scholarly journals The role of gas mediators of nitrogen (II) oxide and hydrogen sulfide in the development of pathochemical changes in the mucous membrane of rats at water-immobilization and adrenaline-induced stress modeling

2020 ◽  
Vol 22 (97) ◽  
pp. 88-94
Author(s):  
N. Motko ◽  
I. Fomenko ◽  
O. Vozna
Keyword(s):  
Hydrogen Sulfide ◽  
Mucous Membrane ◽  
Digestive System ◽  
Molecular Mechanisms ◽  
Ulcer Formation ◽  
Myeloperoxidase Activity ◽  
Duration Of Action ◽  
Stress Modeling ◽  
Induced Stress

Acute and prolonged psycho-emotional overstrain, i.e. stress, are the most frequent factors of ulcer formation in the digestive system. Therefore, the study of molecular mechanisms of stress impact is one of the most promising directions of modern experimental gastroenterology. However, the features of its molecular-biochemical action on the metabolic processes in the digestive system remain insufficiently studied. In this regard, we performed a comparative analysis of changes in indicators of systems of gas mediators of nitrogen (II) oxide and hydrogen sulfide synthesis at water-immobilization and adrenaline-induced stress modeling in experiments on white non-linear rats. Water-immobilization stress (WIS) was modelled by immobilizing animals in a plastic container, and adrenaline-induced stress (AIS) was modelled by injecting adrenaline at a dose of 2 mg/kg intraperitoneally. Modelling WIS caused formation of erosion and spot hemorrhage, located mainly along the folds of the fundus of the stomach. In this case, more noticeable changes were observed in the 5-hour WSI model. Injecting adrenaline at AIS model caused development of structural-hemorrhagic damage in the pyloric part and body of the stomach. The biochemical response to stress is complex, and the release of catecholamines is not the only case of stress. The synthesis of hormones such as glucagon, somatotropin and renin is activated. However, the most important role is played by cortisol, which level of growth in blood is measured to assess the degree of stress development. In our studies, changes in cortisol level in blood under different types of stress modeling (WIS and AIS) had their own peculiarities: at WIS conditions cortisol concentration increased sharply and remained high for 5 hours, while adrenaline did not cause the growth of this “stress hormone”. In our studies, in both models of stress-induced ulcerogenesis there were significant changes to the content of H2S and NO, that confirms the significant role of these substances in development and progression of ulcerogenesis in the digestive system. Thus, H2S concentration decreased at WIS and AIS. There is a significant increase in nitrogen oxide production in both WIS with different duration of action and AIS, which is caused by multiple activation of the inducible isoform of NO-synthase. Therefore, in experimental stress-induced ulcerogenesis, the metabolism of L-arginine in the mucous membrane of stomach is equally shifted towards the formation of NO, that under conditions of strengthening of free radical processes serves as a prerequisite for activation of oxidative-nitric processes and leads to the formation of structural-hemorrhagic damage to the surface of the mucous membrane of stomach. Our studies also show that ulcerative damage to the mucous membrane of stomach in all the types of studied stress was accompanied by an increase in myeloperoxidase activity, indicating an increase in permeability of hemocapillaries due to the development of the inflammatory process.

scholarly journals The Potential of Hydrogen Sulfide Donors in Treating Cardiovascular Diseases

2021 ◽  
Vol 22 (4) ◽  
pp. 2194
Author(s):  
Yi-Zhen Wang ◽  
Ebenezeri Erasto Ngowi ◽  
Di Wang ◽  
Hui-Wen Qi ◽  
Mi-Rong Jing ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Cardiovascular Diseases ◽  
Molecular Mechanisms ◽  
Heart Function ◽  
Cell Types ◽  
Special Focus ◽  
Protective Effects ◽  
Improve Heart Function ◽  
Different Cell Types

Hydrogen sulfide (H2S) has long been considered as a toxic gas, but as research progressed, the idea has been updated and it has now been shown to have potent protective effects at reasonable concentrations. H2S is an endogenous gas signaling molecule in mammals and is produced by specific enzymes in different cell types. An increasing number of studies indicate that H2S plays an important role in cardiovascular homeostasis, and in most cases, H2S has been reported to be downregulated in cardiovascular diseases (CVDs). Similarly, in preclinical studies, H2S has been shown to prevent CVDs and improve heart function after heart failure. Recently, many H2S donors have been synthesized and tested in cellular and animal models. Moreover, numerous molecular mechanisms have been proposed to demonstrate the effects of these donors. In this review, we will provide an update on the role of H2S in cardiovascular activities and its involvement in pathological states, with a special focus on the roles of exogenous H2S in cardiac protection.

