Relevant bibliographies by topics / Intracellular redox homeostasis

Academic literature on the topic 'Intracellular redox homeostasis'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Intracellular redox homeostasis"

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Colgan, Stephen M., and Richard C. Austin. "Homocysteinylation of Metallothionein Impairs Intracellular Redox Homeostasis." Arteriosclerosis, Thrombosis, and Vascular Biology 27, no. 1 (January 2007): 8–11. http://dx.doi.org/10.1161/01.atv.0000254151.00086.26.

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Süzen, Sibel, Mehmet C. Atayik, Hanif Sirinzade, Bita Entezari, Hande Gurer-Orhan, and Ufuk Cakatay. "Melatonin and redox homeostasis." Melatonin Research 5, no. 3 (September 30, 2022): 304–24. http://dx.doi.org/10.32794/mr112500134.

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Redox homeostasis and redox signaling are constituents of preservation of a normal physiological state. Whereas the equilibrium between oxidants and nucleophiles is conserved in redox homeostasis, oxidative stress promotes the formation of a radically altered redox state. It is known that modification of circadian clock may lead to severe alteration in redox balance. Melatonin [N-acetyl-5-methoxytryptamine, (MLT)] regulates numerous physiological functions including circadian rhythm, sleep-wake cycle, gonadal activity, redox homeostasis, neuroprotection, immune-modulation, and anticancer activity in organisms. Insufficient MLT production is closely related to development of aging process, tumorigenesis, visceral adiposity, neurodegenerative disorders, etc. Reactive oxygen species (ROS) are not intrinsically harmful or beneficial in cellular redox metabolism. Redox homeostasis is an integrative status for both of the hormetic response to ROS overproduction and subsequent redox signaling. MLT and its derivatives are traditionally classified as hormone-like substances. Their redox sensitive regulatory activity and direct interaction with intracellular ROS serve as second messenger in cell signaling. This review involves the role of redox homeostasis in the pathogenesis of age-related disorders and its relationship with MLT, therefore, targeting the circadian rhythm may propose new therapeutic approach for these disorders.
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Merker, Marilyn P., Bruce R. Pitt, Augustine M. Choi, Paul M. Hassoun, Christopher A. Dawson, and Aron B. Fisher. "Lung redox homeostasis: emerging concepts." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 3 (September 1, 2000): L413—L417. http://dx.doi.org/10.1152/ajplung.2000.279.3.l413.

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This symposium was organized to present some aspects of current research pertaining to lung redox function. Focuses of the symposium were on roles of pulmonary endothelial NADPH oxidase, xanthine oxidase (XO)/xanthine dehydrogenase (XDH), heme oxygenase (HO), transplasma membrane electron transport (TPMET), and the zinc binding protein metallothionein (MT) in the propagation and/or protection of the lung or other organs from oxidative injury. The presentations were chosen to reflect the roles of both intracellular (metallothionein, XO/XDH, and HO) and plasma membrane (NADPH oxidase, XO/XDH, and unidentified TPMET) redox proteins in these processes. Although the lung endothelium was the predominant cell type under consideration, at least some of the proposed mechanisms operate in or affect other cell types and organs as well.
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Monti, Daria Maria, Nicola Montesano Gesualdi, Josef Matoušek, Franca Esposito, and Giuseppe D’Alessio. "The cytosolic ribonuclease inhibitor contributes to intracellular redox homeostasis." FEBS Letters 581, no. 5 (February 6, 2007): 930–34. http://dx.doi.org/10.1016/j.febslet.2007.01.072.

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Bagur Quetglas, Rafaela, Péter Várnai, Gyorgy Csordás, and Gyorgy Hajnóczky. "Effect of Arsenic on Intracellular Calcium & Redox Homeostasis." Biophysical Journal 112, no. 3 (February 2017): 132a. http://dx.doi.org/10.1016/j.bpj.2016.11.730.

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Xie, Zhi-Zhong, Yang Liu, and Jin-Song Bian. "Hydrogen Sulfide and Cellular Redox Homeostasis." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–12. http://dx.doi.org/10.1155/2016/6043038.

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Intracellular redox imbalance is mainly caused by overproduction of reactive oxygen species (ROS) or weakness of the natural antioxidant defense system. It is involved in the pathophysiology of a wide array of human diseases. Hydrogen sulfide (H2S) is now recognized as the third “gasotransmitters” and proved to exert a wide range of physiological and cytoprotective functions in the biological systems. Among these functions, the role of H2S in oxidative stress has been one of the main focuses over years. However, the underlying mechanisms for the antioxidant effect of H2S are still poorly comprehended. This review presents an overview of the current understanding of H2S specially focusing on the new understanding and mechanisms of the antioxidant effects of H2S based on recent reports. Both inhibition of ROS generation and stimulation of antioxidants are discussed. H2S-induced S-sulfhydration of key proteins (e.g., p66Shc and Keap1) is also one of the focuses of this review.
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Sang, Dongmiao, Xiaofeng Li, Zhikun Xu, Huiming Lin, Changhong Guo, and Fengyu Qu. "Disrupted intracellular redox balance with enhanced ROS generation and sensitive drug release for cancer therapy." Biomaterials Science 8, no. 21 (2020): 6045–55. http://dx.doi.org/10.1039/d0bm00765j.

