Reactive Oxygen Species (ROS), Nanoparticles, and Endoplasmic Reticulum (ER) Stress-Induced Cell Death Mechanisms

Reactive Oxygen Species (ROS), Nanoparticles, and Endoplasmic Reticulum (ER) Stress-Induced Cell Death Mechanisms

1st Edition - June 26, 2020

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  • Author: Loutfy H. Madkour
  • Paperback ISBN: 9780128224816
  • eBook ISBN: 9780128224960

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Description

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.

Key Features

  • 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

Readership

Researchers and professional scientists in toxicology, environmental toxicology, environmental chemistry, nanomaterials, and pharmaceutical sciences; graduate-level researchers working on metals/nanomaterials toxicity in mammalian systems, material science, or pharmaceutical science; R&D scientists, environmental scientists; public health

Table of Contents

  • 1. Pathophysiological, toxicological and immunoregulatory roles of reactive oxygen and nitrogen species (RONS)
    1.1. Oxidative and nitrative stress in toxicology and disease
    1.2. Oxidative and nitrative stress: role in the response to liver toxicants (Roberts)
    1.2.1. Carcinogenesis and inflammation
    1.2.2. Cross-talk with PPARα?
    1.3. Characterization of oxidative stress using neuronal cell culture models (Smith)
    1.4. Nitrative stress and glial-neuronal interactions in the pathogenesis of Parkinson’s disease (PD) (Tjalkens and Stephen Safe)
    1.4.1. Neuroinflammation and PD
    1.4.2. Regulation of neuroinflammatory genes in astrocytes
    1.4.3. Therapeutic strategies to interdict neuroinflammatio
    1.5. Oxidative and nitrative stress in multistage carcinogenesis (Robertson)
    1.6. Role of peroxynitrite in the pathogenesis of doxorubicin-induced cardiotoxicity (Szabo)
    1.6.1. Molecular mechanisms of peroxynitrite formation
    1.7. Immunoregulatory role of ROS
    1.8. Conclusions
    References

    2. Biological mechanisms of reactive oxygen species (ROS)
    2.1. Exogenous source of oxidants
    2.1.1. Cigarette smoke
    2.1.2. Ozone exposure
    2.1.3. Hyperoxia
    2.1.4. Ionizing radiation
    2.1.5. Heavy metal Ions
    2.2. Endogenous sources of ROS and their regulation in inflammation
    2.3. Mitochondria as main source of ROS in autophagy signaling
    2.4. ROS and mitophagy
    2.5. Production of ROS and their mechanisms of biological activities
    2.6. Increased ROS production in photosynthesis during drought
    2.7. ROS elimination
    2.8. Types of reactive oxygen species (ROS)
    References

    3. Cellular signaling pathways with reactive oxygen species (ROS)
    3.1. Oxidative stress and ROS
    3.2. Sources of ROS
    3.2.1. Endogenous sources and localization of ROS
    3.2.1.1. Mitochondria
    3.2.1.2. Endoplasmic reticulum
    3.2.1.3. Soluble enzymes
    3.2.1.4. Lipid metabolism
    3.2.1.5. NADPH oxidase
    3.2.2. Exogenous sources of ROS
    3.2.3. The homeostasis of ROS
    3.3. Oxidative stress in RA
    3.4. Molecular targets of ROS
    3.4.1. Protein tyrosine phosphatases and kinases
    3.4.2. Lipid metabolism
    3.4.3. Ca+2 signaling'
    3.4.4. Small GTP-ases
    3.4.5. Serine/threonine kinases and phosphatases
    3.5. Redox regulation of transcription factors
    3.5.1. NF-κB
    3.5.2. AP-1
    3.5.3. Other transcription factors
    3.6. Rheumatoid arthritis (RA), pathogenesis and therapy
    3.7. Oxidative stress/ROS associated consequences in RA
    3.7.1. Lipid peroxidation
    3.7.2. Effects on immunoglobulins advanced glycation end-products
    3.7.3. Oxidative stress/ROS mediated alteration of auto-antigens
    3.7.4. Genotoxic effects of oxidative stress
    3.7.5. Oxidative stress and tissue injury
    3.7.6. Cartilage/collagen effects
    3.8. ROS mediated pathways in cell death
    3.8.1. Extrinsic pathways
    3.8.2. Intrinsic pathways
    3.9. ROS mediated cellular signaling in RA
    3.9.1. MAPKs signaling pathway
    3.9.2. PI3K-Akt signaling pathway
    3.9.3. ROS and NF-kB signaling pathway
    3.9.4. Oxidative stress/ROS as signaling in T cell tolerance
    3.10. The homeostasis of ROS
    3.11. ROS and NF-κB signaling pathway
    3.12. ROS and MAPKs signaling pathway
    3.13. ROS and keap1-Nrf2-ARE signaling pathway
    3.14. ROS and PI3K-Akt signaling pathway
    3.15. Cross talk between ROS and Ca2+
    3.16. ROS and mPTP
    3.17. ROS and protein kinase
    3.18. ROS and ubiquitination/proteasome system
    3.19. Lipid accumulation in oleaginous microorganisms under different types of stress
    3.19.1. Nutrient limitation
    3.19.2. Physical environmental stresses
    3.19.3. Stress-induced for generation and its potential role in lipid accumulation
    3.19.4. Redox homeostasis and oxidative stress
    3.19.5. Stress sensing and putative concomitant ROS generation
    3.19.6. Transduction of intracellular ROS signals
    3.19.7. Possible links between ROS and lipid accumulation
    References

