scholarly journals Expression of the trxC Gene of Rhodobacter capsulatus: Response to Cellular Redox Status Is Mediated by the Transcriptional Regulator OxyR

2006 ◽  
Vol 188 (21) ◽  
pp. 7689-7695 ◽  
Author(s):  
Tanja Zeller ◽  
Kuanyu Li ◽  
Gabriele Klug
Keyword(s):  
Redox Regulation ◽  
Molecular Mechanisms ◽  
Rhodobacter Capsulatus ◽  
Transcriptional Regulator ◽  
Redox Status ◽  
Cellular Functions ◽  
Cellular Redox

ABSTRACT Despite the importance of thioredoxins in cellular functions, little is known about the regulation of trx genes. To understand the molecular mechanisms involved in the regulation of the Rhodobacter capsulatus trxC gene, the expression of this gene was investigated. We describe OxyR-dependent redox regulation of the trxC gene that adjusts the levels of thioredoxins in the cell.

scholarly journals Redox Potential of Antioxidants in Cancer Progression and Prevention

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1156
Author(s):  
Sajan George ◽  
Heidi Abrahamse
Keyword(s):  
Oxidative Stress ◽  
Cancer Progression ◽  
Natural Antioxidants ◽  
Redox Balance ◽  
Redox Status ◽  
Enzyme Activation ◽  
Metabolic Reprogramming ◽  
Cellular Functions ◽  
Cellular Redox ◽  
The Right

The benevolent and detrimental effects of antioxidants are much debated in clinical trials and cancer research. Several antioxidant enzymes and molecules are overexpressed in oxidative stress conditions that can damage cellular proteins, lipids, and DNA. Natural antioxidants remove excess free radical intermediates by reducing hydrogen donors or quenching singlet oxygen and delaying oxidative reactions in actively growing cancer cells. These reducing agents have the potential to hinder cancer progression only when administered at the right proportions along with chemo-/radiotherapies. Antioxidants and enzymes affect signal transduction and energy metabolism pathways for the maintenance of cellular redox status. A decline in antioxidant capacity arising from genetic mutations may increase the mitochondrial flux of free radicals resulting in misfiring of cellular signalling pathways. Often, a metabolic reprogramming arising from these mutations in metabolic enzymes leads to the overproduction of so called ’oncometabolites’ in a state of ‘pseudohypoxia’. This can inactivate several of the intracellular molecules involved in epigenetic and redox regulations, thereby increasing oxidative stress giving rise to growth advantages for cancerous cells. Undeniably, these are cell-type and Reactive Oxygen Species (ROS) specific, which is manifested as changes in the enzyme activation, differences in gene expression, cellular functions as well as cell death mechanisms. Photodynamic therapy (PDT) using light-activated photosensitizing molecules that can regulate cellular redox balance in accordance with the changes in endogenous ROS production is a solution for many of these challenges in cancer therapy.

scholarly journals Post-Translational S-Nitrosylation of Proteins in Regulating Cardiac Oxidative Stress

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1051 ◽  
Author(s):  
Xiaomeng Shi ◽  
Hongyu Qiu
Keyword(s):  
Therapeutic Potential ◽  
Heart Diseases ◽  
Redox Homeostasis ◽  
Redox Status ◽  
Cardiac Protection ◽  
Cellular Functions ◽  
Post Translational Modifications ◽  
Cellular Redox ◽  
Novel Therapeutic Strategies

Like other post-translational modifications (PTMs) of proteins, S-nitrosylation has been considered a key regulatory mechanism of multiple cellular functions in many physiological and disease conditions. Emerging evidence has demonstrated that S-nitrosylation plays a crucial role in regulating redox homeostasis in the stressed heart, leading to discoveries in the mechanisms underlying the pathogenesis of heart diseases and cardiac protection. In this review, we summarize recent studies in understanding the molecular and biological basis of S-nitrosylation, including the formation, spatiotemporal specificity, homeostatic regulation, and association with cellular redox status. We also outline the currently available methods that have been applied to detect S-nitrosylation. Additionally, we synopsize the up-to-date studies of S-nitrosylation in various cardiac diseases in humans and animal models, and we discuss its therapeutic potential in cardiac protection. These pieces of information would bring new insights into understanding the role of S-nitrosylation in cardiac pathogenesis and provide novel avenues for developing novel therapeutic strategies for heart diseases.

