scholarly journals NRF2, a Key Regulator of Antioxidants with Two Faces towards Cancer

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Jaieun Kim ◽  
Young-Sam Keum
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Signal Transduction ◽  
Transcription Factor ◽  
Structure And Function ◽  
Related Factor ◽  
Oxygen Species ◽  
Cellular Functions ◽  
Intracellular Signal ◽  
And Function

While reactive oxygen species (ROS) is generally considered harmful, a relevant amount of ROS is necessary for a number of cellular functions, including the intracellular signal transduction. In order to deal with an excessive amount of ROS, organisms are equipped with a sufficient amount of antioxidants together with NF-E2-related factor-2 (NRF2), a transcription factor that plays a key role in the protection of organisms against environmental or intracellular stresses. While the NRF2 activity has been generally viewed as beneficial to preserve the integrity of organisms, recent studies have demonstrated that cancer cells hijack the NRF2 activity to survive under the oxidative stress and, therefore, a close check must be kept on the NRF2 activity in cancer. In the present review, we briefly highlight important progresses in understanding the molecular mechanism, structure, and function of KEAP1 and NRF2 interaction. In addition, we provide general perspectives that justify conflicting views on the NRF2 activity in cancer.

scholarly journals Control of Reactive Oxygen Species for the Prevention of Parkinson’s Disease: The Possible Application of Flavonoids

Antioxidants ◽  
2020 ◽  
Vol 9 (7) ◽  
pp. 583 ◽  
Author(s):  
Tae Yeon Kim ◽  
Eunju Leem ◽  
Jae Man Lee ◽  
Sang Ryong Kim
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Glycogen Synthase ◽  
Reactive Oxygen ◽  
Adult Brain ◽  
Related Factor ◽  
Oxygen Species ◽  
Antioxidant Defense Systems

Oxidative stress reflects an imbalance between the production of reactive oxygen species (ROS) and antioxidant defense systems, and it can be associated with the pathogenesis and progression of neurodegenerative diseases such as multiple sclerosis, stroke, and Parkinson’s disease (PD). The application of antioxidants, which can defend against oxidative stress, is able to detoxify the reactive intermediates and prevent neurodegeneration resulting from excessive ROS production. There are many reports showing that numerous flavonoids, a large group of natural phenolic compounds, can act as antioxidants and the application of flavonoids has beneficial effects in the adult brain. For instance, it is well known that the long-term consumption of the green tea-derived flavonoids catechin and epigallocatechin gallate (EGCG) can attenuate the onset of PD. Also, flavonoids such as ampelopsin and pinocembrin can inhibit mitochondrial dysfunction and neuronal death through the regulation of gene expression of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Additionally, it is well established that many flavonoids exhibit anti-apoptosis and anti-inflammatory effects through cellular signaling pathways, such as those involving (ERK), glycogen synthase kinase-3β (GSK-3β), and (Akt), resulting in neuroprotection. In this review article, we have described the oxidative stress involved in PD and explained the therapeutic potential of flavonoids to protect the nigrostriatal DA system, which may be useful to prevent PD.

Reactive oxygen species in cell signaling

2000 ◽  
Vol 279 (6) ◽  
pp. L1005-L1028 ◽  
Author(s):  
Victor J. Thannickal ◽  
Barry L. Fanburg
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Signal Transduction ◽  
Plasma Membrane ◽  
Growth Factors ◽  
Redox State ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cellular Redox ◽  
By Products

Reactive oxygen species (ROS) are generated as by-products of cellular metabolism, primarily in the mitochondria. When cellular production of ROS overwhelms its antioxidant capacity, damage to cellular macromolecules such as lipids, protein, and DNA may ensue. Such a state of “oxidative stress” is thought to contribute to the pathogenesis of a number of human diseases including those of the lung. Recent studies have also implicated ROS that are generated by specialized plasma membrane oxidases in normal physiological signaling by growth factors and cytokines. In this review, we examine the evidence for ligand-induced generation of ROS, its cellular sources, and the signaling pathways that are activated. Emerging concepts on the mechanisms of signal transduction by ROS that involve alterations in cellular redox state and oxidative modifications of proteins are also discussed.