    4. Manganese as the essential element in oxidative stress, and metabolic diseases
    4.1. Effects of manganese on the role of reactive oxygen species
    4.2. Physiological roles of manganese
    4.3. Mn as metalloenzymes and as an enzyme activator
    4.4. Mn stability and transport
    4.5. Mn administration, distribution, and excretion
    4.6. Brain manganese targets
    4.7. Mn and metabolic syndrome
    4.8. Mn and type 2 diabetes mellitus/insulin resistance
    4.9. Mn and obesity
    4.10. Mn and atherosclerosis
    4.11. Mn and nonalcoholic fatty liver disease
    4.12. Mn and autoxidation of catecholamines and other neurotransmitters
    4.13. Mitochondria, the mitochondrial permeability transition, and apoptosis
    4.14. Mn, ROS, the mitochondria, and apoptosis
    4.15. A case for the use of mitochondrially targeted antioxidants
    4.16. Conclusion
    References

    5. Affected energy metabolism is primal cause of manganese toxicity
    5.1. Affected energy metabolism
    5.1.1. Gene expression profile under manganese stress.
    5.1.2. Manganese-induced iron depletion blocks ISC and heme protein biogenesis.
    5.1.3. Mature ISC and heme protein deficiency affects energy metabolism.
    5.1.4. Reduced ETC function evokes ROS under manganese stress.
    5.1.5. Affected energy metabolism determines manganese toxicity.
    5.2. Mechanism of manganese-induced cellular toxicity
    5.3. Polynitrogen manganese complexes
    5.3.1. Cytotoxicity of Mn complexes 1 and 2.
    5.3.2. Effects of different concentrations of H2O2 on apoptosis of PC12 cells.
    5.3.3. Protection of preconditioning with Mn complexes against H2O2-induced death of neuronal cells.
    5.3.4. Time course analysis of intracellular ROS levels changes.
    5.3.5. Effects of Mn complexes on the mRNA levels of HIF-1α and HIF target genes in cultured cells.
    5.3.6. Effects of Mn complexes on the protein levels of HIF-1α and HIF target genes in cultured cells.
    5.3.7. HIF-1α knockdown induced apoptotic cell death under preconditioning with Mn complexes of neuronal cells.
    5.4. Neuroprotection-related signaling pathways of Mn complexes 1 and 2.
    5.5. Conclusion
    References

    6. Heavy metals and free radicals-induced cell death mechanisms
    6.1. Heavy metal ions
    6.2. Occurrence and recovery of heavy metals
    6.3. Free radicals
    6.3.1. Definition free radicals
    6.4. Heavy metals and their risk role on organisms of biological systems
    6.5. Bio-importance of some heavy metals
    6.6. Ecotoxicology and metabolism of heavy metals
    6.7. Toxicity of xenobiotic metals (mercury, lead, cadmium, tin and arsenic)
    6.7.1. Mercury
    6.7.2. Lead
    6.7.3. Cadmium
    6.7.4. Tin
    6.7.5. Arsenic
    References

