scholarly journals Thermal Decomposition of Dimethyl Ether in the Presence of Hydrogen Sulfide and Nitric Oxide

1962 ◽  
Vol 35 (6) ◽  
pp. 860-863 ◽  
Author(s):  
Naomi Imai ◽  
Osamu Toyama
Keyword(s):  
Nitric Oxide ◽  
Thermal Decomposition ◽  
Hydrogen Sulfide ◽  
Dimethyl Ether

Influence of Nitric Oxide on the Thermal Decomposition of Dimethyl Ether. Gaseous Catalysis

Nature ◽  
1936 ◽  
Vol 138 (3491) ◽  
pp. 546-547 ◽  
Author(s):  
P. F. GAY ◽  
MORRIS W. TRAVERS
Keyword(s):  
Nitric Oxide ◽  
Thermal Decomposition ◽  
Dimethyl Ether

KINETICS AND MECHANISMS OF THE PYROLYSIS OF DIMETHYL ETHER: II. THE REACTION INHIBITED BY NITRIC OXIDE AND PROPYLENE

1963 ◽  
Vol 41 (8) ◽  
pp. 1993-2008 ◽  
Author(s):  
D. J. McKenney ◽  
B. W. Wojciechowski ◽  
K. J. Laidler
Keyword(s):  
Nitric Oxide ◽  
Thermal Decomposition ◽  
Dimethyl Ether ◽  
Chain Process ◽  
Maximal Inhibition ◽  
First Order ◽  
Temperature Range ◽  
Maximum Inhibition ◽  
A Chain

The thermal decomposition of dimethyl ether, inhibited by nitric oxide and by propylene, was studied in the temperature range of 500 to 600 °C. About 1.5 mm of nitric oxide gave maximal inhibition, the rate then being approximately 8% of the uninhibited rate. With propylene, approximately 70 mm gave maximal inhibition, the rate being slightly higher than that using nitric oxide (~12.5% of the uninhibited rate). In both cases the degree of inhibition was independent of the ether pressure. In the maximally inhibited regions both reactions are three-halves order with respect to ether pressure. As the pressure of nitric oxide was increased beyond 10–15 mm, the overall rate increased, and in this region the reaction is first order with respect to both nitric oxide and ether. A 50:50 mixture of CH3OCH3 and CD3OCD3, with enough NO to ensure maximum inhibition, was pyrolyzed. Even at very low percentage decomposition the CD3H/CD4 ratio was approximately the same as that in the uninhibited decomposition, proving that the inhibited reaction is largely a chain process. Detailed inhibition mechanisms are proposed in which the inhibitor is involved both in initiation and termination reactions.

CHANGES OF NITRIC OXIDE SYNTHASE AND HYDROGEN SULFIDE IN BLOOD LYMPHOCYTES IN THE ACUTE PERIOD OF POLYTRAUMA

2019 ◽  
Vol 72 (8) ◽  
pp. 1473-1476
Author(s):  
Nataliya Matolinets ◽  
Helen Sklyarova ◽  
Eugene Sklyarov ◽  
Andrii Netliukh
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Sulfide ◽  
Tissue Injury ◽  
Traumatic Injury ◽  
Cell Types ◽  
No Synthase ◽  
Septic Complications ◽  
Acute Period ◽  
Gaseous Transmitters ◽  
The Moment

Introduction: Polytrauma patients have high risk of shock, septic complications and death during few years of follow-up. In recent years a lot of attention is paid to gaseous transmitters, among which are nitrogen oxide (NO) and hydrogen sulfide (H2S). It is known that the rise of NO and its metabolites levels occurs during the acute period of polytrauma. Nitric oxide and hydrogen sulfide are produced in different cell types, among which are lymphocytes. The aim: To investigate the levels of NO, NOS, iNOS, еNOS, H2S in lymphocytes lysate in patients at the moment of hospitalization and 24 hours after trauma. Materials and methods: We investigated the levels of NO, NO-synthase, inducible NO-synthase, endothelial NO-synthase, H2S in lymphocytes lysate in patients at the moment of hospitalization and 24 hours after trauma. Results: The study included 20 patients with polytrauma who were treated in the intensive care unit (ICU) of the Lviv Emergency Hospital. Tissue injury was associated with an increased production of NO, NOS, iNOS, еNOS during the acute period of polytrauma. At the same time, the level of H2S decreased by the end of the first day of traumatic injury. Conclusions: In acute period of polytrauma, significant increasing of iNOS and eNOS occurs with percentage prevalence of iNOS over eNOS on the background of H2S decreasing.

