scholarly journals Yap1-Regulated Glutathione Redox System Curtails Accumulation of Formaldehyde and Reactive Oxygen Species in Methanol Metabolism of Pichia pastoris

2009 ◽  
Vol 8 (4) ◽  
pp. 540-549 ◽  
Author(s):  
Taisuke Yano ◽  
Emiko Takigami ◽  
Hiroya Yurimoto ◽  
Yasuyoshi Sakai
Keyword(s):  
Reactive Oxygen Species ◽  
Pichia Pastoris ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Redox System ◽  
Reduced Form ◽  
Growth Defect ◽  
Oxygen Species ◽  
Glutathione Redox System ◽  
Glutathione Redox

ABSTRACT The glutathione redox system, including the glutathione biosynthesis and glutathione regeneration reaction, has been found to play a critical role in the yeast Pichia pastoris during growth on methanol, and this regulation was at least partly executed by the transcription factor PpYap1. During adaptation to methanol medium, PpYap1 transiently localized to the nucleus and activated the expression of the glutathione redox system and upregulated glutathione reductase 1 (Glr1). Glr1 activates the regeneration of the reduced form of glutathione (GSH). Depletion of Glr1 caused a severe growth defect on methanol and hypersensitivity to formaldehyde (HCHO), which could be complemented by addition of GSH to the medium. Disruption of the genes for the HCHO-oxidizing enzymes PpFld1 and PpFgh1 caused a comparable phenotype, but disruption of the downstream gene PpFDH1 did not, demonstrating the importance of maintaining intracellular GSH levels. Absence of the peroxisomal glutathione peroxidase Pmp20 also triggered nuclear localization of PpYap1, and although cells were not sensitive to HCHO, growth on methanol was again severely impaired due to oxidative stress. Thus, the PpYap1-regulated glutathione redox system has two important roles, i.e., HCHO metabolism and detoxification of reactive oxygen species.

scholarly journals Chloroplasts Require Glutathione Reductase to Balance Reactive Oxygen Species and Maintain Efficient Photosynthesis

2019 ◽  
Author(s):  
Stefanie J. Müller-Schüssele ◽  
Ren Wang ◽  
Desirée D. Gütle ◽  
Jill Romer ◽  
Marta Rodriguez-Franco ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Plant Growth ◽  
Glutathione Reductase ◽  
Critical Role ◽  
Reactive Oxygen ◽  
List Type ◽  
Oxygen Species ◽  
Protein Repair ◽  
Glutathione Redox

SummaryThiol-based redox-regulation is vital to coordinate chloroplast functions depending on illumination. Yet, how the redox-cascades of the thioredoxin and glutathione redox machineries integrate metabolic regulation and reactive oxygen species (ROS) detoxification remains largely unresolved. We investigate if maintaining a highly reducing stromal glutathione redox potential (EGSH) via glutathione reductase (GR) is necessary for functional photosynthesis and plant growth.Since absence of the plastid/mitochondrial GR is embryo-lethal in Arabidopsis thaliana, we used the model moss Physcomitrella patens to create knock-out lines. We dissect the role of GR in chloroplasts by in vivo monitoring stromal EGSH dynamics, and reveal changes in protein abundances by metabolic labelling.Whereas stromal EGSH is highly reducing in wildtype and clearly responsive to light, the absence of GR leads to a partial oxidation, which is not rescued by light. Photosynthetic performance and plant growth are decreased with increasing light intensities, while ascorbate and zeaxanthin levels are elevated. An adjustment of chloroplast proteostasis is pinpointed by the induction of plastid protein repair and degradation machineries.Our results indicate that the plastid thioredoxin and glutathione redox systems operate largely independently. They reveal a critical role of GR in maintaining efficient photosynthesis.

scholarly journals Reactive Oxygen Species: Beyond Their Reactive Behavior

2021 ◽  
Vol 46 (1) ◽  
pp. 77-87
Author(s):  
Arnaud Tauffenberger ◽  
Pierre J. Magistretti
Keyword(s):  
Reactive Oxygen Species ◽  
Second Messengers ◽  
Critical Role ◽  
Complex Function ◽  
Reactive Oxygen ◽  
High Reactivity ◽  
Oxygen Species ◽  
Health And Disease ◽  
Cellular Dysfunction ◽  
The Brain

AbstractCellular homeostasis plays a critical role in how an organism will develop and age. Disruption of this fragile equilibrium is often associated with health degradation and ultimately, death. Reactive oxygen species (ROS) have been closely associated with health decline and neurological disorders, such as Alzheimer’s disease or Parkinson’s disease. ROS were first identified as by-products of the cellular activity, mainly mitochondrial respiration, and their high reactivity is linked to a disruption of macromolecules such as proteins, lipids and DNA. More recent research suggests more complex function of ROS, reaching far beyond the cellular dysfunction. ROS are active actors in most of the signaling cascades involved in cell development, proliferation and survival, constituting important second messengers. In the brain, their impact on neurons and astrocytes has been associated with synaptic plasticity and neuron survival. This review provides an overview of ROS function in cell signaling in the context of aging and degeneration in the brain and guarding the fragile balance between health and disease.

scholarly journals Tomato SlIDA has a critical role in tomato fertilization by modifying reactive oxygen species homeostasis

