[PDF] Reactive Oxygen Species Ros Nanoparticles And Endoplasmic Reticulum Er Stress Induced Cell Death Mechanisms eBook

Author : Loutfy H. Madkour
Publisher : Academic Press
Page : 782 pages
File Size : 47,72 MB
Release : 2020-06-27
Category : Medical
ISBN : 0128224967

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Reactive Oxygen Species (ROS), Nanoparticles, and Endoplasmic Reticulum (ER) Stress-Induced Cell Death Mechanisms presents the role of ROS?mediated pathways cellular signaling stress, endoplasmic reticulum (ER) stress, oxidative stress, oxidative damage, nanomaterials, and the mechanisms by which metalloids and nanoparticles induce their toxic effects. The book covers the ecotoxicology of environmental heavy metal ions and free radicals on macromolecules cells organisms, heavy metals?induced cell responses, oxidative stress, the source of oxidants, and the roles of ROS, oxidative stress and oxidative damage mechanisms. It also examines the nanotoxicity, cytotoxicity and genotoxicity mechanisms of nanomaterials and the effects of nanoparticle interactions. Antioxidant defense therapy and strategies for treatment round out the book, making it an ideal resource for researchers and professional scientists in toxicology, environmental chemistry, environmental science, nanomaterials and the pharmaceutical sciences. Covers the ecotoxicology of environmental heavy metal ions and the interactions between specific heavy metals?induced cell responses and oxidative stress Provides a better understanding of the mechanism of nanomaterial-induced toxicity as a first defense for hazard prevention Covers recent advances in new nanomedication technologies for the effects of NPs on oxidative stress, ROS and ER stress Discusses the effects of interactions between antioxidant defense therapy, ROS and strategies for treatment

Author : Loutfy H. Madkour
Publisher : Springer
Page : 696 pages
File Size : 30,90 MB
Release : 2020-03-14
Category : Technology & Engineering
ISBN : 9783030372965

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This book provides insights and tools for better understanding redox biology and medicine and, in the long run, to finding new therapeutic strategies to target dysregulated redox processes in various diseases. It presents the recent advances in new nanomedication technologies of the effects of nanoparticles NPs on oxidative stress, RONS and ER stress. The book comprises 13 chapters covering ecotoxicology, cytotoxicity, nanotoxicity and genotoxicity mechanisms causing by the role and interactions of nanoparticles and free radicals with (RONS) and (ER) stress. Endoplasmic Reticulum (ER) Stress as a mechanism for NPs induced toxicity has been discussed. The advances of nanotechnology and the effects of nanoparticles on oxidative stress, ROS and ER stress parameters are discussed. Antioxidants, therapeutic options and regulation of the immune responses are explained throughout the book.

Author : Kuladip Jana
Publisher :
Page : 0 pages
File Size : 16,39 MB
Release : 2024
Category : Active oxygen
ISBN :

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"Reactive oxygen species (ROS) play an essential role in different biological functions, including physiological regulatory mechanisms to damaging alterations involved in the pathogenesis of an increasing number of human diseases. ROS are metabolic products from numerous cells, but two vital cellular organelles are intimately involved in their production and metabolism, i.e. the endoplasmic reticulum and the mitochondria. Excess cellular levels of ROS may cause damage to proteins, nucleic acids, lipids, membranes, and organelles, which may lead to the activation of cell death processes such as apoptosis. Apoptosis is a highly regulated process that is essential for the development and survival of multicellular organisms. These organisms often need to discard superfluous or potentially harmful cells, have accumulated mutations, or become infected by pathogens. Apoptosis features a characteristic set of morphological and biochemical features whereby cells undergo a cascade of self-destruction. Thus, proper regulation of apoptosis is essential for maintaining normal cellular homeostasis. Mitochondrial ROS (mtROS) play a central role in cell signaling and regulating the main pathways of apoptosis, mediated by mitochondria, death receptors, and the endoplasmic reticulum (ER) stress. This book focuses on the current understanding of the role of ROS in each of these three main pathways of apoptosis related to different human diseases, with particular emphasis on Metabolic, Inflammatory, Neurodegenerative, and Neoplastic diseases. It's promise and limitations are also discussed by targeting ROS with different antioxidants in preventing non-communicable diseases. The role of mtROS in the complex interplay and crosstalk between these different signaling pathways of apoptosis related to different human diseases remains to be unraveled further in future research"--

Author : Dennis Lam
Publisher : Open Dissertation Press
Page : pages
File Size : 35,19 MB
Release : 2017-01-26
Category :
ISBN : 9781361275146

