was blocked by an inhibitor of soluble guanylyl cyclase, ODQ (0.1 and 10 μM), and by the NO scavenger cPTIO (100 μM), but less affected by prior acidification (pH 2-4), and unaffected by N-acetylcysteine (1 mM) or methemoglobin (20 μM heme). By contrast, relaxation to the Sulfide/GSNO reaction products (100-500 nM based on the starting material) was inhibited to a lesser extent by ODQ, only slightly decreased by cPTIO, more markedly inhibited by methemoglobin and N-acetylcysteine, and abolished by acidification before addition to the organ bath. The reaction mixture was found to generate NO as detected by EPR spectroscopy using N-(dithiocarboxy)-N-methyl-D-glucamine (MGD2)-Fe 2+ as spin trap. In conclusion, the Sufide/GSNO reaction products are faster and more pronounced vasorelaxants than GSNO itself. We conclude that in addition to NO formation from SSNO -, reaction products other than polysulfides may give rise to nitroxyl (HNO) and be involved in the pronounced relaxation induced by the Sulfide/GSNO cross-talk.

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“…However, there was no consensus regarding the anti-inflammatory ability or pro-inflammatory ability of H 2 S. In some researches, pretreatment of mice with H 2 S improved leukocyte rolling/ adhesion as well as neutrophil migration, which subsequently contributed to reduce bacteria levels and improve survival rate. 17 This suggested that endogenous H 2 S played a protective role in systemic inflammatory responses. The study by Li et al revealed that the damage of ALI/ARDS mouse was aggravated after NaHS was administered, which suggested the proinflammatory role of H 2 S. 4 In the current study, H 2 S is significantly lower in patients with ISS ≥ 25 compared with the patients with ISS ≤ 16.…”

Section: Groupmentioning

confidence: 99%

The analysis on the expression of gasotransmitters in early trauma patients

Wang

Fang

Guo

et al. 2017

Rev. Assoc. Med. Bras.

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Objective: Nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H 2 S) were endogenously-generated molecules gas. They owned important biological activity and participated in many pathophysiological processes. This study aimed to examine the levels of three gasotransmitters in the early phase of trauma patients. Method: Blood samples were collected from 60 trauma patients and ten healthy volunteers. Concentration of serum iNOS and HO-1 were analyzed by enzyme linked immunosorbent assay and plasma H 2 S was determined by colorimetric method. Meanwhile, the occurrence of multiple organ dysfunction syndrome (MODS) was also monitored. Results: The levels of iNOS, HO-1 and endogenous H 2 S in the patients group were significantly different from the healthy control group, and the difference was more obvious with the increase of ISS score. iNOS levels were positively correlated with ISS scores and blood lactic acid values, and HO-1 and endogenous H2S were negatively correlated with ISS scores and blood lactic acid values. Of 60 trauma patients, eight (13.33%) developed MODS. The level of iNOS in the MODS group was higher than that in non-MODS group, while HO-1 and H 2 S were significant lower in the MODS group. Conclusion: The three gasotransmitters participated in systemic inflammatory responses during early trauma and could be used as important indicators for trauma severity. Their measurements were meaningful for evaluating the severity and prognosis of trauma.

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The hypothesis of the main role of H2S in coupled sulphide-nitroso signalling pathway

Cited by 22 publications

References 42 publications

Low molecular thiols, pH and O2 modulate H2S-induced S-nitrosoglutathione decomposition – •NO release

Low molecular thiols, pH and O2 modulate H2S-induced S-nitrosoglutathione decomposition – •NO release

The reaction products of sulfide and S-nitrosoglutathione are potent vasorelaxants

The analysis on the expression of gasotransmitters in early trauma patients

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