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Walker, Cheryl L., Laura C. D. Pomatto, Durga Nand Tripathi, and Kelvin J. A. Davies. "Redox Regulation of Homeostasis and Proteostasis in Peroxisomes." Physiological Reviews 98, no. 1 (January 1, 2018): 89–115. http://dx.doi.org/10.1152/physrev.00033.2016.

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Peroxisomes are highly dynamic intracellular organelles involved in a variety of metabolic functions essential for the metabolism of long-chain fatty acids, d-amino acids, and many polyamines. A byproduct of peroxisomal metabolism is the generation, and subsequent detoxification, of reactive oxygen and nitrogen species, particularly hydrogen peroxide (H2O2). Because of its relatively low reactivity (as a mild oxidant), H2O2 has a comparatively long intracellular half-life and a high diffusion rate, all of which makes H2O2 an efficient signaling molecule. Peroxisomes also have intricate connections to mitochondria, and both organelles appear to play important roles in regulating redox signaling pathways. Peroxisomal proteins are also subject to oxidative modification and inactivation by the reactive oxygen and nitrogen species they generate, but the peroxisomal LonP2 protease can selectively remove such oxidatively damaged proteins, thus prolonging the useful lifespan of the organelle. Peroxisomal homeostasis must adapt to the metabolic state of the cell, by a combination of peroxisome proliferation, the removal of excess or badly damaged organelles by autophagy (pexophagy), as well as by processes of peroxisome inheritance and motility. More recently the tumor suppressors ataxia telangiectasia mutate (ATM) and tuberous sclerosis complex (TSC), which regulate mTORC1 signaling, have been found to regulate pexophagy in response to variable levels of certain reactive oxygen and nitrogen species. It is now clear that any significant loss of peroxisome homeostasis can have devastating physiological consequences. Peroxisome dysregulation has been implicated in several metabolic diseases, and increasing evidence highlights the important role of diminished peroxisomal functions in aging processes.
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Fatma, Homa, Mohd Jameel, and Hifzur R. Siddique. "An Update on Phytochemicals in Redox Homeostasis: “Virtuous or Evil” in Cancer Chemoprevention?" Chemistry 5, no. 1 (February 4, 2023): 201–22. http://dx.doi.org/10.3390/chemistry5010017.

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Redox homeostasis, a dynamic process ensuring a balance between cellular oxidizing and reducing reactions, is crucial for maintaining healthy cellular physiology and regulating many biological processes, requiring continuous monitoring and fine-tuning. Reactive species play a critical role in intra/intercellular signaling, and each cell has a specific system guarding cellular redox homeostasis. ROS signaling and oxidative stress are involved in cancer initiation and progression. However, the generation of reactive species beyond the threshold level inside the tumor microenvironment is considered one of the therapeutic approaches. Various studies have shown that some phytochemicals can target the redox homeostasis of the tumor microenvironment. Recent advances have focused on developing and introducing phytochemical interventions as favorable therapeutic options against cancer. However, studies have also suggested the “virtuous” and “evil” impacts of phytochemicals. Some phytochemicals enhance therapeutic efficacy by promoting intracellular oxidant accumulation. However, under certain conditions, some phytochemicals may harm the cellular microenvironment to promote cancer and tend to target different pathways for cancer initiation and development instead of targeting redox homeostasis. In this context, this review is focused on providing an overall understanding of redox homeostasis and intends to highlight the potential positive and negative impacts of phytochemicals in redox homeostasis and disease development. We also discuss the recent nanotechnology-based advancements in combating cancer development.
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Shi, Jiayan, Hailong Tian, Liyuan Peng, Canhua Huang, Edouard C. Nice, Bingwen Zou, and Haiyuan Zhang. "A nanoplatform reshaping intracellular osmolarity and redox homeostasis against colorectal cancer." Journal of Controlled Release 352 (December 2022): 766–75. http://dx.doi.org/10.1016/j.jconrel.2022.11.003.

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Dissertations / Theses on the topic "Intracellular redox homeostasis"

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Auchinvole, Craig Alexander R. "SERS nanosensors for intracellular redox potential measurements." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/9706.

