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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.
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
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.
Nanoparticles (NPs) are becoming more commonly used in numerous consumer and medical applications, thereby increasing human exposure. To name a few uses, NPs are utilized as protective and antibacterial coatings, drug delivery vehicles, electronics, medical imaging, treatment of a wide range of diseases, cosmetics, and tissue engineering [1-8]. NPs are also found as a manufacturing byproduct and found from combustion processes, which poses a health hazard [9, 10]. The Food and Drug Administration (FDA) defines NPs as particles with a size of 1 - 100 nm, and the toxicity guidelines state they are documented as adaptive and flexible. Due to the rapid development of nanotechnology, the number of NPs exceeds our capability for testing their toxicity, thereby necessitating an understanding of the general mechanisms of their toxicity. The size range of NPs allows them to have unique interactions with proteins and cells, thus making them ideal for their development as therapeutics and imaging contrast agents in medical applications. The potential of using these NPs depends on fully characterizing their toxicity and adverse interactions with biological systems. The purpose of this dissertation study was to understand the role of key physicochemical properties (e.g. biocorona and chemical defects) of NPs on cellular stress and the subsequent toxicity. The first aim of this study examined the formation of a biocorona (BC) on silver nanoparticles (AgNPs), and their contribution to endoplasmic reticulum (ER) stress. Once a NP enters the blood stream or other biological fluids, proteins will form a corona around the NPs resulting in a new biological entity which then affects their interactions with various cells and tissues. Two BCs that were investigated are modeled after common circulating proteins that have been shown to interact with AgNPs; bovine serum albumin (BSA) and high-density lipoprotein (HDL). In addition, I used fetal bovine serum (FBS) to serve as a model for a complex corona comprised of multiple proteins and lipids attached to NPs. The results of hyperspectral imaging and dynamic light scattering showed that proteins bind to AgNPs. In addition, circular dichroism spectroscopy showed that the structure of the proteins is perturbed when associated with NPs. Importantly, AgNPs induce ER stress responses in endothelial cells through activation of the IRE pathway. Further, the presence of a BC on AgNPs modified the ER stress response which varied according to the composition of the BC. Lastly, I observed differences in the subcellular localization of NPs due to size differences that likely contributed to the ER stress response. The second aim of this dissertation was to examine the contribution of chemical defects in ZnO NPs to cellular stress and toxicity. Due to the manufacturing process, contaminants may be incorporated into the crystal structure of NPs resulting in changes in their physicochemical properties. The results of this study indicate that chemical defects modify the degree of ER stress and oxidative stress in endothelial cells. In contrast to AgNPs, ZnO NPs induced ER stress through the PERK pathway, and the response is enhanced by oxidation of ZnO NPs compared to pristine ZnO NPs with no chemical defects. Furthermore, the cellular redox potential was reduced in endothelial cells exposed to ZnO NPs with defects compared to cells treated with pristine ZnO NPs. I conclude that the interactions of NPs with proteins as well as chemical defects of the NPs contribute significantly to cellular stress and toxicity. Taken together, the results indicate additional physicochemical properties such as chemical defects and BC formation contribute to cell stress and toxicity and should be considered when screening for the safety of NPs for consumer and medical applications.
"Nanoparticles are engineered structure with at least one dimension of 100 nanometers or less. These materials are increasingly being used for commercial purposes such as catalyst, semiconductor, cosmetics, microelectronic, and drug carrier. However, the toxicological impact of these materials has not yet been studied in detail, thereby limiting their use. In our present study, we use human brain endothelial cell line as a blood-brain barrier (BBB) model to investigate if two kinds of nanoparticles [ 1). Diesel exhaust particles (DEPs) and 2). single wall carbon nanotube (CNT) ] induced oxidative stress in cell model. Our studies showed that DEPs or CNT significantly decreased the levels of intracellular glutathione (GSH) and glutathione peroxidase (GPx). Malondialdehyde (MDA) levels increased dramatically after DEPs or CNT treatment, and generation of reactive oxygen species (ROS) increased after DEPs or CNT exposure as well. In order to determine whether DEPs/CNT-induced oxidative stress in BBB cells alters BBB integrity, permeability and trans-endothelial electrical resistance (TEER) tests were performed. Cells exposed to DEPs or CNT showed significant increases in cell permeability and significant decreases in TEER compared to those of control. These results strongly suggest that DEPs or CNT induce oxidative stress in human brain endothelial cells and disrupt the integrity of the BBB. We hypothesize that nano material such as DEPs or CNT induced oxidative damage may contribute to the increase incidences of neurodegenerative diseases. Therefore, an antioxidant should be recommended in the areas with nanoparticle exposure related disease"--Abstract, leaf iii.