2020 ◽  
Vol 103 (6) ◽  
pp. 2100-2118
Author(s):  
Rong Wang ◽  
ChunLin Shi ◽  
Xiaoyang Wang ◽  
Ruizhen Li ◽  
Yan Meng ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Oxygen Species

scholarly journals Effects of reactive oxygen species on renal tubular transport

2019 ◽  
Vol 317 (2) ◽  
pp. F444-F455 ◽  
Author(s):  
Agustin Gonzalez-Vicente ◽  
Nancy Hong ◽  
Jeffrey L. Garvin
Keyword(s):  
Reactive Oxygen Species ◽  
Collecting Duct ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Thick Ascending Limb ◽  
Oxygen Species ◽  
Renal Tubular Transport ◽  
Regulation Of Transport ◽  
Renal Tubular ◽  
Made In

Reactive oxygen species (ROS) play a critical role in regulating nephron transport both via transcellular and paracellular pathways under physiological and pathological circumstances. Here, we review the progress made in the past ~10 yr in understanding how ROS regulate solute and water transport in individual nephron segments. Our knowledge in this field is still rudimentary, with basic information lacking. This is most obvious when looking at the reported disparate effects of superoxide ([Formula: see text]) and H2O2 on proximal nephron transport, where there are no easy explanations as to how to reconcile the data. Similarly, we know almost nothing about the regulation of transport in thin descending and ascending limbs, information that is likely critical to understanding the urine concentrating mechanism. In the thick ascending limb, there is general agreement that ROS enhance transcellular reabsorption of NaCl, but we know very little about their effects on the paracellular pathway and therefore Ca2+ and Mg2+ transport. In the distal convoluted tubule, precious little is known. In the collecting duct, there is general agreement that ROS stimulate the epithelial Na+ channel.

scholarly journals Cytotoxicity of Air Pollutant 9,10-Phenanthrenequinone: Role of Reactive Oxygen Species and Redox Signaling

2018 ◽  
Vol 2018 ◽  
pp. 1-15 ◽  
Author(s):  
Manli Yang ◽  
Hassan Ahmed ◽  
Weidong Wu ◽  
Bijie Jiang ◽  
Zhenquan Jia
Keyword(s):  
Reactive Oxygen Species ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Air Pollutant ◽  
Diesel Exhaust Particles ◽  
Political Community ◽  
Oxygen Species ◽  
Cytotoxic Effects

Atmospheric pollution has been a principal topic recently in the scientific and political community due to its role and impact on human and ecological health. 9,10-phenanthrenequinone (9,10-PQ) is a quinone molecule found in air pollution abundantly in the diesel exhaust particles (DEP). This compound has studied extensively and has been shown to develop cytotoxic effects both in vitro and in vivo. 9, 10-PQ has been proposed to play a critical role in the development of cytotoxicity via generation of reactive oxygen species (ROS) through redox cycling. This compound also reduces expression of glutathione (GSH), which is critical in Phase II detoxification reactions. Understanding the underlying cellular mechanisms involved in cytotoxicity can allow for the development of therapeutics designed to target specific molecules significantly involved in the 9,10-PQ-induced ROS toxicity. This review highlights the developments in the understanding of the cytotoxic effects of 9, 10-PQ with special emphasis on the possible mechanisms involved.

scholarly journals Inhibition of p66ShcA Longevity Gene Rescues Podocytes from HIV-1-induced Oxidative Stress and Apoptosis

2009 ◽  
Vol 284 (24) ◽  
pp. 16648-16658 ◽  
Author(s):  
Mohammad Husain ◽  
Leonard G. Meggs ◽  
Himanshu Vashistha ◽  
Sonia Simoes ◽  
Kevin O. Griffiths ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Small Interfering Rna ◽  
Critical Role ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Dominant Negative ◽  
Redox Activity ◽  
Oxygen Species ◽  
Interfering Rna ◽  
Hiv 1

Glomerular visceral epithelial cells (podocytes) play a critical role in the pathogenesis of human immunodeficiency virus (HIV)-associated nephropathy. A key question concerns the mechanism(s) by which the HIV-1 genome alters the phenotype of the highly specialized, terminally differentiated podocytes. Here, using an in vitro system of conditionally immortalized differentiated human podocytes (CIDHPs), we document a pivotal role for the p66ShcA protein in HIV-1-induced reactive oxygen species generation and CIDHP apoptosis. CIDHP transfected with truncated HIV-1 construct (NL4-3) exhibit increased reactive oxygen species metabolism, DNA strand breaks, and a 5-fold increase in apoptosis, whereas the opposite was true for NL4-3/CIDHP co-transfected with mu-36p66ShcA (mu-36) dominant negative expression vector or isoform-specific p66-small interfering RNA. Phosphorylation at Ser-36 of the wild type p66ShcA protein, required for p66ShcA redox function and inhibition of the potent stress response regulator Foxo3a, was unchanged in mu-36/NL4-3/CIDHP but increased in NL4-3/CIDHP. Acute knockdown of Foxo3a by small interfering RNA induced a 50% increase in mu-36/NL4-3/CIDHP apoptosis, indicating that Foxo3a-dependent responses promote the survival phenotype in mu-36 cells. We conclude that inhibition of p66ShcA redox activity prevents generation of HIV-1 stress signals and activation of the CIDHP apoptosis program.

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