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Redox regulation and homeostasis are critically important in the regulation of cell function; however, there are significant challenges in quantitatively measuring and monitoring intracellular redox potentials. The work in this thesis details a novel approach to intracellular redox monitoring. The approach is based on the use of nanosensors, which comprise molecules capable of sensing the local redox potential, assembled on gold nanoshells. Since the Raman spectra of the sensor molecules change depending on their oxidation state, and since the nanoshells allow a large enhancement of the Raman scattering, intracellular potential can be calculated by simple optical measurements. A full description of the design, fabrication and characterisation (spectroscopic and electrochemical) of the nanosensors is provided within. The ability to deliver nanosensors into cells in a controllable fashion was confirmed using electron microscopy. Results from a range of assays are also presented which reveal that introduction of nanosensors does not result in any cytotoxicity. Sensor utility in monitoring redox potentials as cells responded to physiological and superphysiological oxidative and reductive stimuli was investigated. Importantly, the capability of the nanosensors in monitoring intracellular potentials in a reversible, non-invasive manner, and over a previously unattainable potential range, is demonstrated.
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Zhao, Tingyi. "Maintenance of intracellular redox homeostasis by an antioxidant enzyme glutaredoxin 1 (Grx1) in human cells." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/263504.

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Papp, Laura V., and n/a. "Multiple Levels of Regulation of Human SECIS Binding Protein 2, SBP2." Griffith University. School of Biomolecular and Biomedical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20070208.145623.

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Selenium is an essential trace mineral of fundamental importance to human health. Its beneficial functions are largely attributed to its presence within a group of proteins named selenoproteins in the form of the amino acid selenocysteine (Sec). Recently, it was revealed that the human selenoproteome consists of 25 selenoproteins, and for many of them their function remains unknown. The most prominent known roles of selenoproteins are to maintain the intracellular redox homeostasis, redox regulation of intracellular signalling and thyroid hormone metabolism. Sec incorporation into selenoproteins employs a unique mechanism that involves decoding of the UGA stop codon. The process requires interplay between distinct, intrinsic features such as the Sec Insertion Sequence (SECIS) element, the tRNASec and multiple protein factors. The work presented in this thesis has focused on characterising the regulation of human SECIS binding protein 2, SBP2, a factor central to this process. Experimental approaches combined with bioinformatics analysis revealed that SBP2 is subjected to alternative splicing. A total of nine alternatively spliced transcripts appear to be expressed in cells, potentially encoding five different protein isoforms. The alternative splicing events are restricted to the 5?-region, which is proposed to be dispensable for Sec incorporation. One of the variants identified, contains a mitochondrial targeting sequence that was capable of targetting SBP2 into the mitochondrial compartment. This isoform also appears to be expressed endogenously within the mitochondria in cells. Previous reports have depicted SBP2 as a ribosomal protein, despite the presence of a putative Nuclear Localisation Signal (NLS). In this study it was found that SBP2 subcellular localisation is not restricted to ribosomes. Intrinsic functional NLS and Nuclear Export Signals (NESs), enable SBP2 to shuttle between the nucleus and the cytoplasm via the CRM1 pathway. In addition, the subcellular localisation of SBP2 appears to play an important role in regulating Sec incorporation into selenoproteins. The subcellular localisation of SBP2 is altered by conditions imposing oxidative stress. Several oxidising agents induce the nuclear accumulation of SBP2, which occurs via oxidation of cysteine residues within a novel redox-sensitive cysteine rich domain (CRD). Cysteine residues were to form disulfide bonds and glutathione-mixed disulfides during oxidising conditions, which are efficiently reversed in vitro by the thioredoxin and glutaredoxin systems, respectively. These modifications negatively regulate selenoprotein synthesis. Cells depleted of SBP2 are more sensitive to oxidative stress than control cells, which correlated with a substantial decrease in selenoprotein synthesis after treatment with oxidising agents. These results provide direct evidence that SBP2 is required for Sec incorporation in vivo and suggest that nuclear sequestration of SBP2 under such conditions may represent a mechanism to regulate the expression of selenoproteins. Collectively, these results suggest that SBP2 is regulated at multiple levels: by alternative splicing, changes in subcellar localisation and redox control.
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Papp, Laura V. "Multiple Levels of Regulation of Human SECIS Binding Protein 2, SBP2." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/367554.