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This dissertation, "A Study of Biological Role of Reactive Oxygen Species in Cellular Response in Stress" by Dennis, Lam, 林勁行, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: When proteins are unable to fold properly in the endoplasmic reticulum (ER), the resultant formation of misfolded proteins causes stress of the ER. Cells with ER stress often have a higher abundance of reactive oxygen species (ROS). Previous studies suggest that ROS could aggravate ER stress by further disrupting the ER protein folding process. More recent studies suggest that the unfolded protein response signaling pathways activated by ER stress could lead to the production of ROS. Such studies lead to the hypothesis that ER stress could be promoted by ROS, and vice versa. The aim of the present study is to test the above hypothesis by studying how ROS could be generated in ER-stressed cells. This is followed by investigating if ROS could increase or decrease the level of ER stress in cells. Finally, the extent of ER stress induced cell death in the presence and absence of ROS is assessed. The treatment of HeLa cells with tunicamycin (Tm), a common ER-stress inducing agent, resulted in the elevation of intracellular ROS that could be detected with the ROS-reactive probe dichlorodihydrofluorescein (DCF), but not dihydroethidium which is relatively specific towards superoxide anion. The Tm-induced elevation of ROS could be prevented by co-incubation of cells with thiol reductants such as dithiothreitol and N-acetylcysteine but not with the free radical scavenger ascorbate. The tunicamycin-induced elevation of ROS level could also be prevented by the over-expression of catalase in HeLa. These data is consistent with the idea that hydrogen peroxide is a major form of ROS produced in Tm-treated cells. In addition to elevation of ROS level, HeLa cells treated with tunicamycin also resulted in the phosphorylation of PERK and eIF2α, and the splicing of XBP-1. In the presence of cycloheximide to inhibit protein synthesis so as to deplete protein substrates for folding in the ER, tunicamycin-induced ER stress was greatly minimized as was evident by the absence of both the phosphorylation of PERK and splicing of XBP-1. However, the phosphorylation of eIF2α and elevation of DCF-detectable ROS remained unaffected. The cycloheximde-resistant phosphorylation of eIF2α could be prevented when cells were co-treated with thiol reductants, or upon the over-expression of catalase. These data suggest that the production of ROS in Tm-treated cells does not require the presence of ER stress as a prerequisite. Furthermore, the ROS so produced could induce phosphorylation of eIF2α without the need to cause ER stress in the first place. The quenching of ROS through the use of thiol reductants, or the over-expression of catalase, had no effect on inhibition of protein synthesis in cells treated with tunicamycin. However, the extent of cell death was significantly increased. The data obtained in this study is not consistent with the idea that ROS is a downstream product of ER stress, capable of inducing more ER-stress by a feedback mechanism. Therefore, a mutually enhancing effect between ER stress and ROS may not exist. The ROS found in stressed cells may serve to extend cellular survival under the condition of continuous stress.

Author : Loutfy H. Madkour
Publisher :
Page : 742 pages
File Size : 43,6 MB
Release : 2020
Category : Nanoparticles
ISBN : 9783030372989

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This book provides insights and tools for better understanding redox biology and medicine and, in the long run, to finding new therapeutic strategies to target dysregulated redox processes in various diseases. It presents the recent advances in new nanomedication technologies of the effects of nanoparticles NPs on oxidative stress, RONS and ER stress. The book comprises 13 chapters covering ecotoxicology, cytotoxicity, nanotoxicity and genotoxicity mechanisms causing by the role and interactions of nanoparticles and free radicals with (RONS) and (ER) stress. Endoplasmic Reticulum (ER) Stress as a mechanism for NPs induced toxicity has been discussed. The advances of nanotechnology and the effects of nanoparticles on oxidative stress, ROS and ER stress parameters are discussed. Antioxidants, therapeutic options and regulation of the immune responses are explained throughout the book.