scholarly journals Temporal profiling of redox-dependent heterogeneity in single cells

2017 ◽  
Author(s):  
Meytal Radzinski ◽  
Rosi Fasler ◽  
Ohad Yogev ◽  
William Breuer ◽  
Nadav Shai ◽  
...  
Keyword(s):  
Single Cells ◽  
Redox Homeostasis ◽  
Redox Status ◽  
Yeast Cells ◽  
Protein Homeostasis ◽  
Cellular Functions ◽  
Defense Proteins ◽  
Cellular Redox ◽  
Oxidation Status ◽  
Logarithmic Growth

AbstractCellular redox status affects diverse cellular functions, including proliferation, protein homeostasis, and aging. Thus, individual differences in redox status can give rise to distinct sub-populations even among cells with identical genetic backgrounds. Here, we have created a novel methodology to track redox status at single cell resolution using the redox-sensitive probe roGFP. Our method allows identification and sorting of sub-populations with different oxidation levels in either the cytosol, mitochondria or peroxisomes. Using this approach we defined redox-dependent heterogeneity of yeast cells, and characterized growth, as well as proteomic and transcriptomic profiles of subpopulations of cells that differ in their redox status, but are similar in age. We report that, starting in late logarithmic growth, cells of the same age have a bi-modal distribution of oxidation status. A comparative proteomic analysis between these populations identified three key proteins, Hsp30, Dhh1, and Pnc1, which affect basal oxidation levels and may serve as first line of defense proteins in redox homeostasis.

H2S signaling in redox regulation of cellular functions

2013 ◽  
Vol 91 (1) ◽  
pp. 8-14 ◽  
Author(s):  
Youngjun Ju ◽  
Weihua Zhang ◽  
Yanxi Pei ◽  
Guangdong Yang
Keyword(s):  
Mammalian Cells ◽  
Redox Regulation ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Redox Homeostasis ◽  
Therapeutic Interventions ◽  
Post Translational Modification ◽  
Cellular Functions ◽  
Future Design ◽  
Cellular Effects

Hydrogen sulfide (H2S) is traditionally recognized as a toxic gas with a rotten-egg smell. In just the last few decades, H2S has been found to be one of a family of gasotransmitters, together with nitric oxide and carbon monoxide, and various physiologic effects of H2S have been reported. Among the most acknowledged molecular mechanisms for the cellular effects of H2S is the regulation of intracellular redox homeostasis and post-translational modification of proteins through S-sulfhydration. On the one side, H2S can promote an antioxidant effect and is cytoprotective; on the other side, H2S stimulates oxidative stress and is cytotoxic. This review summarizes our current knowledge of the antioxidant versus pro-oxidant effects of H2S in mammalian cells and describes the Janus-faced properties of this novel gasotransmitter. The redox regulation for the cellular effects of H2S through S-sulfhydration and the role of H2S in glutathione generation is also recapitulated. A better understanding of H2S-regualted redox homeostasis will pave the way for future design of novel pharmacological and therapeutic interventions for various diseases.

scholarly journals Temporal profiling of redox-dependent heterogeneity in single cells

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Meytal Radzinski ◽  
Rosi Fassler ◽  
Ohad Yogev ◽  
William Breuer ◽  
Nadav Shai ◽  
...  
Keyword(s):  
Single Cells ◽  
Redox Homeostasis ◽  
Redox Status ◽  
Yeast Cells ◽  
Protein Homeostasis ◽  
Cellular Functions ◽  
Defense Proteins ◽  
Cellular Redox ◽  
Oxidation Status ◽  
Logarithmic Growth

Cellular redox status affects diverse cellular functions, including proliferation, protein homeostasis, and aging. Thus, individual differences in redox status can give rise to distinct sub-populations even among cells with identical genetic backgrounds. Here, we have created a novel methodology to track redox status at single cell resolution using the redox-sensitive probe Grx1-roGFP2. Our method allows identification and sorting of sub-populations with different oxidation levels in either the cytosol, mitochondria or peroxisomes. Using this approach, we defined a redox-dependent heterogeneity of yeast cells and characterized growth, as well as proteomic and transcriptomic profiles of distinctive redox subpopulations. We report that, starting in late logarithmic growth, cells of the same age have a bi-modal distribution of oxidation status. A comparative proteomic analysis between these populations identified three key proteins, Hsp30, Dhh1, and Pnc1, which affect basal oxidation levels and may serve as first line of defense proteins in redox homeostasis.

