Effects of aspirin on the levels of hydrogen sulfide and sulfane sulfur in mouse tissues

Bilska, Anna; Iciek, Małgorzata; Kwiecień, Inga; Kaniecki, Karol; Paliborek, Magdalena; Somogyi, E; Piotrowska, Joanna; Wiliński, Bogdan; Góralska, Marta; Srebro, Z; Włodek, Lidia

doi:10.1016/s1734-1140(10)70270-x

Cited by 14 publications

(8 citation statements)

References 29 publications

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“…Conversely, the sulfane sulfur content in the liver dropped. ASA did not change the CSE and TST activity in either organ (Bilska et al, 2010). On the other hand, the sulfane sulfur increase was observed in the kidneys of mice receiving ASA (Bilska-Wilkosz et al, 2013).…”

Section: Effect Of Some Drugs On the Sulfane Sulfur Levelmentioning

confidence: 67%

Sulfane sulfur – new findings on an old topic

2019

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Sulfane sulfur is a divalent sulfur atom bonded to another sulfur which is very reactive and labile. Compounds containing this reactive sulfur include persulfides, polysulfides, thiosulfate, thiosulfinates, polythionates, and elemental sulfur. Sulfane sulfur appears in a number of biologically important compounds, including thiocysteine, thiocystine and thiotaurine, products of the cysteine metabolism, as well as glutathione persulfide. Sulfane sulfur compounds can modify cysteine residues in proteins via an S-sulfhydration reaction to produce protein persulfides. It has been also postulated that cysteine persulfides can be incorporated into proteins during translation. Recently, the sulfane sulfur compounds, especially the persulfides and polysulfides, have attracted increasing interest due to their regulatory and antioxidant properties. Compounds containing sulfane sulfur are also regarded as a form of H2S storage, which can easily release this gasotransmitter in response to biological signals. Both reactive sulfur species (H2S and sulfane sulfur) always coexist in biological systems. This review is focused on new findings in the field of sulfane sulfur’s biological role, and disruption of its level in some patho/physiological conditions. A few sulfane sulfur donors with potential applications are presented. In recent years, in parallel to increasing interest in biological importance of sulfane sulfur, new analytical methods have been developed for sensitive and reliable determination of its level in the cells and tissues.

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Section: Effect Of Some Drugs On the Sulfane Sulfur Levelmentioning

confidence: 67%

Sulfane sulfur – new findings on an old topic

2019

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“…Recently, carvedilol was found to improve neuronal transmission and attenuate brain oligomeric beta-amyloid content and cognitive deterioration in two mouse models of Alzheimer's disease (WANG et al 2010). Analogically, non-steroidal anti-inflammatory drugs were also demonstrated to exert some anti-amyloidogenic effects and to affect H S biology (BILSKA et al 2010;SREBRO et al 2006).…”

Section: Resultsmentioning

confidence: 99%

Carvedilol Induces Endogenous Hydrogen Sulfide Tissue Concentration Changes in Various Mouse Organs

Wiliński¹,

Wiliński²,

Somogyi³

et al. 2011

folia biol (krakow)

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Carvedilol induces endogenous hydrogen sulfide tissue concentration changes in various mouse organs. Folia biologica (Kraków) 59: 151-155. Carvedilol, a third generation non-selective adrenoreceptor blocker, is widely used in cardiology. Its action has been proven to reach beyond adrenergic antagonism and involves multiple biological mechanisms. The interaction between carvedilol and endogenous gasotransmitter hydrogen sulfide (H S) is unknown. The aim of the study is to assess the influence of carvedilol on the H S tissue level in mouse brain, liver, heart and kidney. Twenty eight SJL strain female mice were administered intraperitoneal injections of 2.5 mg/kg b.w./d (group D1, n = 7), 5 mg/kg b.w./d (group D2, n = 7) or 10 mg/kg b.w./d of carvedilol (group D3, n = 7). The control group (n = 7) received physiological saline in portions of the same volume (0.2 ml). Measurements of the free tissue H S concentrations were performed according to the modified method of Siegel. A progressive decline in H S tissue concentration along with an increase in carvedilol dose was observed in the brain (12.5%, 13.7% and 19.6%, respectively). Only the highest carvedilol dose induced a change in H S tissue level in the heart an increase by 75.5%. In the liver medium and high doses of carvedilol increased the H S level by 48.1% and 11.8%, respectively. In the kidney, group D2 showed a significant decrease of H S tissue level (22.5%), while in the D3 group the H S concentration increased by 12.9%. Our study has proven that carvedilol affects H S tissue concentration in different mouse organs.

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“…MicroRNA (miRNA) controls gene expression at the posttranscriptional level [34] and is one of the main factors involved in the upregulation of CSE expression [16]. Interestingly, currently used drugs, including angiotensinconverting enzyme (ACE) inhibitors (e.g., ramipril) [35], statins [36], calcium channel antagonists (e.g., amlodipine) [37], digoxin [38], vitamin D 3 [39], aspirin [40], metformin [40], and others [23], may increase the production of H 2 S. For example, statins can increase H 2 S synthesis via Aktmediated upregulation of CSE [36] or suppress H 2 S degradation by decreasing the concentration of coenzyme Q, which is a sulfide quinone reductase cofactor [41]. It is worth noting that either exogenously supplied or endogenously produced H 2 S can be stored in the body in the form of bound sulfane, which is a reductant labile sulfur (e.g., persulfide (R-S-S-SH), polysulfide (RSS n SR), and protein-associated sulfur, among others) [42].…”

Section: Modulation Of H 2 Smentioning

confidence: 99%

Hydrogen Sulfide as a Potential Alternative for the Treatment of Myocardial Fibrosis

Kang

Sohn

Lee

2020

Oxidative Medicine and Cellular Longevity

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Harmful, stressful conditions or events in the cardiovascular system result in cellular damage, inflammation, and fibrosis. Currently, there is no targeted therapy for myocardial fibrosis, which is highly associated with a large number of cardiovascular diseases and can lead to fatal heart failure. Hydrogen sulfide (H2S) is an endogenous gasotransmitter similar to nitric oxide and carbon monoxide. H2S is involved in the suppression of oxidative stress, inflammation, and cellular death in the cardiovascular system. The level of H2S in the body can be boosted by stimulating its synthesis or supplying it exogenously with a simple H2S donor with a rapid- or slow-releasing mode, an organosulfur compound, or a hybrid with known drugs (e.g., aspirin). Hypertension, myocardial infarction, and inflammation are exaggerated when H2S is reduced. In addition, the exogenous delivery of H2S mitigates myocardial fibrosis caused by various pathological conditions, such as a myocardial infarct, hypertension, diabetes, or excessive β-adrenergic stimulation, via its involvement in a variety of signaling pathways. Numerous experimental findings suggest that H2S may work as a potential alternative for the management of myocardial fibrosis. In this review, the antifibrosis role of H2S is briefly addressed in order to gain insight into the development of novel strategies for the treatment of myocardial fibrosis.

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Effects of aspirin on the levels of hydrogen sulfide and sulfane sulfur in mouse tissues

Cited by 14 publications

References 29 publications

Sulfane sulfur – new findings on an old topic

Sulfane sulfur – new findings on an old topic

Carvedilol Induces Endogenous Hydrogen Sulfide Tissue Concentration Changes in Various Mouse Organs

Hydrogen Sulfide as a Potential Alternative for the Treatment of Myocardial Fibrosis

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