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Abstract:
Selenium is an essential trace mineral of fundamental importance to human health. Its beneficial functions are largely attributed to its presence within a group of proteins named selenoproteins in the form of the amino acid selenocysteine (Sec). Recently, it was revealed that the human selenoproteome consists of 25 selenoproteins, and for many of them their function remains unknown. The most prominent known roles of selenoproteins are to maintain the intracellular redox homeostasis, redox regulation of intracellular signalling and thyroid hormone metabolism. Sec incorporation into selenoproteins employs a unique mechanism that involves decoding of the UGA stop codon. The process requires interplay between distinct, intrinsic features such as the Sec Insertion Sequence (SECIS) element, the tRNASec and multiple protein factors. The work presented in this thesis has focused on characterising the regulation of human SECIS binding protein 2, SBP2, a factor central to this process. Experimental approaches combined with bioinformatics analysis revealed that SBP2 is subjected to alternative splicing. A total of nine alternatively spliced transcripts appear to be expressed in cells, potentially encoding five different protein isoforms. The alternative splicing events are restricted to the 5?-region, which is proposed to be dispensable for Sec incorporation. One of the variants identified, contains a mitochondrial targeting sequence that was capable of targetting SBP2 into the mitochondrial compartment. This isoform also appears to be expressed endogenously within the mitochondria in cells. Previous reports have depicted SBP2 as a ribosomal protein, despite the presence of a putative Nuclear Localisation Signal (NLS). In this study it was found that SBP2 subcellular localisation is not restricted to ribosomes. Intrinsic functional NLS and Nuclear Export Signals (NESs), enable SBP2 to shuttle between the nucleus and the cytoplasm via the CRM1 pathway. In addition, the subcellular localisation of SBP2 appears to play an important role in regulating Sec incorporation into selenoproteins. The subcellular localisation of SBP2 is altered by conditions imposing oxidative stress. Several oxidising agents induce the nuclear accumulation of SBP2, which occurs via oxidation of cysteine residues within a novel redox-sensitive cysteine rich domain (CRD). Cysteine residues were to form disulfide bonds and glutathione-mixed disulfides during oxidising conditions, which are efficiently reversed in vitro by the thioredoxin and glutaredoxin systems, respectively. These modifications negatively regulate selenoprotein synthesis. Cells depleted of SBP2 are more sensitive to oxidative stress than control cells, which correlated with a substantial decrease in selenoprotein synthesis after treatment with oxidising agents. These results provide direct evidence that SBP2 is required for Sec incorporation in vivo and suggest that nuclear sequestration of SBP2 under such conditions may represent a mechanism to regulate the expression of selenoproteins. Collectively, these results suggest that SBP2 is regulated at multiple levels: by alternative splicing, changes in subcellar localisation and redox control.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Book chapters on the topic "Intracellular redox homeostasis"

1

M. Owen, John, and Kenneth J. Dormer. "The Shear Stress/KLF2/Nrf2/ARE Pathway: A Hemodynamic Defense against Oxidative Stress." In Blood - Updates on Hemodynamics and Thalassemia. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.99566.

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Many diseases have oxidative stress and inflammation as underlying pathological features, including metabolic and inflammatory/autoimmune disorders, diseases of the lung, liver, kidney, gastrointestinal tract, cardiovascular and nervous systems. A leading physiological mechanism for oxidative stress is the nuclear erythroid-related factor 2-like 2/antioxidant response element (Nrf2/ARE) signaling pathway. It maintains intracellular homeostasis and protects cells from oxidative damage by inducing phase II detoxifying and oxidative-stress responsive genes. Nrf2 transcription factor functions as the key controller of the redox homeostatic gene regulatory network, and is tightly controlled by the repressor protein, Kelch-like ECH-associated protein 1 (Keap1). Pharmacological agents to inhibit Keap1 and boost effectiveness of the Nrf2/ARE pathway have been developed and more are in development. This chapter elucidates the importance of hemodynamic laminar shear stress in oxidative homeostasis and examines hemodynamic induction of the shear stress (SS)/Krupple-like factor2 (KLF2) /Nrf2/ARE pathway as a means to combat oxidative stress through hemodynamics.
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Sadhukhan, Pritam, and Parames C. Sil. "The regulation of intracellular redox homeostasis in cancer progression and its therapy." In Pathology, 105–14. Elsevier, 2020. http://dx.doi.org/10.1016/b978-0-12-815972-9.00010-x.

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Di Paola, Rosanna, Salvatore Cuzzocrea, Roberta Fusco, and Marika Cordaro. "Dietary Regulation of Keap1/Nrf2/ARE Pathway: Focus on Acai Berries and Pistachios and Cashews as Natural Food Sources." In Recent Developments in Antioxidants From Natural Sources [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.109239.

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Inflammation is a biological reaction to oxidative stress in which cell starts producing proteins, enzymes, and other substances to restore homeostasis, while oxidative stress could be intrinsically a biochemical imbalance of the physiologically redox status of the intracellular environment. The nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway, which controls the transcription of numerous antioxidant genes that protect cellular homeostasis and detoxification genes that process and eliminate all toxic compounds and substances before they can cause damage. The Nrf2 pathway is the heart of the daily biological response to oxidative stress. Transient activation of Nrf2 by diet can upregulate antioxidant enzymes to protect cells against oxidative stress inducers. In this chapter, we summarize the effects of some novel foods in the regulation of the Nrf2/ARE pathway and its cellular mechanisms.
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