Role of Hydrogen Sulfide in NRF2- and Sirtuin-Dependent Maintenance of Cellular Redox Balance

Abstract

Hydrogen sulfide (H2S) has arisen as a critical gasotransmitter signaling molecule modulating cellular biological events related to health and diseases in heart, brain, liver, vascular systems and immune response. Three enzymes mediate the endogenous production of H2S: cystathione β-synthase (CBS), cystathione γ-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3-MST). CBS and CSE localizations are organ-specific. 3-MST is a mitochondrial and cytosolic enzyme. The generation of H2S is firmly regulated by these enzymes under normal physiological conditions. Recent studies have highlighted the role of H2S in cellular redox homeostasis, as it displays significant antioxidant properties. H2S exerts antioxidant effects through several mechanisms, such as quenching reactive oxygen species (ROS) and reactive nitrogen species (RNS), by modulating cellular levels of glutathione (GSH) and thioredoxin (Trx-1) or increasing expression of antioxidant enzymes (AOE), by activating the transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF2). H2S also influences the activity of the histone deacetylase protein family of sirtuins, which plays an important role in inhibiting oxidative stress in cardiomyocytes and during the aging process by modulating AOE gene expression. This review focuses on the role of H2S in NRF2 and sirtuin signaling pathways as they are related to cellular redox homeostasis.

Antioxidant Defence Systems and Oxidative Stress in Poultry Biology: An Update

“…These protective systems control free radical (i.e., ROS and RNS) production and maintain redox (antioxidant/prooxidant) balance. Indeed, the redox balance in the cell/whole body is shown to be responsible for a regulation of an array of various physiological/biochemical processes, including cell signalling, gene expression and homeostasis maintenance [3,4]. In our previous publications [5][6][7], the concept of the antioxidant defence network in poultry was developed and validated.…”

Novel approach for discrimination of eosinophilic granulocytes and evaluation of their surface receptors in a multicolor fluorescent histological assessment

“…Several scientific groups confirm that mitochondria, important organelles in different cells, play a crucial role in the maintenance of redox balan ce, energy biosynthesis, antioxidant activities and cellular homeostasis [5,15,30]. Recent studies have implicated the activation of mitochondrial dysfunction in the pathogenesis of several comorbid pathologies (non-alcoholic fatty liver disease, cardiovascular disease, obesity) associated with RAT, as it contributes to the perpetuation of the oxidative stress and metaflammation (a metabolic inflammatory process) [4,19]. Moreover, according to the recent view, AM has worse blood capillary supply and intrinsically low antioxidant enzyme defense that make it vulnerable to hypoxia and free radical damage, the main triggers for oxidative stress injuries [31].…”

“…Treatment for 9 days with H 2 S compounds (NaHS, H 2 S-ASA or ASA+NaHS) showed a downward trend of lowering the level of TBARS in experimental groups exposed to HFD and WIS. The administration of H 2 S-ASA decreased the levels of TBARS by approxi mately half (P < 0.05), NaHS -by 30% (P < 0.001) and (6) is vacuolated cytoplasm (5) with a large number of ring-like mitochondria (4) and digital-shaped invagination of the plasmalemma (7). 10000x magnification.…”

“…Except for rat groups with H 2 S pre-treatment by NaHS, H 2 S-ASA (ATB-340), or ASA+NaHS where CSE and CBS were up-regulated (4), fat droplets (5) and mitochondria with signs of self-destruction (6) are visible. 10000x magnification; (C) Fragment of adipocyte, with large fat droplet in adipocyte (4) and hemocapillary (7). Magnification 4000x; and (D) Fragment of adipocyte with peripherally located mitochondria showing signs of self-destruction (6), cell nucleus (8) with heterochromatin, and mast cell (9).…”

“…Recently, it was shown that oxidative stress related to metabolic responses linked to high carbohydrate intake can modulate DNA methylation and reduce the NAD+ dependent deacetylase SIRT1 that controls mitochondrial respiration and reactive oxygen species production, causing inflammatory responses, lipid storage, and changes in telomerase activity [4]. In this context, HFD that decreases NAD + content can negatively regulate sirtuin activity, and could induce metaflammation (metabolic inflammation), a low-grade chronic sterile inflammation primarily driven by endogenous signals which is suggested as one of the central mechanisms of obesity.…”