    7. Cytotoxic mechanisms of xenobiotic heavy metals on oxidative stress
    7.1. Effects of lead on oxidative stress
    7.2. Effects of iron on oxidative stress
    7.3. Effects of mercury on oxidative stress
    7.4. Effects of copper on oxidative stress
    7.5. Effects of cadmium and zinc on oxidative stress
    7.6. Effects of arsenic on oxidative stress
    7.7. Effects of chromium on oxidative stress
    7.8. Effects of vanadium on oxidative stress
    7.9. Cytotoxic and cellular functions of heavy metals
    References

    8. Oxidative stress and oxidative damage-induced cell death
    8.1. Oxidative stress
    8.2. ROS regulation of signaling molecules
    8.2.1. Kinases and phosphatases
    8.2.2. Transcription factors
    8.2.3. ROS-induced transcriptional activation
    8.2.4. Signaling pathways
    8.2.5. Mitogen signaling
    8.2.6. Integrin signaling
    8.2.7. Wnt signaling
    8.3. Cellular processes regulated by ROS
    8.3.1. Proliferation
    8.3.2. Differentiation
    8.3.3. Cell death
    8.4. Autophagy and oxidative stress
    8.4.1. Redox signaling in autophagy
    8.5. Oxidative damage
    8.6. ROS and oxidative damage on biomolecules
    8.6.1. Effects of oxidative stress on lipids
    8.6.2. Effects of oxidative stress on proteins
    8.6.3. Effects of oxidative stress on DNA
    8.7. ROS/RNS and nucleic acid destabilization
    References

    9. Cell death mechanisms–apoptosis pathways and their implications in toxicology
    9.1. Apoptosis: Historical perspectives
    9.2. Apoptosis: Mechanisms and different pathways
    9.2.1. Extrinsic pathway
    9.2.2. Intrinsic pathway
    9.2.3. Perforin/granzyme pathway
    9.2.4. Execution pathway
    9.2.5. Main mechanisms of parasites induced cell apoptosis
    9.3. Signaling pathways leading to apoptosis in mammalian cells
    9.4. The role of calcium in cell death
    9.4.1. The endoplasmic reticulum ER, Ca2+‏, and apoptosis
    9.4.2. Apoptosis by mitochondrial permeabilization
    9.4.3. Ca2+‏-activated effector mechanisms
    9.4.4. Ca2+ and the phagocytosis of apoptotic cells
    9.5. Oxidative stress and cell death
    9.6. Targets of ROS
    9.7. Inflammation and cell death
    9.8. Some alternative forms of cell death
    9.8.1. Autophagy
    9.8.2. Pyroptosis
    9.8.3. Entosis
    9.8.4. Mitotic catastrophe (mitotic failure)
    9.9. Links between apoptosis and other cell death modalities
    9.10. Toxicity-related cell death
    9.11. Role of autophagy in toxicity
    9.11.1. Role of apoptosis in cancers
    9.11.2. Over-expression of apoptosis
    9.11.3. Use of anti-apoptotic therapy anti-apoptotic agent
    9.11.4. Assays used
    9.12. Chelerythrine induced cell death through ROS-dependent ER stress in human prostate cancer cells
    9.12.1. CHE reduced cell viability in human prostate cancer cells
    9.12.2. CHE induced cell apoptosis in human prostate cancer cells
    9.12.3. CHE increased ROS accumulation in PC-3 cells
    9.12.4. Blockage of ROS generation reversed CHE-induced cell apoptosis in PC-3 cells
    9.12.5. CHE induced cell apoptosis through ROS-mediated ER stress in PC-3 cells
    9.13. Conclusion
    References