Counteraction of the deleterious effects of reactive oxygen species on hemoglobin structure and function by ellagic acid

2017 ◽  
Vol 182 ◽  
pp. 1-7 ◽  
Author(s):  
Masoumeh Valipour ◽  
Parvaneh Maghami ◽  
Mehran Habibi-Rezaei ◽  
Mostafa Sadeghpour ◽  
Mohamad Ali Khademian ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Ellagic Acid ◽  
Reactive Oxygen ◽  
Structure And Function ◽  
Oxygen Species ◽  
And Function

Molecular targets of oxidative stress

2011 ◽  
Vol 434 (2) ◽  
pp. 201-210 ◽  
Author(s):  
Simon V. Avery
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Apoptotic Cell ◽  
Molecular Targets ◽  
Membrane Lipid ◽  
Oxygen Species ◽  
Cellular Functions ◽  
Toxic Protein ◽  
Detailed Picture ◽  
Ros Reactive Oxygen Species

Aerobic life requires organisms to resist the damaging effects of ROS (reactive oxygen species), particularly during stress. Extensive research has established a detailed picture of how cells respond to oxidative stress. Attention is now focusing on identifying the key molecular targets of ROS, which cause killing when resistance is overwhelmed. Experimental criteria used to establish such targets have differing merits. Depending on the nature of the stress, ROS cause loss of essential cellular functions or gain of toxic functions. Essential targets on which life pivots during ROS stress include membrane lipid integrity and activity of ROS-susceptible proteins, including proteins required for faithful translation of mRNA. Protein oxidation also triggers accumulation of toxic protein aggregates or induction of apoptotic cell death. This burgeoning understanding of the principal ROS targets will offer new possibilities for therapy of ROS related diseases.

Cellular Response to Hyperosmotic Stresses

2007 ◽  
Vol 87 (4) ◽  
pp. 1441-1474 ◽  
Author(s):  
Maurice B. Burg ◽  
Joan D. Ferraris ◽  
Natalia I. Dmitrieva
Keyword(s):  
Reactive Oxygen Species ◽  
Cellular Response ◽  
Organic Osmolytes ◽  
Oxygen Species ◽  
Adaptive Responses ◽  
Cellular Functions ◽  
Renal Inner Medulla ◽  
Shock Proteins ◽  
And Function ◽  
Signal Activation

Cells in the renal inner medulla are normally exposed to extraordinarily high levels of NaCl and urea. The osmotic stress causes numerous perturbations because of the hypertonic effect of high NaCl and the direct denaturation of cellular macromolecules by high urea. High NaCl and urea elevate reactive oxygen species, cause cytoskeletal rearrangement, inhibit DNA replication and transcription, inhibit translation, depolarize mitochondria, and damage DNA and proteins. Nevertheless, cells can accommodate by changes that include accumulation of organic osmolytes and increased expression of heat shock proteins. Failure to accommodate results in cell death by apoptosis. Although the adapted cells survive and function, many of the original perturbations persist, and even contribute to signaling the adaptive responses. This review addresses both the perturbing effects of high NaCl and urea and the adaptive responses. We speculate on the sensors of osmolality and document the multiple pathways that signal activation of the transcription factor TonEBP/OREBP, which directs many aspects of adaptation. The facts that numerous cellular functions are altered by hyperosmolality and remain so, even after adaptation, indicate that both the effects of hyperosmolality and adaptation to it involve profound alterations of the state of the cells.

scholarly journals Azilsartan Suppresses Osteoclastogenesis and Ameliorates Ovariectomy-Induced Osteoporosis by Inhibiting Reactive Oxygen Species Production and Activating Nrf2 Signaling

2021 ◽  
Vol 12 ◽  
Author(s):  
Bin Pan ◽  
Lin Zheng ◽  
Jiawei Fang ◽  
Ye Lin ◽  
Hehuan Lai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Signaling Pathways ◽  
Bone Microarchitecture ◽  
Reactive Oxygen ◽  
Related Factor ◽  
Nuclear Factor ◽  
Oxygen Species