scholarly journals Emerging role of hydrogen sulfide-microRNA crosstalk in cardiovascular diseases

2016 ◽  
Vol 310 (7) ◽  
pp. H802-H812 ◽  
Author(s):  
Bryan T. Hackfort ◽  
Paras K. Mishra
Keyword(s):  
Heart Failure ◽  
Hydrogen Sulfide ◽  
Cardiac Remodeling ◽  
Molecular Mechanisms ◽  
High Dose ◽  
Physiological Level ◽  
Cellular Processes ◽  
Regulatory Rnas ◽  
Apoptosis And Inflammation

Despite an obnoxious smell and toxicity at a high dose, hydrogen sulfide (H2S) is emerging as a cardioprotective gasotransmitter. H2S mitigates pathological cardiac remodeling by regulating several cellular processes including fibrosis, hypertrophy, apoptosis, and inflammation. These encouraging findings in rodents led to initiation of a clinical trial using a H2S donor in heart failure patients. However, the underlying molecular mechanisms by which H2S mitigates cardiac remodeling are not completely understood. Empirical evidence suggest that H2S may regulate signaling pathways either by directly influencing a gene in the cascade or interacting with nitric oxide (another cardioprotective gasotransmitter) or both. Recent studies revealed that H2S may ameliorate cardiac dysfunction by up- or downregulating specific microRNAs. MicroRNAs are noncoding, conserved, regulatory RNAs that modulate gene expression mostly by translational inhibition and are emerging as a therapeutic target for cardiovascular disease (CVD). Few microRNAs also regulate H2S biosynthesis. The inter-regulation of microRNAs and H2S opens a new avenue for exploring the H2S-microRNA crosstalk in CVD. This review embodies regulatory mechanisms that maintain the physiological level of H2S, exogenous H2S donors used for increasing the tissue levels of H2S, H2S-mediated regulation of CVD, H2S-microRNAs crosstalk in relation to the pathophysiology of heart disease, clinical trials on H2S, and future perspectives for H2S as a therapeutic agent for heart failure.

scholarly journals Myostatin deficiency not only prevents muscle wasting but also improves survival in septic mice.

2020 ◽  
Author(s):  
Masayuki Kobayashi ◽  
Shingo Kasamatsu ◽  
Shohei Shinozaki ◽  
Shingo Yasuhara ◽  
Masao Kaneki
Keyword(s):  
Molecular Mechanisms ◽  
Muscle Wasting ◽  
Plasma Concentrations ◽  
Kidney Injury ◽  
Major Complication ◽  
Neutrophil Infiltration ◽  
Myeloperoxidase Activity ◽  
Bacterial Clearance ◽  
Liver And Kidney

Sepsis remains a leading cause of mortality in critically ill patients. Muscle wasting is a major complication of sepsis and negatively affects clinical outcomes. Despite intense investigation for many years, the molecular mechanisms underlying sepsis-related muscle wasting are not fully understood. In addition, a potential role of muscle wasting in disease development of sepsis has not been studied. Myostatin is a myokine that downregulates skeletal muscle mass. We studied the effects of myostatin deficiency on muscle wasting and other clinically relevant outcomes, including mortality and bacterial clearance, in mice. Myostatin deficiency prevented muscle atrophy along with inhibition of increases in MuRF-1 and atrogin-1 expression and phosphorylation of STAT3 (major players of muscle wasting) in septic mice. Moreover, myostatin deficiency improved survival and bacterial clearance of septic mice. Sepsis-induced liver dysfunction, acute kidney injury and neutrophil infiltration into the liver and kidney were consistently mitigated by myostatin deficiency, as indicated by plasma concentrations of AST, ALT and NGAL and myeloperoxidase activity in the organs. Myostatin deficiency also inhibited sepsis-induced increases in plasma HMGB1 and MIC-1/GDF-15 concentrations. These results indicate that myostatin plays an important role not only in muscle wasting but also in other clinically relevant outcomes in septic mice. Furthermore, our data raise the possibility that muscle wasting may not be simply a complication, but myostatin-mediated muscle cachexia and related changes in muscle may actually drive the development of sepsis as well.

scholarly journals Synergisms, Discrepancies and Interactions between Hydrogen Sulfide and Carbon Monoxide in the Gastrointestinal and Digestive System Physiology, Pathophysiology and Pharmacology

Biomolecules ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 445 ◽  
Author(s):  
Urszula Głowacka ◽  
Tomasz Brzozowski ◽  
Marcin Magierowski
Keyword(s):  
Carbon Monoxide ◽  
Hydrogen Sulfide ◽  
Digestive System ◽  
In Vitro Models ◽  
Biological Functions ◽  
Systems Physiology ◽  
System Physiology