    10. Programmed cell death mechanisms and nanoparticles toxicity
    10.1 Molecular mechanisms underlying nanomaterials toxicity
    10.2 Major forms of programmed cell death
    10.3 More than one way to skin a cat
    10.4 Programmed cell death: Apoptosis
    10.5 Programmed cell death: Autophagy
    10.6 Programmed cell death: Necrosi
    10.7 The importance of being small
    10.8 Effects of nanoparticles on apoptosis
    10.9 Nanomaterials and apoptosis
    10.10 Nanomaterials and mitotic catastrophe
    10.11 Effects of nanoparticles on autophagy
    10.12 Nanomaterials and autophagy or "autophagic cell death"
    10.13 Effects of nanoparticles on necroptosis
    10.14 Nanomaterials and necrosis
    10.15 Nanomaterials and pyroptosis
    10.16 Mechanisms of graphene-induced programmed cell death
    10.17 GBMs induce apoptosis in cells
    10.18 The signaling pathways involved in GBM-induced apoptosis
    10.19 GBMs induce autophagy in cells
    10.20 The signaling pathways involved in GBMs-induced autophagy
    10.21 GBMs induce necroptosis and relative pathways involved
    10.22 Some differences and relationships of GBMs-induced PCDs
    10.22.1 Differences in PCD
    10.22.2 Several cross-linked pathways in PCD
    10.23 Conclusions and perspectives
    References

    11.Endoplasmic reticulum stress (ERS) and associated ROS in disease pathophysiology applications
    11.1 Endoplasmic reticulum ER
    11.2 Reactive oxygen species (ROS)
    11.3 Sources of reactive oxygen species (ROS) generation
    11.4 Endoplasmic reticulum stress (ERS)
    11.5 Unfolded protein response (UPR)
    11.5.1 Inositol-requiring protein 1 (IRE1)
    11.5.2 Protein kinase-like endoplasmic reticulum kinase (PERK)
    11.5.3 Activating transcription factor 6 (ATF6)
    11.6 Protein folding challenge in intestinal secretory cells
    11.7 Endoplasmic reticulum stress and autophagy
    11.8 How is reactive oxygen species (ROS) induced through endoplasmic reticulum (ER) stress?
    11.8.1. The specific mechanism of ER stress-induced ROS during the ER folding process
    11.9 Specific mechanism of ER stress-induced ROS: NADPH oxidase 4 (Nox4)
    11.10 Coupled glutathione within the ER
    11.11 NADPH-dependent p450 reductase and p450 connection involvement in ER stress
    11.12 ER and mitochondria connection and relationship to ROS
    11.13 Oxidative stress
    11.14 Vicious sequence of events between endoplasmic reticulum stress and oxidative stress
    11.15 Endoplasmic reticulum stress and oxidative stress in inflammatory bowel disease
    11.16 Disease application
    11.16.1 ER stress and diseases
    11.16.2 Neurodegenerative diseases
    11.16.3 Diabetes mellitus
    11.16.4 Atherosclerosis
    11.16.5 Kinds of inflammation
    11. 16.6 Liver disease
    11.16.7 Ischemia
    11.16.8 Kidney disease
    11. 17 Conclusions
    References