Osteoporosis is characterized by a decrease in bone mass and destruction of the bone microarchitecture, and it commonly occurs in postmenopausal women and the elderly. Overactivation of osteoclasts caused by the inflammatory response or oxidative stress leads to osteoporosis. An increasing number of studies have suggested that intracellular reactive oxygen species (ROS) are strongly associated with osteoclastogenesis. As a novel angiotensin (Ang) II receptor blocker (ARB), azilsartan was reported to be associated with the inhibition of intracellular oxidative stress processes. However, the relationship between azilsartan and osteoclastogenesis is still unknown. In this study, we explored the effect of azilsartan on ovariectomy-induced osteoporosis in mice. Azilsartan significantly inhibited the receptor activator of nuclear factor-κB ligand (RANKL)-mediated osteoclastogenesis and downregulated the expression of osteoclast-associated markers (Nfatc1, c-Fos, and Ctsk) in vitro. Furthermore, azilsartan reduced RANKL-induced ROS production by increasing the expression of nuclear factor erythroid 2-related factor 2 (Nrf2). Mechanistically, azilsartan inhibited the activation of MAPK/NF-κB signaling pathways, while Nrf2 silencing reversed the inhibitory effect of azilsartan on MAPK/NF-κB signaling pathways. Consistent with the in vitro data, azilsartan administration ameliorated ovariectomy (OVX)-induced osteoporosis, and decreased ROS levels in vivo. In conclusion, azilsartan inhibited oxidative stress and may be a novel treatment strategy for osteoporosis caused by osteoclast overactivation.

scholarly journals Insights into the respiratory chain and oxidative stress

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Véronique Larosa ◽  
Claire Remacle
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Signal Transduction ◽  
Hydrogen Peroxide ◽  
Superoxide Anion ◽  
Oxygen Species ◽  
Hydroperoxyl Radical ◽  
Photosynthetic Organisms ◽  
The Common ◽  
And Oxidative Stress

Reactive oxygen species (ROS) are highly reactive reduced oxygen molecules that result from aerobic metabolism. The common forms are the superoxide anion (O2∙−) and hydrogen peroxide (H2O2) and their derived forms, hydroxyl radical (HO∙) and hydroperoxyl radical (HOO∙). Their production sites in mitochondria are reviewed. Even though being highly toxic products, ROS seem important in transducing information from dysfunctional mitochondria. Evidences of signal transduction mediated by ROS in mitochondrial deficiency contexts are then presented in different organisms such as yeast, mammals or photosynthetic organisms.

scholarly journals The SEM-4 Transcription Factor Is Required for Regulation of the Oxidative Stress Response in Caenorhabditis elegans

2020 ◽  
Vol 10 (9) ◽  
pp. 3379-3385
Author(s):  
Adilya Rafikova ◽  
Queenie Hu ◽  
Terrance J Kubiseski
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Transcription Factor ◽  
Phase Ii ◽  
Oxidative Stress Response ◽  
Premature Aging ◽  
Detoxification Enzymes ◽  
Potential Candidate ◽  
Oxygen Species ◽  
C Elegans

Abstract Oxidative stress causes damage to cells by creating reactive oxygen species (ROS) and the overproduction of ROS have been linked to the onset of premature aging. We previously found that a brap-2 (BRCA1 associated protein 2) mutant significantly increases the expression of phase II detoxification enzymes in C. elegans. An RNAi suppression screen to identify transcription factors involved in the production of gst-4 mRNA in brap-2 worms identified SEM-4 as a potential candidate. Here, we show that knockdown of sem-4 suppresses the activation of gst-4 caused by the mutation in brap-2. We also demonstrate that sem-4 is required for survival upon exposure to oxidative stress and that SEM-4 is required for expression of the transcription factor SKN-1C. These findings identify a novel role for SEM-4 in ROS detoxification by regulating expression of SKN-1C and the phase II detoxification genes.

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