The Role of Reactive Oxygen Species, Kinases, Hydrogen Sulfide, and Nitric Oxide in the Regulation of Autophagy and Their Impact on Ischemia and Reperfusion Injury in the Heart

2020 ◽  
Vol 16 ◽  
Author(s):  
Andrey Krylatov ◽  
Leonid Maslov ◽  
Sergey Y. Tsibulnikov ◽  
Nikita Voronkov ◽  
Alla Boshchenko ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Hydrogen Sulfide ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Ischemia And Reperfusion ◽  
Oxygen Species ◽  
Ischemia And Reperfusion Injury ◽  
Adaptive Process

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.

Hydrogen Sulfide in Physiological and Pathological Mechanisms in Brain

2018 ◽  
Vol 17 (9) ◽  
pp. 654-670 ◽  
Author(s):  
Mohit Kumar ◽  
Rajat Sandhir
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Hydrogen Sulfide ◽  
Neurodegenerative Disorders ◽  
Neurological Disorders ◽  
Scientific Community ◽  
Molecular Targets ◽  
Long Term Potentiation ◽  
Term Potentiation

Background & Objective: Hydrogen sulfide [H2S] has been widely known as a toxic gas for more than 300 years in the scientific community. However, the understanding about this small molecule has changed after the discovery of involvement of H2S in physiological and pathological mechanisms in brain. H2S is a third gasotransmitter and neuromodulator after carbon monoxide [CO] and nitric oxide [NO]. H2S plays an important role in memory and cognition by regulating long-term potentiation [LTP] and calcium homeostasis in neuronal cells. The disturbances in endogenous H2S levels and trans-sulfuration pathway have been implicated in neurodegenerative disorders like Alzheimer’s disease, Parkinson disease, stroke and traumatic brain injury. According to the results obtained from various studies, H2S not only behaves as neuromodulator but also is a potent antioxidant, anti-inflammatory and anti-apoptotic molecule suggesting its neuroprotective potential. Conclusion: Recently, there is an increased interest in developing H2S releasing pharmaceuticals to target various neurological disorders. This review covers the information about the involvement of H2S in neurodegenerative diseases, its molecular targets and its role as potential therapeutic molecule.

scholarly journals Hydrogen Sulfide Increases Nitric Oxide Production and Subsequent S-Nitrosylation in Endothelial Cells

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Ping-Ho Chen ◽  
Yaw-Syan Fu ◽  
Yun-Ming Wang ◽  
Kun-Han Yang ◽  
Danny Ling Wang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Hydrogen Sulfide ◽  
Protein Kinase ◽  
Fluorescent Probe ◽  
Acid Methyl Ester ◽  
High Specificity ◽  
Protein S ◽  
No Production ◽  
No Donor

Hydrogen sulfide (H2S) and nitric oxide (NO), two endogenous gaseous molecules in endothelial cells, got increased attention with respect to their protective roles in the cardiovascular system. However, the details of the signaling pathways between H2S and NO in endothelia cells remain unclear. In this study, a treatment with NaHS profoundly increased the expression and the activity of endothelial nitric oxide synthase. Elevated gaseous NO levels were observed by a novel and specific fluorescent probe, 5-amino-2-(6-hydroxy-3-oxo-3H-xanthen-9-yl)benzoic acid methyl ester (FA-OMe), and quantified by flow cytometry. Further study indicated an increase of upstream regulator for eNOS activation, AMP-activated protein kinase (AMPK), and protein kinase B (Akt). By using a biotin switch, the level of NO-mediated protein S-nitrosylation was also enhanced. However, with the addition of the NO donor, NOC-18, the expressions of cystathionine-γ-lyase, cystathionine-β-synthase, and 3-mercaptopyruvate sulfurtransferase were not changed. The level of H2S was also monitored by a new designed fluorescent probe, 4-nitro-7-thiocyanatobenz-2-oxa-1,3-diazole (NBD-SCN) with high specificity. Therefore, NO did not reciprocally increase the expression of H2S-generating enzymes and the H2S level. The present study provides an integrated insight of cellular responses to H2S and NO from protein expression to gaseous molecule generation, which indicates the upstream role of H2S in modulating NO production and protein S-nitrosylation.

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