    12.Endoplasmic reticulum (ER) stress-induced cell death mechanism
    12.1 ER stress and unfolded protein response
    12.2 Protein folding: ER chaperones and foldases
    12.2.1 General chaperones
    12.2.2 Lectin chaperones
    12.2.3 Other folding chaperones and enzymes
    12.3 Role of ER stress inhibitors in the context of metabolic diseases
    12.4 ER stress sensors
    12.4.1 Activation of PERK
    12.4.2 Activation of IRE1α pathway
    12.5 ER stress leads to disease progression
    12.6 Metabolic disorders
    12.6.1 Diabetes
    12.6.2 Obesity
    12.6.3 Lipid disorders
    12.7 ER stress inhibitors
    12.7.1 KIRA6
    12.7.2 3-hydroxy-2-naphthoic acid
    12.7.3 MKC-3946
    12.7.4 4-Phenylbutyric acid
    12.7.5 Taurine-conjugated ursodeoxycholic acid
    12.7.6 Olmesartan
    12.7.7 N-acetylcysteine (NAC)
    12.7.8 Oleanolic acid
    12.7.9 Ursolic acid
    12.7.10 Telmisartan
    12.7.11 Quercetin
    12.7.12 Other inhibitors
    12.7.13 Antidiabetic drugs targeting ER stress
    12.8 ER stress, UPR signaling, and cell death regulation
    12.9 UPR independent ER stress-signaling and cell death
    12.9.1 Calcium
    12.9.2 MEKK1 (MAP3K4)
    12.9.3 ER membrane re-organization
    12.10 Suppressors of ER-stress induced apoptosis
    12.10.1 Bax-inhibitor 1 (BI-1/Tmbim6)
    12.10.2 Bcl-2/Bcl-XL
    12.10.3 MicroRNAs
    12.10.4 Additional suppressors of ER stress-induced apoptosis
    12.11 ER stress and autophagy
    12.12 ER stress involvement in diseases
    12.12.1 Neurodegenerative diseases
    12.12.2 Ophthalmology disorders
    12.12.3 Immunity and inflammation
    12.12.4 Viral infections
    12.12.5 Metabolic diseases
    12.12.6 Atherosclerosis
    12.13 ER stress and cancer
    12.13.1 ER chaperones and cancer regulation
    12.13.2 ER sensors and cancer
    12.14 The cross talk between ER stress and autophagy in cancer
    12.15 The relationship between FOXO, ER stress and cancer
    12.15.1 PERK pathway and FOXO3 story
    12.15.2 IRE-1 and FOXO regulation
    12.15.3 Chaperones and FOX regulation
    12.15.4 ER stress and FOX regulation in worms
    12.15.5 Daf-16 and dFOXO and regulation of Ire-1 arm
    12.15.6 Regulation of PERK by dFOXO
    12.16 Target cancer through the UPR signaling and its FOXO link
    12.16.1 Targeting IRE1α-XBP1
    12.16.2 Targeting PERK-ATF4
    12.16.3 Chaperones inhibitors and FOXO3
    References

    13.Modulation of endoplasmic reticulum (ER) stress of nanotoxicology for nanoparticles (NPs)
    13.1. Nanotoxicology and nanomedicine
    13.2. ER stress as a mechanism for nanotoxicology
    13.2.1. Morphological changes of ER by NP exposure
    13.2.2. Effects of NP exposure on ER stress pathway
    13.2.3. Modulation of ER stress and the toxicity of NPs
    13.3. Modulation of ER stress by NP in nanomedicine
    13.3.1. Selective activation of ER stress by NPs for cancer therapy
    13.3.2. Alleviation of ER stress by NPs for metabolic disease therapy
    13.4. Silver nanoparticles – allies or adversaries?
    13.5. Role of AgNPs in cell toxicity
    13.5.1. Silver nanoparticles-induced apoptosis
    13.5.2. Silver nanoparticles induce endoplasmic reticulum ER stress
    13.6. Uptake of AgNP and their intracellular localization
    13.7. Inhibition of proliferation and cell death
    13.8. ROS key factor in biological oxidation processes
    13.9. Oxidative stress as an underlying mechanism for NP toxicity
    13.10. Genotoxicity
    13.11. Concluding remarks
    References

    14. Nanoparticle cellular uptake and intracellular targeting on reactive oxygen species (ROS) in biological activities
    14.1. Nanoparticle (NP) classes and biomedical applications
    14.1.1. Optical imaging
    14.1.2. Biosensing
    14.1.3. Diagnostic applications
    14.1.4. Drug delivery
    14.1.5. Other applications
    14.2. Mechanisms associated with NP-induced ROS generation
    14.2.1. NP-related factors implicated in ROS generation
    14.2.2. NP- and cellular-component-induced ROS generation
    14.3. Biological functions modulated by NP-induced ROS production
    14.3.1. DNA damage and cytotoxicity
    14.3.2. Antimicrobial function
    14.3.3. Cellular differentiation
    14.3.4. Anticancer
    14.4. NP-induced modulation of ROS generation in stem cell biology
    14.5. Nanoparticle cellular uptake and intracellular targeting
    14.6. Endocytic routes and non-ligand targeted nanomedicines
    14.7 Receptor-mediated cellular internalization of ligand-targeted nanomedicines
    14.7.1. Prostate-specific membrane antigen (PSMA) targeting
    14.7.2. Neonatal Fc-receptor (FcRn) targeting—an avenue to oral delivery of  nanomedicine
    14.8. Intracellular trafficking and subcellular targeting
    14.8.1. From endosomes/lysosomes to cytoplasm
    14.8.2. Endoplasmic reticulum and Golgi apparatus
    14.8.3. Mitochondria
    14.8.4. Nucleus
    14.9. Outlook
    14.10. Conclusions
    References