Endogenous gas transmitters, hydrogen sulfide (H2S), carbon monoxide (CO) and nitric oxide (NO) are important signaling molecules known to exert multiple biological functions. In recent years, the role of H2S, CO and NO in regulation of cardiovascular, neuronal and digestive systems physiology and pathophysiology has been emphasized. Possible link between these gaseous mediators and multiple diseases as well as potential therapeutic applications has attracted great attention from biomedical scientists working in many fields of biomedicine. Thus, various pharmacological tools with ability to release CO or H2S were developed and implemented in experimental animal in vivo and in vitro models of many disorders and preliminary human studies. This review was designed to review signaling functions, similarities, dissimilarities and a possible cross-talk between H2S and CO produced endogenously or released from chemical donors, with special emphasis on gastrointestinal digestive system pathologies prevention and treatment.

scholarly journals Molecular Functions of Hydrogen Sulfide in Cancer

2021 ◽  
Vol 28 (3) ◽  
pp. 437-456
Author(s):  
Rodney E. Shackelford ◽  
Islam Z. Mohammad ◽  
Andrew T. Meram ◽  
David Kim ◽  
Fawaz Alotaibi ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Molecular Mechanisms ◽  
Chemotherapy Resistance ◽  
Tumor Stage ◽  
Enzyme Expression ◽  
Mesenchymal Transition ◽  
Repair Protein ◽  
Dna Repair Protein ◽  
Worse Prognosis

Hydrogen sulfide (H2S) is a gasotransmitter that exerts a multitude of functions in both physiologic and pathophysiologic processes. H2S-synthesizing enzymes are increased in a variety of human malignancies, including colon, prostate, breast, renal, urothelial, ovarian, oral squamous cell, and thyroid cancers. In cancer, H2S promotes tumor growth, cellular and mitochondrial bioenergetics, migration, invasion, angiogenesis, tumor blood flow, metastasis, epithelia–mesenchymal transition, DNA repair, protein sulfhydration, and chemotherapy resistance Additionally, in some malignancies, increased H2S-synthesizing enzyme expression correlates with a worse prognosis and a higher tumor stage. Here we review the role of H2S in cancer, with an emphasis on the molecular mechanisms by which H2S promotes cancer development, progression, dedifferentiation, and metastasis.

Role of hydrogen sulfide in cecal ligation and puncture-induced sepsis in the mouse

2006 ◽  
Vol 290 (6) ◽  
pp. L1193-L1201 ◽  
Author(s):  
Huili Zhang ◽  
Liang Zhi ◽  
Philip K. Moore ◽  
Madhav Bhatia
Keyword(s):  
Hydrogen Sulfide ◽  
Systemic Inflammation ◽  
Mammalian Cells ◽  
Cecal Ligation ◽  
Organ Injury ◽  
Sham Operation ◽  
Myeloperoxidase Activity ◽  
Cecal Ligation And Puncture ◽  
Sodium Hydrosulfide

Endogenous hydrogen sulfide (H2S) is naturally synthesized in various types of mammalian cells from l-cysteine in a reaction catalyzed by two enzymes, cystathionine-γ-lyase (CSE) and/or cystathionine-β-synthase. The latest studies have implied that H2S functions as a vasodilator and neurotransmitter. However, so far there is little information about the role played by H2S in systemic inflammation such as sepsis. Thus the aim of this study was to investigate the potential role of endogenous H2S in cecal ligation and puncture (CLP)-induced sepsis. Male Swiss mice were subjected to CLP-induced sepsis and treated with saline (ip), dl-propargylglycine (PAG, 50 mg/kg ip), a CSE inhibitor, or sodium hydrosulfide (NaHS; 10 mg/kg ip). PAG was administered either 1 h before or 1 h after the induction of sepsis, whereas NaHS was given at the same time of CLP. CLP-induced sepsis significantly increased the plasma H2S level and the liver H2S synthesis 8 h after CLP compared with sham operation. Induction of sepsis also resulted in a significant upregulation of CSE mRNA in liver. On the other hand, prophylactic as well as therapeutic administration of PAG significantly reduced sepsis-associated systemic inflammation, as evidenced by myeloperoxidase activity and histological changes in lung and liver, and attenuated the mortality of CLP-induced sepsis. Injection of NaHS significantly aggravated sepsis-associated systemic inflammation. Therefore, the effect of inhibition of H2S formation and administration of NaHS suggests that H2S plays a proinflammatory role in regulating the severity of sepsis and associated organ injury.