This book is divided into four main sections thoroughly analyzing the use of nanomaterials for water, air and soil solutions, and emphasizing environmental risks. Providing background on nanomaterials' two-decade study, it discusses the characterization and application of unconventional disinfectants, called antimicrobial nanomaterials, which fall into three categories and, while seemingly harmless, have potential hazards if applied improperly. Special attention is given to the process of remediation, synthetics techniques, and properties of nanomaterials, with examples to which new and trained readers in the field can relate and understand. an interdisciplinary approach, aimed at scientists in physical chemistry, nanotechnology, and environmental sciences includes applications of non-conventional techniques in environmental protection furthers the development of applied nanoscience and nanotechnology suggests new industrial projects and university courses addressing nanotechnology in and for the environment includes applications for water, air and soil protection
This book covers the latest information related to understanding immune responses to engineered nanomaterials (ENMs). Many ENMs used in both the consumer and biomedical fields have been reported to elicit adverse immune responses ranging from innate immune responses such as complement activation to changes in adaptive immunity that influence pathogen responses and promote disease states such as asthma. Interaction of Nanomaterials with the Immune System covers the most up to date information on our understanding of immune responses to ENMs across a wide range of topics including innate immunity, allergic immune responses, adaptive provides the reader with (1) up to date understanding of immune responses to ENMs; (2) current testing methods; and (3) appropriate models including alternative testing strategies for evaluating immunotoxicity of ENMs.
Oxidative Stress and Biomaterials provides readers with the latest information on biomaterials and the oxidative stress that can pose an especially troubling challenge to their biocompatibility, especially given the fact that, at the cellular level, the tissue environment is a harsh landscape of precipitating proteins, infiltrating leukocytes, released oxidants, and fluctuations of pH which, even with the slightest shift in stasis, can induce a perpetual state of chronic inflammation. No material is 100% non-inflammatory, non-toxic, non-teratogenic, non-carcinogenic, non-thrombogenic, and non-immunogenic in all biological settings and situations. In this embattled terrain, the most we can hope for from the biomaterials we design is a type of “meso-compatibility, a material which can remain functional and benign for as long as required without succumbing to this cellular onslaught and inducing a local inflammatory reaction. Explores the challenges of designing and using biomaterials in order to minimize oxidative stress, reducing patterns of chronic inflammation and cell death Brings together the two fields of biomaterials and the biology of oxidative stress Provides approaches for the design of biomaterials with improved biocompatibility
This reference book, which is the second volume of Targeting Oxidative Stress in Cancer, explores oxidative stress as the potential therapeutic target for cancer therapy. The initial chapters discuss the molecular mechanisms of oxidative stress and its effects on different signaling pathways. Subsequently, the sections examine the impact of redox signaling on tumor cell proliferation and consider the therapeutic potential of dietary phytochemicals and nutraceuticals in reactive oxygen species (ROS)-induced cancer. In turn, it examines the evidence supporting the use of Vitamin C in cancer management, before presenting various synthetic and natural compounds that have therapeutic implications for oxidative stress-induced cancer. It also explores the correlation between non-coding RNA and oxidative stress. Furthermore, the book summarizes the role of stem cells in ROS-induced cancer therapy and reviews the therapeutic applications of nanoparticles to alter redox haemostasis in cancer cells. Lastly, it explores heat-shock proteins, ubiquitin ligases, and probiotics as potential therapeutic agents in ROS-mediated cancer. This book is a useful resource for basic and translational scientists as well as clinicians interested in the field of oxidative stress and cancer therapy. ​