    15. Metal nanoparticles (MNPs) and particulate matter (PM) induce toxicity
    15.1 Nano-bio interactions
    15.2 Nanotoxicology of nanoparticles
    15.3 Overproduction of ROS and cell damage
    15.4 Nanotoxicity and generation of ROS
    15.5 Dependence of ROS production on the properties of nanoparticles
    15.5.1 Size and shape
    15.5.2 Particle surface, surface positive charges, and surface containing groups
    15.5.3 Solubility and particle dissolution
    15.5.4 Metal ions released from metal and metal oxide nanoparticles
    15.5.5 Light activation
    15.5.6 Aggregation and mode of interaction with cells
    15.5.7 Inflammation leading to ROS formation15.5.8 pH of the system
    15.6 Particulate matter (PM
    References

    16. Mechanisms for nanoparticles-mediated oxidative stress
    16.1. Introduction to transition metals
    16.1.1. Generation of ROS
    16.1.2. ROS and biological system
    16.2. Exposure routes for nanoparticles
    16.3. Prooxidant effects of metal oxide nanoparticles
    16.4. Effects of NPs on cell organisms
    16.4.1. Absorption of NPs and cytotoxicity
    16.4.2. Absorption of NPs under environmental conditions
    16.4.3. NPs in outdoor spaces
    16.4.4. Interactions among organisms, NPs, and contaminants
    16.5. Nanoparticles-induced oxidative stress
    16.6. Oxidant generation via particle-cell interactions
    16.6.1. Lung injury caused by nanoparticle-induced reactive nitrogen species
    16.6.2. Mechanisms for ROS production and apoptosis within metal nanoparticles
    16.7. Modelling nanotoxicity
    16.8. Cellular signaling affected by metal nanoparticles
    16.8.1. NF-κB.
    16.8.2. AP-1.
    16.8.3. MAPK.
    16.8.4. PTP.
    16.8.5. Src.
    16.9. Carbon nanotubes (CNT)
    16.10. Carbon nanotube-induced oxidative stress
    16.11. Role of ROS in CNT-induced inflammation
    16.12. Role of ROS in CNT-induced genotoxicity
    16.13. Role of ROS in CNT-induced fibrosis
    16.14. Difficulties in determination of the mechanism of nanotoxicity in cells and in vivo
    16.15. Conclusion
    References

    17.Nanotechnological modifications of nanoparticles on reactive oxygen and nitrogen species (RONS)
    17.1. Nanotechnology and nanomaterials
    17.2. Nanotechnological modifications
    17.2.1. Nanodiffusion in the environment
    17.2.2. Nanomaterials in soil
    17.2.3. Nanoparticles mobility in soil
    17.3. Nanotechnology and agricultural sustainable development
    17.3.1. Nano fertilizers
    17.3.2. Nano pesticides
    17.3.3. Ecotoxicological implications of the nanoparticles
    17.4. Growth of cultivated plants and its ecotoxicological sustainability
    17.5. Applications of nanotechnology in the agricultural sector
    17.5.1. Nanosilver
    17.5.2. Nanosilica
    17.5.3. Nanotitanium dioxide
    17.5.4. Nanocalcium
    17.5.5. Nano-iron
    17.6. Nanotechnologies in food industry
    17.6.1. Food process
    17.6.2. Food packaging and labeling
    17.7. Selenium NPs as a food additive
    17.7.1. Problems with traditional forms of oral supplementation of selenium and potential benefits of SeNPs
    17.7.2. Mechanism of passage of NPs through intestinal mucosa
    17.7.3. Application of SeNPs through oral administration
    17.7.3.1. Nano-Se as an antioxidant
    17.7.3.2. Effect of SeNPs on reproductive performance
    17.7.3.3. Use of nano-Se for increasing hair follicle development and fetal growth
    17.7.3.4. Antiviral and antibacterial effects of SeNPs
    17.7.4. Anticancer effects of SeNPs
    17.7.4.1. Nano-Se as an anticancer drug
    17.7.4.2. Nano-Se as an anticancer drug delivery carrier
    17.7.4.3. Nano-Se as a promising orthopedic implant material and an agent reducing bone cancer cell functions
    17.8. Effect of SeNPs on oxidative stress parameters
    17.9. Protective effects of nano-Se
    17.9.1. SeNPs in prevention of cisplatin (CIS) induced reproductive toxicity
    17.9.2. Protective effect of nano-Se against polycyclic aromatic hydrocarbons
    17.9.3. Use of SeNPs for minimization of risk of iron overabundance
    17.9.4. SeNPs in treatment of heavy metal intoxication
    17.9.5. Nano-Se as an immunostimulatory
    17.9.6. Effect of Nano-Se on microbial fermentation, nutrients digestibility, and probiotics support
    17.9.7. Nano-Se in treatment of metabolic disorders
    17.10. Safety and toxicity concerns of orally delivered SeNPs for use as food additives and drug carriers
    References