Author : Shamim I. Ahmad
Publisher : CRC Press
Page : 782 pages
File Size : 24,55 MB
Release : 2017-12-19
Category : Science
ISBN : 1315352648

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Unlike other narrowly focused books, Reactive Oxygen Species in Biology and Human Health provides a comprehensive overview of ROS. It covers the current status of research and provides pointers to future research goals. Additionally, it authoritatively reviews the impact of reactive oxygen species with respect to various human diseases and discusses antioxidants and other compounds that counteract oxidative stress. Comprised of seven sections, the first section describes the introduction, detection, and production of ROS, emphasizing phenolic compounds and vitamin E for their abilities to act as antioxidants. This section also highlights the role of lipoprotein-associated oxidative stress. Section two addresses the importance of iron accumulation in the brain resulting in the development of a group of neurodegenerative disorders (NDs) and identifies several causative genes for neurodegeneration with brain iron accumulation (NBIA) associated with Parkinsonism-related disorders. The third section discusses a number of NDs, including amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), Huntington's disease (HD), epilepsy, and multiple sclerosis (MS). Section four addresses autoimmune diseases caused by ROS, including asthma, autoimmune liver diseases, rheumatoid arthritis, thyroid disease, primary biliary cirrhosis, and systemic lupus. Section five analyzes a number of different cancers, including lung cancer, breast cancer, and melanoma, along with possible treatment regimens. Section six discusses cardiovascular diseases (CVDs) induced by ROS, presents the ROS-associated complex biochemical processes inducing inflammation as an important cause of CVDs, and explains the roles carotenoids play in preventing CVDs. The final section addresses other human diseases induced by oxidative stress, including sickle cell disease, nonalcoholic steatohepatitis, retinopathy, fibromyalgia, chronic obstructive pulmonary disease, asthma, pulmonary hypertension, infertility, and aging of human skin.

Author : Suresh C. Pillai
Publisher :
Page : 0 pages
File Size : 47,90 MB
Release : 2019
Category : Medical
ISBN : 9780429265471

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Choice Recommended Title, April 2020 This comprehensive book, edited by two leading experts in nanotechnology and bioengineering with contributions from a global team of specialists, provides a detailed overview of the environmental and health impacts associated with the toxicology of nanomaterials. Special attention is given to nanomaterial toxicity during synthesis, production and application, and chapters throughout are focused on key areas that are important for future research and development of nanomaterials. This book will be of interest to advanced students studying biomedical engineering and materials science, PhD researchers, post-docs and academics working in the area of nanotechnology, medicine, manufacturing and regulatory bodies. Features: Collates and critically evaluates various aspects of the toxicology of nanomaterials in one comprehensive text Discusses the various effects of nanocrystals including the morphologies on cytotoxicity, in addition to the environmental and cytotoxicity risks of graphene and 2D nanomaterials Explores practical methods of detection and quantification, with applications in the environmental and healthcare fields

Author :
Publisher :
Page : 384 pages
File Size : 35,40 MB
Release : 2009
Category :
ISBN :

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Mechanisms of cell death extend beyond the simple apoptosis/necrosis relationship to include regulated modes of cell death that do not readily fit either of the classic descriptors. One such mechanism of cell death involves poly(ADP-ribose)polymerase-1 (PARP-1)-mediated cell death. 2,3,5-Tris(Glutathion-S-yl)-hydroquinone (TGHQ), a reactive oxygen species (ROS) generating nephrotoxic and nephrocarcinogenic metabolite of hydroquinone, causes necrotic renal cell death, the basis for which is unclear. We therefore investigated TGHQ-mediated cell death in human renal proximal tubule epithelial HK-2 cells. TGHQ induced ROS generation, DNA strand breaks, hyperactivation of PARP-1, rapid depletion of nicotinamide adenine dinucleotide (NAD), elevations in intracellular Ca2+ concentrations, loss of mitochondrial membrane potential, and subsequent necrotic cell death. Interestingly, PARP-1 hyperactivation was not accompanied by the translocation of apoptosis-inducing factor (AIF) from mitochondria to the nucleus, a process usually associated with PARP-dependent cell death. Inhibition of PARP-1 with PJ34 blocked TGHQ-mediated accumulation of poly(ADP-ribose) polymers, NAD consumption, and the consequent necrotic cell death. However, HK-2 cell death was only delayed by PJ34, and cell death remained necrotic in nature. In contrast, chelation of intracellular Ca2+ with BAPTA-AM completely abrogated TGHQ-induced necrotic cell death. Ca2+ chelation not only prevented the collapse in the mitochondrial potential but also attenuated PARP-1 hyperactivation. Conversely, inhibition of PARP-1 modulated TGHQ-mediated changes in Ca2+ homeostasis. Moreover, TGHQ caused a sequential oxidation of peroxiredoxin III (PrxIII), a protein considered the primary antioxidant defense within mitochondria. Thus, TGHQ induced two acidic shifts in PrxIII, with both pI shifted spots representing oxidized forms of PrxIII. Transient expression of a dominant negative version of PrxIII resulted in a significant increase in TGHQ-induced cytotoxicity, whereas overexpression of wild-type PrxIII significantly attenuated cytotoxicity. Our studies provide new insights into PARP-1-mediated necrotic cell death. Changes in intracellular Ca2+ concentrations appear to couple PARP-1-hyperactivation to subsequent cell death, but in the absence of AIF release from mitochondria. NAD depletion, mitochondrial membrane depolarization, Ca2+-mediated calpain activation, and PrxIII oxidation, all contribute to TGHQ-driven ROS-mediated necrotic cell death.

