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

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.

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

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00219.2012 ◽

2012 ◽

Vol 303 (10) ◽

pp. L889-L898 ◽

Cited By ~ 42

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.

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

Journal of Bacteriology ◽

10.1128/jb.00660-06 ◽

2006 ◽

Vol 188 (21) ◽

pp. 7689-7695 ◽

Cited By ~ 5

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.

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Roles of Phase Separation for Cellular Redox Maintenance

Frontiers in Genetics ◽

10.3389/fgene.2021.691946 ◽

2021 ◽

Vol 12 ◽

Author(s):

Yuichi Saito ◽

Wataru Kimura

Keyword(s):

Phase Separation ◽

Redox Regulation ◽

Redox Homeostasis ◽

Ubiquitin Proteasome System ◽

Future Research ◽

Cellular Redox ◽

Redox Imbalance ◽

Metabolic Switching ◽

Major Player ◽

Cellular Components

The oxidation reaction greatly alters characteristics of various cellular components. In exchange for efficient energy production, mitochondrial aerobic respiration substantially increases the risk of excess oxidation of cellular biomolecules such as lipids, proteins, nucleic acids, and numerous small molecules. To maintain a physiologically balanced cellular reduction-oxidation (redox) state, cells utilize a variety of molecular machineries including cellular antioxidants and protein degradation complexes such as the ubiquitin-proteasome system or autophagy. In the past decade, biomolecular liquid-liquid phase separation (LLPS) has emerged as a subject of great interest in the biomedical field, as it plays versatile roles in the maintenance of cellular homeostasis. With regard to redox homeostasis, LLPS arose as a major player in both well-characterized and newly emerging redox pathways. LLPS is involved in direct redox imbalance sensing, signal transduction, and transcriptional regulation. Also, LLPS is at play when cells resist redox imbalance through metabolic switching, translational remodeling, activating the DNA damage response, and segregation of vulnerable lipids and proteins. On the other hand, chronic accumulation of phase-separated molecular condensates such as lipid droplets and amyloid causes neurotoxic outcomes. In this review we enumerate recent progress on understanding how cells utilize LLPS to deal with oxidative stress, especially related to cell survival or pathogenesis, and we discuss future research directions for understanding biological phase separation in cellular redox regulation.

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The key role of the redox status in regulation of metabolism in photosynthesizing organisms.

Acta Biochimica Polonica ◽

10.18388/abp.2010_2387 ◽

2010 ◽

Vol 57 (2) ◽

Cited By ~ 16

Author(s):

Andrzej Kornas ◽

Elzbieta Kuźniak ◽

Ireneusz Slesak ◽

Zbigniew Miszalski

Keyword(s):

Redox Reactions ◽

Redox Regulation ◽

Essential Feature ◽

Life Forms ◽

Redox Status ◽

Oxygenic Photosynthesis ◽

Sulphur Compounds ◽

Environmental Signals ◽

Redox Active ◽

Regulation Of Metabolism

The redox status of the cell is described by the ratio of reduced to non-reduced compounds. Redox reactions which determine the redox state are an essential feature of all living beings on Earth. However, the first life forms evolved under strongly anoxic conditions of the young Earth, and the redox status probably was based on iron and sulphur compounds. Nowadays, redox reactions in cells have developed in strict connection to molecular oxygen and its derivatives i.e. reactive oxygen species (ROS). Oxygen has started to accumulate on the Earth due to oxygenic photosynthesis. All aspects of aerobic life involve ROS, reactive nitrogen species (RNS), antioxidants and redox regulation. Many different redox-active compounds are involved in the complex of redox processes, including pyridine nucleotides, thioredoxins, glutaredoxins and other thiol/disulphide-containing proteins. Redox regulation is integrated with the redox-reactions in photosynthesis and respiration to achieve an overall energy balance and to maintain a reduced state necessary for the biosynthetic pathways that are reductive in nature. It underlies the physiological and developmental flexibility in plant response to environmental signals.

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The nonclassic secretion of thioredoxin is not sensitive to redox state

AJP Cell Physiology ◽

10.1152/ajpcell.00521.2002 ◽

2003 ◽

Vol 284 (5) ◽

pp. C1272-C1279 ◽

Cited By ~ 28

Author(s):

Marcel Tanudji ◽

Sarah Hevi ◽

Steven L. Chuck

Keyword(s):

Active Site ◽

Redox State ◽

Chinese Hamster Ovary Cells ◽

Chinese Hamster ◽

Brefeldin A ◽

Redox Status ◽

Cellular Level ◽

Active Protein ◽

Ovary Cells ◽

Redox Active

Thioredoxin (Trx) is a cytosolic, redox-active protein that is secreted from many cells and has several extracellular functions. In activated lymphocytes, the pathway of secretion does not involve the Golgi apparatus. Levels of extracellular Trx are decreased by the antioxidant N-acetylcysteine. Hence, the secretion of Trx could be altered by the redox status of the cell or the protein. To study Trx mutants, we characterized the secretion of human Trx from Chinese hamster ovary cells. Secretion of human Trx is unaffected by brefeldin A, slow but efficient, and sensitive to low temperature and factors in serum. We demonstrate that N-acetylcysteine reduces the cellular level of Trx but not the proportion secreted; thus this chemical does not block the nonclassic pathway for Trx secretion. Furthermore, we find that mutations in either the active site or the dimerization site of Trx do not alter its secretion. Thus the nonclassic secretion of Trx is not dependent on the redox status of either the cell or the protein.