How do histone modifications contribute to transgenerational epigenetic inheritance in C. elegans?

2020 ◽  
Vol 48 (3) ◽  
pp. 1019-1034 ◽  
Author(s):  
Rachel M. Woodhouse ◽  
Alyson Ashe
Keyword(s):  
Histone Modifications ◽  
Molecular Mechanisms ◽  
Epigenetic Inheritance ◽  
Nematode Caenorhabditis Elegans ◽  
Histone Methyltransferases ◽  
Transgenerational Epigenetic Inheritance ◽  
C Elegans ◽  
Recent Developments ◽  
Gene Regulatory

Gene regulatory information can be inherited between generations in a phenomenon termed transgenerational epigenetic inheritance (TEI). While examples of TEI in many animals accumulate, the nematode Caenorhabditis elegans has proven particularly useful in investigating the underlying molecular mechanisms of this phenomenon. In C. elegans and other animals, the modification of histone proteins has emerged as a potential carrier and effector of transgenerational epigenetic information. In this review, we explore the contribution of histone modifications to TEI in C. elegans. We describe the role of repressive histone marks, histone methyltransferases, and associated chromatin factors in heritable gene silencing, and discuss recent developments and unanswered questions in how these factors integrate with other known TEI mechanisms. We also review the transgenerational effects of the manipulation of histone modifications on germline health and longevity.

Mesophyll conductance: the leaf corridors for photosynthesis

2020 ◽  
Vol 48 (2) ◽  
pp. 429-439 ◽  
Author(s):  
Jorge Gago ◽  
Danilo M. Daloso ◽  
Marc Carriquí ◽  
Miquel Nadal ◽  
Melanie Morales ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Main Role ◽  
Mesophyll Conductance ◽  
Future Studies ◽  
Cell Structures ◽  
Leaf Tissues ◽  
Change Framework ◽  
Chloroplast Stroma

Besides stomata, the photosynthetic CO2 pathway also involves the transport of CO2 from the sub-stomatal air spaces inside to the carboxylation sites in the chloroplast stroma, where Rubisco is located. This pathway is far to be a simple and direct way, formed by series of consecutive barriers that the CO2 should cross to be finally assimilated in photosynthesis, known as the mesophyll conductance (gm). Therefore, the gm reflects the pathway through different air, water and biophysical barriers within the leaf tissues and cell structures. Currently, it is known that gm can impose the same level of limitation (or even higher depending of the conditions) to photosynthesis than the wider known stomata or biochemistry. In this mini-review, we are focused on each of the gm determinants to summarize the current knowledge on the mechanisms driving gm from anatomical to metabolic and biochemical perspectives. Special attention deserve the latest studies demonstrating the importance of the molecular mechanisms driving anatomical traits as cell wall and the chloroplast surface exposed to the mesophyll airspaces (Sc/S) that significantly constrain gm. However, even considering these recent discoveries, still is poorly understood the mechanisms about signaling pathways linking the environment a/biotic stressors with gm responses. Thus, considering the main role of gm as a major driver of the CO2 availability at the carboxylation sites, future studies into these aspects will help us to understand photosynthesis responses in a global change framework.

The Role of the Endothelium in Premature Atherosclerosis: Molecular Mechanisms

2020 ◽  
Vol 27 (7) ◽  
pp. 1041-1051 ◽  
Author(s):  
Michael Spartalis ◽  
Eleftherios Spartalis ◽  
Antonios Athanasiou ◽  
Stavroula A. Paschou ◽  
Christos Kontogiannis ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Low Density Lipoprotein ◽  
Critical Role ◽  
Density Lipoprotein ◽  
Number Of Genes ◽  
Causes Of Mortality ◽  
Artery Disease ◽  
Genetic And Environmental Factors ◽  
Made In

Atherosclerotic disease is still one of the leading causes of mortality. Atherosclerosis is a complex progressive and systematic artery disease that involves the intima of the large and middle artery vessels. The inflammation has a key role in the pathophysiological process of the disease and the infiltration of the intima from monocytes, macrophages and T-lymphocytes combined with endothelial dysfunction and accumulated oxidized low-density lipoprotein (LDL) are the main findings of atherogenesis. The development of atherosclerosis involves multiple genetic and environmental factors. Although a large number of genes, genetic polymorphisms, and susceptible loci have been identified in chromosomal regions associated with atherosclerosis, it is the epigenetic process that regulates the chromosomal organization and genetic expression that plays a critical role in the pathogenesis of atherosclerosis. Despite the positive progress made in understanding the pathogenesis of atherosclerosis, the knowledge about the disease remains scarce.

Sign in / Sign up

Export Citation Format

Share Document