scholarly journals Redox regulation by TXNRD3 during epididymal maturation underlies capacitation-associated mitochondrial activation and sperm motility in mice

2021 ◽  
Author(s):  
Huafeng Wang ◽  
Qianhui Dou ◽  
Kyung Jo Jung ◽  
Jungmin Choi ◽  
Vadim N. Gladyshev ◽  
...  
Keyword(s):  
Redox Regulation ◽  
Molecular Mechanisms ◽  
Redox Homeostasis ◽  
Thioredoxin Reductase ◽  
Redox Status ◽  
Male Reproduction ◽  
Sperm Maturation ◽  
Epididymal Maturation ◽  
Sperm Development ◽  
Sheath Formation

During epididymal transit, redox remodeling protects mammalian spermatozoa, preparing them for survival in the subsequent journey to fertilization. However, molecular mechanisms of the redox regulation in sperm development and maturation remain largely elusive. In this study, we report thioredoxin reductase 3 (TXNRD3) - a thioredoxin reductase family member particularly abundant in elongating spermatids at the site of mitochondrial sheath formation - contributes to regulate redox homeostasis in male reproduction. Using Txnrd3-/- mice, our biochemical, ultrastructural, and live cell imaging analyses revealed impairments in sperm morphology and motility in absence of TXNRD3. Absence of TXNRD3 alters redox status in both the head and tail during sperm maturation and capacitation, resulting in defective mitochondrial ultrastructure and activity under capacitating conditions. These findings provide insights into molecular mechanisms of redox homeostasis and bioenergetics during sperm maturation, capacitation, and fertilization.

scholarly journals The Secret Life of NAD+: An Old Metabolite Controlling New Metabolic Signaling Pathways

2010 ◽  
Vol 31 (2) ◽  
pp. 194-223 ◽  
Author(s):  
Riekelt H. Houtkooper ◽  
Carles Cantó ◽  
Ronald J. Wanders ◽  
Johan Auwerx
Keyword(s):  
Redox Status ◽  
Cellular Functions ◽  
Cellular Redox ◽  
Life Span Extension ◽  
Nad Metabolism ◽  
Wide Range ◽  
Dependent Protein ◽  
Physiological Impact ◽  
Cellular Compartmentalization ◽  
Reduced Forms

A century after the identification of a coenzymatic activity for NAD+, NAD+ metabolism has come into the spotlight again due to the potential therapeutic relevance of a set of enzymes whose activity is tightly regulated by the balance between the oxidized and reduced forms of this metabolite. In fact, the actions of NAD+ have been extended from being an oxidoreductase cofactor for single enzymatic activities to acting as substrate for a wide range of proteins. These include NAD+-dependent protein deacetylases, poly(ADP-ribose) polymerases, and transcription factors that affect a large array of cellular functions. Through these effects, NAD+ provides a direct link between the cellular redox status and the control of signaling and transcriptional events. Of particular interest within the metabolic/endocrine arena are the recent results, which indicate that the regulation of these NAD+-dependent pathways may have a major contribution to oxidative metabolism and life span extension. In this review, we will provide an integrated view on: 1) the pathways that control NAD+ production and cycling, as well as its cellular compartmentalization; 2) the signaling and transcriptional pathways controlled by NAD+; and 3) novel data that show how modulation of NAD+-producing and -consuming pathways have a major physiological impact and hold promise for the prevention and treatment of metabolic disease.