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Faculty Opinions recommendation of [CONFERENCE POSTER]: Miner1, mutated in Wolfram syndrome, is an endoplasmic reticular protein that regulates cellular redox status and Ca2+ homeostasis.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.717952860.793458345 ◽

2012 ◽

Author(s):

David Marcinek

Keyword(s):

Wolfram Syndrome ◽

Redox Status ◽

Cellular Redox

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Redox Regulation of Lipid Mobilization in Adipose Tissues

Antioxidants ◽

10.3390/antiox10071090 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1090

Author(s):

Ursula Abou-Rjeileh ◽

G. Andres Contreras

Keyword(s):

Adipose Tissue ◽

Energy Metabolism ◽

Redox Regulation ◽

Cellular Metabolism ◽

Antioxidant Response ◽

Redox Signaling ◽

Nitrogen Species ◽

Adipose Tissues ◽

Lipid Mobilization ◽

Cellular Processes

Lipid mobilization in adipose tissues, which includes lipogenesis and lipolysis, is a paramount process in regulating systemic energy metabolism. Reactive oxygen and nitrogen species (ROS and RNS) are byproducts of cellular metabolism that exert signaling functions in several cellular processes, including lipolysis and lipogenesis. During lipolysis, the adipose tissue generates ROS and RNS and thus requires a robust antioxidant response to maintain tight regulation of redox signaling. This review will discuss the production of ROS and RNS within the adipose tissue, their role in regulating lipolysis and lipogenesis, and the implications of antioxidants on lipid mobilization.

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NAC and Vitamin D Restore CNS Glutathione in Endotoxin-Sensitized Neonatal Hypoxic-Ischemic Rats

Antioxidants ◽

10.3390/antiox10030489 ◽

2021 ◽

Vol 10 (3) ◽

pp. 489

Author(s):

Lauren E. Adams ◽

Hunter G. Moss ◽

Danielle W. Lowe ◽

Truman Brown ◽

Donald B. Wiest ◽

...

Keyword(s):

Oxidative Stress ◽

Vitamin D ◽

Redox Status ◽

Therapeutic Window ◽

Post Injury ◽

Artery Ligation ◽

Cellular Redox ◽

Carotid Artery Ligation ◽

Drug Concentrations

Therapeutic hypothermia does not improve outcomes in neonatal hypoxia ischemia (HI) complicated by perinatal infection, due to well-described, pre-existing oxidative stress and neuroinflammation that shorten the therapeutic window. For effective neuroprotection post-injury, we must first define and then target CNS metabolomic changes immediately after endotoxin-sensitized HI (LPS-HI). We hypothesized that LPS-HI would acutely deplete reduced glutathione (GSH), indicating overwhelming oxidative stress in spite of hypothermia treatment in neonatal rats. Post-natal day 7 rats were randomized to sham ligation, or severe LPS-HI (0.5 mg/kg 4 h before right carotid artery ligation, 90 min 8% O2), followed by hypothermia alone or with N-acetylcysteine (25 mg/kg) and vitamin D (1,25(OH)2D3, 0.05 μg/kg) (NVD). We quantified in vivo CNS metabolites by serial 7T MR Spectroscopy before, immediately after LPS-HI, and after treatment, along with terminal plasma drug concentrations. GSH was significantly decreased in all LPS-HI rats compared with baseline and sham controls. Two hours of hypothermia alone did not improve GSH and allowed glutamate + glutamine (GLX) to increase. Within 1 h of administration, NVD increased GSH close to baseline and suppressed GLX. The combination of NVD with hypothermia rapidly improved cellular redox status after LPS-HI, potentially inhibiting important secondary injury cascades and allowing more time for hypothermic neuroprotection.

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Protective effects of lipoic acid against acrylamide-induced neurotoxicity: involvement of mitochondrial energy metabolism and autophagy

Food & Function ◽

10.1039/c7fo01429e ◽

2017 ◽

Vol 8 (12) ◽

pp. 4657-4667 ◽

Cited By ~ 11

Author(s):

Ge Song ◽

Zhigang Liu ◽

Luanfeng Wang ◽

Renjie Shi ◽

Chuanqi Chu ◽

...

Keyword(s):

Energy Metabolism ◽

Lipoic Acid ◽

Redox Status ◽

Protective Effects ◽

Mitochondrial Energy Metabolism

Lipoic acid (LA) suppressed acrylamide (ACR)-induced inflammation, redox status disturbance, autophagy, and apoptosis mediated by mitochondria in the SH-SY5Y cells.

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