Effects of acetylsalicylic acid on the levels of sulfane sulfur and non-protein sulfhydryl groups in mouse tissues

Bilska‐Wilkosz, Anna; Ochenduszka, Magdalena; Iciek, Małgorzata; Sokołowska-Jeżewicz, Maria; Wiliński, Bogdan; Góralska, Marta; Srebro, Z; Włodek, Lidia

doi:10.1016/s1734-1140(13)70975-7

Cited by 9 publications

(10 citation statements)

References 29 publications

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“…The ulceration induced by aspirin may be attributed mainly to various processes, including generation of reactive oxygen species (ROS), initiation of lipid peroxidation and inhibition of prostaglandin synthesis. The decrease in the prostaglandin level impairs almost all aspects of gastroprotection and increases acid secretions associated with inhibition in mucus secretion, bicarbonate and phospholipid production which, in turn, aggravate the ulcer [38]. These results are in parallel with that obtained by Abdallah et al [39].…”

Section: Resultssupporting

confidence: 75%

Efficacy and Safety of some Medical Herbs on Gastric Ulcer Induced by Aspirin in Rats

Heibashy¹,

Mazen²,

Ibrahim³

2014

IOSRJPBS

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Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used drugs in inflammation treatment. NSAIDs are associated with several side effects especially on the stomach. Considering these limitations of NSAIDs side effect, alternate natural nontoxic antioxidant with potent antiulcer activity such as ginger or curcumin was needed. Thus, this study was conducted to evaluate the correction role of ranitidine alone or with ginger or/and curcumin on aspirin induced gastric ulcer in adult male albino rats. Gastric ulcer in rats was induced by administered aspirin (500mg/Kg body weight/day) for three successive days to the animals. The obtained data revealed that aspirin induced a significant (p<0.05) increase in macroscopic ulcer score, gastric acidity and gastric production of mucosal non-protein sulfhrydryl group than those in control ones. The levels of proinflammatory cytokines (TNF-α, IL-1β & IL-8) were significantly (p<0.05) increase associated with remarkable elevation in the levels of total oxidant capacity and malondialdehyde (MDA) in ulcergenic rats. On the other hand, aspirin caused significant (p<0.05) decrease in the gastric total anti-oxidant capacity, prostaglandine E2, cyclooxygenase and vascular endothelial cell growth factor (VEGF) levels as compared to control rats. These disturbances in all the pervious parameters were ameliorated after the ulcerogenic rats treated with ginger, curcumin or their mixture accompanied with ranitidine treatment dependent on the time of administration (1&2 weeks). These findings are consistent with the concept that curcumin and ginger are antioxidant agents. The underlying mechanisms of these effects were discussed with available recent researches.

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Section: Resultssupporting

confidence: 75%

Efficacy and Safety of some Medical Herbs on Gastric Ulcer Induced by Aspirin in Rats

Heibashy¹,

Mazen²,

Ibrahim³

2014

IOSRJPBS

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“…GSH constitutes approximately 95% of the cellular NPSH pool [27] . In mammals, low-molecular-weight thiols (in reduced form), such as homocysteine, cysteine, glutathione (GSH), and cysteinylglycine, are collectively referred to as NPSH.…”

Section: Oxidative Stress and Lipid Peroxidationmentioning

confidence: 99%

A comprehensive review of sodium layered oxides: powerful cathodes for Na-ion batteries

Han

Gonzalo

Singh

et al. 2015

Energy Environ. Sci.

1,128

857

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Objective The goal of the current study was to investigate the molecular mechanisms of copper nanoparticle (CuNP)-induced hepato-and nephrotoxicity by proteomic analysis that was phenotypically anchored to conventional toxicological outcomes. Methods We employed specialized proteomic techniques, namely two-dimensional difference gel electrophoresis coupled with mass spectrometry to analyze changes in protein expression in rat liver and kidney after 5 days of oral copper nanoparticles administration. Serum biochemical analyses and histopathological examinations of livers and kidneys of all rats were also performed. ResultsAll of the results indicated that the adverse effects observed in the rats treated with 100 mg/kg/d nanocopper were less than those induced by 200 mg/kg/d CuNPs. Exposure to CuNPs at a dose of 200 mg/kg/d for 5 d can induce overt hepatotoxicity and nephrotoxicity through a mechanism that mainly involves scattered dot hepatocytic necrosis and widespread renal proximal tubule necrosis. In addition, significantly elevated copper accumulation, decreased thiolgroups and elevated malondialdehyde levels were also observed in the liver and kidney tissues. The perturbed proteins identified in the rat livers and kidneys are mainly involved in the respiratory and energy metabolism, antioxidant defense, phase II metabolism, lipid metabolism, urea cycle, creatine biosynthesis, intracellular calcium homeostasis, and cytoskeletal organization. No abnormalities were identified in the liver and kidney tissues from the rats treated with 200 mg/kg microcopper. Conclusions The results of this study suggest that mitochondrial dysfunction and oxidative damage may be the initial events in the hepato-and nephrotoxicity of copper nanoparticles. The down-regulation of phase II metabolic enzymes in the liver and the decrease in calcium-binding proteins in the kidney appear to be specific modes of action in these target organs. Our findings offer new directions for future research aiming to identify specific biomarkers of the hepatotoxicity and nephrotoxicity of copper nanoparticles.