Author : Vijay Pratap Singh
Publisher : John Wiley & Sons
Page : 611 pages
File Size : 49,6 MB
Release : 2017-10-11
Category : Science
ISBN : 1119324947

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Describes the basics of ROS metabolism in plants and examines the broad range of ROS signaling mechanisms New discoveries about the effects of reactive oxygen species (ROS) on plants have turned ROS from being considered a bane into a boon, because their roles have been discovered in many plant developmental processes as signaling molecules. This comprehensive book teaches about the role of ROS metabolism in plants and how they affect various developmental processes. It also discusses in detail the advancements made in understanding the ROS signaling. Reactive Oxygen Species in Plants: Boon Or Bane - Revisiting the Role of ROS begins by presenting the basic introduction to ROS and deciphers the detailed knowledge in ROS research. It then examines the broad range of ROS signaling mechanisms as well as how they may be beneficial for plants and human beings. This book also describes both the bane and boon aspects of ROS with their impact on plants, and how the recent revelations have compelled us to rethink ROS turning from stressors to plant regulators. ● Compiles, for the first time, the wholesome knowledge in ROS research and their cellular signaling ● Includes new discoveries and in-depth discussions about the advancements made in the field ● Discusses reactive oxygen species which are involved in a broad range of biological processes Reactive Oxygen Species in Plants: Boon Or Bane - Revisiting the Role of ROS will help scientists to utilize the functions of ROS signaling for plants and also enable readers to gain a deeper knowledge of ROS research and signaling. It is highly recommended for researchers, scientists, and academicians in plant science as well for advanced undergraduate and postgraduate students.

Author : Ghada Mahmoud Abou-Lteif
Publisher :
Page : 176 pages
File Size : 49,48 MB
Release : 2008
Category :
ISBN :

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N-(4-hydroxyphenyl)retinamide (HPR) is a synthetic retinoid that inhibits growth and induces apoptosis in many human cell lines including those that are resista nt to natural retinoids. Adult T-cell leukemia-lymphoma (ATL) is an aggressive peripheral T-cell malignancy caused by human T-cell lymphotropic virus type I (H TLV-I). ATL carries a poor prognosis with a mean survival time of less than eig ht months, in the acute form, mainly due to acquired resistance to chemotherapy. The viral transactivator protein Tax plays a critical role in HTLV-I-induced t ransformation and apoptosis resistance. We have previously shown that HPR inhibits proliferation and induces apoptosis i n all tested ATL and HTLV-I-negative malignant T cell lines, while no effect is observed on normal lymphocytes (Darwiche 2004). The mechanisms of HPR-induced c ell death are complex and involve signaling pathways mediated by free radicals o r reactive oxygen species (ROS). Using ATL as a model, we aim at deciphering th e mechanisms generating ROS and apoptosis of malignant T cells in response to HP R. We will explore the involvement of ROS in HPR-induced apoptosis, the contrib ution of the different biochemical pathways of ROS generation in relation to HPR -induced cell death; and Tax modulation of HPR induced ROS accumulation and ROS- induced cell death. We identified HPR-induced ROS generation as the key mediator of cell cycle arres t and apoptosis of malignant T cells. Pre-treatment with antioxidants inhibited ROS generation, prevented HPR-induced ceramide accumulation, cell cycle arrest, cytochrome c release, caspase-activation and apoptosis. The expression of the HTLV-I oncoprotein Tax abrogated HPR-induced ROS accumulation in HTLV-I-infected cells, which explains their lower sensitivity to HPR. Of the enzyme systems fr equently implicated in ROS generation, only phospholipase A2 (PLA2) and lipooxyg enase (LOX) were shown to be involved in ROS generation and growth suppression i n response to HPR in HTLV-I-negative malignant T cells Defining the mechanism of free radical induction by HPR may support a potential therapeutic role for this synthetic retinoid in ATL and HTLV-I-negative T-cell l ymphomas.