Proteasome Inhibitors in Cancer Therapy and their Relation to Redox Regulation

2019 ◽  
Vol 24 (44) ◽  
pp. 5252-5267
Author(s):  
Gulce Sari ◽  
Zehra Okat ◽  
Ali Sahin ◽  
Betul Karademir
Keyword(s):  
Signaling Pathways ◽  
Redox Regulation ◽  
Molecular Mechanisms ◽  
Redox Homeostasis ◽  
Proteasome Inhibitors ◽  
Redox System ◽  
Redox Balance ◽  
Redox Status ◽  
Signaling Molecules ◽  
Cancer Therapies

Redox homeostasis is important for the maintenance of cell survival. Under physiological conditions, redox system works in a balance and involves activation of many signaling molecules. Regulation of redox balance via signaling molecules is achieved by different pathways and proteasomal system is a key pathway in this process. Importance of proteasomal system on signaling pathways has been investigated for many years. In this direction, many proteasome targeting molecules have been developed. Some of them are already in the clinic for cancer treatment and some are still under investigation to highlight underlying mechanisms. Although there are many studies done, molecular mechanisms of proteasome inhibitors and related signaling pathways need more detailed explanations. This review aims to discuss redox status and proteasomal system related signaling pathways. In addition, cancer therapies targeting proteasomal system and their effects on redox-related pathways have been summarized.

scholarly journals Redox control of plant energy metabolism: The complex intertwined regulation of redox and metabolism in plant cells

2015 ◽  
Vol 37 (1) ◽  
pp. 14-18
Author(s):  
Toshihiro Obata ◽  
Peter Geigenberger ◽  
Alisdair R. Fernie
Keyword(s):  
Energy Metabolism ◽  
Redox Regulation ◽  
Redox Status ◽  
Cellular Level ◽  
Fine Tuning ◽  
Cellular Redox ◽  
Redox Active ◽  
Metabolic Activities ◽  
Cellular Components ◽  
Regulate Energy Metabolism

Maintenance of the cellular redox status is crucial both to keep metabolic processes running and to prevent oxidation of cellular components by reactive oxygen species under fluctuating environments. The plastid is a plant-specific organelle in which considerable redox-active reactions occur and therefore the redox status in this energy organelle, as well as that of the mitochondria, must be tightly regulated. Plants employ multiple mechanisms to actively regulate energy metabolism in response to the redox status and to integrate subcellular redox signals to orchestrate redox status at the cellular level. In this article, we describe the redox regulation of the major flux bearing reactions in these two energy organelles and survey recent advances concerning interorganellar redox communication. The sum action of this complex regulatory network allows both the fine-tuning of metabolic activities for cellular redox homoeostasis and that of redox to allow optimal metabolic function.

Short-term cigarette smoke exposure induces reversible changes in energy metabolism and cellular redox status independent of inflammatory responses in mouse lungs

2012 ◽  
Vol 303 (10) ◽  
pp. L889-L898 ◽  
Author(s):  
Amit R. Agarwal ◽  
Liqin Zhao ◽  
Harsh Sancheti ◽  
Isaac K. Sundar ◽  
Irfan Rahman ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Cigarette Smoke ◽  
Redox Regulation ◽  
Inflammatory Responses ◽  
Redox Status ◽  
Cigarette Smoke Exposure ◽  
Chronic Obstructive ◽  
Altered Expression ◽  
Cellular Redox ◽  
Mouse Lungs

Cigarette smoking leads to alteration in cellular redox status, a hallmark in the pathogenesis of chronic obstructive pulmonary disease. This study examines the role of cigarette smoke (CS) exposure in the impairment of energy metabolism and, consequently, mitochondrial dysfunction. Male A/J mice were exposed to CS generated by a smoking machine for 4 or 8 wk. A recovery group was exposed to CS for 8 wk and allowed to recover for 2 wk. Acute CS exposure altered lung glucose metabolism, entailing a decrease in the rate of glycolysis and an increase in the pentose phosphate pathway, as evidenced by altered expression and activity of GAPDH and glucose-6-phosphate dehydrogenase, respectively. Impairment of GAPDH was found to be due to glutathionylation of its catalytic site cysteines. Metabolic changes were associated with changes in cellular and mitochondrial redox status, assessed in terms of pyridine nucleotides and glutathione. CS exposure elicited an upregulation of the expression of complexes II, III, IV, and V and of the activity of complexes II, IV, and V. Microarray analysis of gene expression in mouse lungs after exposure to CS for 8 wk revealed upregulation of a group of genes involved in metabolism, electron transfer chain, oxidative phosphorylation, mitochondrial transport and dynamics, and redox regulation. These changes occurred independently of inflammatory responses. These findings have implications for the early onset of alterations in energy and redox metabolism upon acute lung exposure to CS.

Sign in / Sign up

Export Citation Format

Share Document