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“…Additional clinically used drugs that can induce increases in H 2 S levels in biologic systems include aspirin (in female, but not male mice) (Srebro et al, 2006), sildenafil (Fusco et al, 2012), and cinaciguat (Salloum et al, 2012). Although the mechanism of sildenafil's effect remains to be characterized, the effect of aspirin may be related to an enhancement of H 2 S release from sulfane sulfur pools (Bilska-H 2 S Donors and H 2 S Biosynthesis Inhibitors Wilkosz et al, 2013). The effect of cinaciguat may be, at least in part, related to the protein kinase G-mediated upregulation of CSE (Das et al, 2015).…”

Section: Alternative Means To Increase Biologic H 2 S Levelsmentioning

confidence: 99%

International Union of Basic and Clinical Pharmacology. CII: Pharmacological Modulation of H₂S Levels: H₂S Donors and H₂S Biosynthesis Inhibitors

2017

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Over the last decade, hydrogen sulfide (HS) has emerged as an important endogenous gasotransmitter in mammalian cells and tissues. Similar to the previously characterized gasotransmitters nitric oxide and carbon monoxide, HS is produced by various enzymatic reactions and regulates a host of physiologic and pathophysiological processes in various cells and tissues. HS levels are decreased in a number of conditions (e.g., diabetes mellitus, ischemia, and aging) and are increased in other states (e.g., inflammation, critical illness, and cancer). Over the last decades, multiple approaches have been identified for the therapeutic exploitation of HS, either based on HS donation or inhibition of HS biosynthesis. HS donation can be achieved through the inhalation of HS gas and/or the parenteral or enteral administration of so-called fast-releasing HS donors (salts of HS such as NaHS and NaS) or slow-releasing HS donors (GYY4137 being the prototypical compound used in hundreds of studies in vitro and in vivo). Recent work also identifies various donors with regulated HS release profiles, including oxidant-triggered donors, pH-dependent donors, esterase-activated donors, and organelle-targeted (e.g., mitochondrial) compounds. There are also approaches where existing, clinically approved drugs of various classes (e.g., nonsteroidal anti-inflammatories) are coupled with HS-donating groups (the most advanced compound in clinical trials is ATB-346, an HS-donating derivative of the non-steroidal anti-inflammatory compound naproxen). For pharmacological inhibition of HS synthesis, there are now several small molecule compounds targeting each of the three HS-producing enzymes cystathionine--synthase (CBS), cystathionine--lyase, and 3-mercaptopyruvate sulfurtransferase. Although many of these compounds have their limitations (potency, selectivity), these molecules, especially in combination with genetic approaches, can be instrumental for the delineation of the biologic processes involving endogenous HS production. Moreover, some of these compounds (e.g., cell-permeable prodrugs of the CBS inhibitor aminooxyacetate, or benserazide, a potentially repurposable CBS inhibitor) may serve as starting points for future clinical translation. The present article overviews the currently known HS donors and HS biosynthesis inhibitors, delineates their mode of action, and offers examples for their biologic effects and potential therapeutic utility.

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Effects of acetylsalicylic acid on the levels of sulfane sulfur and non-protein sulfhydryl groups in mouse tissues

Abstract: The results of the present study suggest that ASA affects sulfur metabolism, in particular, renal and hepatic production of sulfane sulfur and NPSH in mice.

Cited by 9 publications

References 29 publications

Efficacy and Safety of some Medical Herbs on Gastric Ulcer Induced by Aspirin in Rats

Efficacy and Safety of some Medical Herbs on Gastric Ulcer Induced by Aspirin in Rats

A comprehensive review of sodium layered oxides: powerful cathodes for Na-ion batteries

International Union of Basic and Clinical Pharmacology. CII: Pharmacological Modulation of H₂S Levels: H₂S Donors and H₂S Biosynthesis Inhibitors

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Effects of acetylsalicylic acid on the levels of sulfane sulfur and non-protein sulfhydryl groups in mouse tissues

Abstract: The results of the present study suggest that ASA affects sulfur metabolism, in particular, renal and hepatic production of sulfane sulfur and NPSH in mice.

Cited by 9 publications

References 29 publications

Efficacy and Safety of some Medical Herbs on Gastric Ulcer Induced by Aspirin in Rats

Efficacy and Safety of some Medical Herbs on Gastric Ulcer Induced by Aspirin in Rats

A comprehensive review of sodium layered oxides: powerful cathodes for Na-ion batteries

International Union of Basic and Clinical Pharmacology. CII: Pharmacological Modulation of H2S Levels: H2S Donors and H2S Biosynthesis Inhibitors

Contact Info

Product

Resources

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International Union of Basic and Clinical Pharmacology. CII: Pharmacological Modulation of H₂S Levels: H₂S Donors and H₂S Biosynthesis Inhibitors