    18.Medical imaging the complexity of nanoparticles and ROS dynamics in vivo for clinical diagnosis application
    18.1. Redox signaling
    18.2. Dynamics of the EPR signal of nitroxide radicals in leukemic and normal lymphocytes
    18.3. Redox-sensitive two-photon microscopy
    18.3.1. Two-photon redox-sensitive probes
    18.3.2. Two-photon sensitive probes for assessment of glutathione redox state
    18.3.3. Two-photon NADPH redox state sensitive probes
    18.3.4. Two-photon H2O2-sensitive probes
    18.3.5. Two-photon NO-sensitive probes
    18.4. Chemiluminescent imaging of ROS in vivo
    18.4.1. NIR fluorescence and chemiluminescence
    18.4.2. Chemiluminescent nanoparticles and ROS imaging
    18.5. Ultrasound in ROS imaging
    18.6. PET/SPECT in vivo imaging of oxidative stress using radiotracers
    18.6.1. Imaging glucose consumption as a surrogate of oxidative stress
    18.6.2. Radiotracers with redox potential-dependent cellular retention
    18.6.3. Radiotracers with hypoxia-dependent cellular retention
    18.6.4. Radiotracers targeting ROS scavengers or mitochondrial complex I-IV
    18.7. Magnetic resonance modalities
    18.7.1. Basic principles and technical considerations
    18.7.2. Examples of EPRI/MRI of ROS/RNS
    18.7.3. Brain imaging (without tumors)
    18.7.4. Tumor imaging
    18.7.5. Other organs
    18.7.6. Imaging of trapped radicals
    18.7.7. Dynamic nuclear polarization DNP-MRI (OMRI, PEDRI)
    18.8. Dynamics of the EPR signal of mito-TEMPO in cells of different origins and proliferative activities: Correlation with the levels of intracellular superoxide and hydrogen peroxide.
    18.9. Dynamics of the EPR signal of nitroxide radical in cells of the same origin and different proliferative activities: Correlation with the levels of intracellular superoxide, hydrogen peroxide, and antioxidant enzymes

Product details

  • No. of pages: 780
  • Language: English
  • Copyright: © Academic Press 2020
  • Published: June 26, 2020
  • Imprint: Academic Press
  • Paperback ISBN: 9780128224816
  • eBook ISBN: 9780128224960

About the Author

Loutfy H. Madkour

Dr. Loutfy H. Madkour is a professor of physical chemistry and nanoscience at the Chemistry Department, Faculty of Science, Al Baha University, Saudi Arabia, since 2012. He received his BSc, MSc, and PhD degrees in physical chemistry from the universities of Cairo, Minia, and Tanta, respectively, in Egypt. He worked as a lecturer in chemistry at the Tanta University since 1982 and as a professor of physical chemistry in 1999. He is an editorial board member of several international journals including International Journal of Industrial Chemistry (IJIC), International Journal of Ground Sediment & Water, E-Cronicon Chemistry (EC Chemistry), BAOJ Chemistry, Global Drugs and Therapeutics (GDT), Chronicles of Pharmaceutical Science, and Journal of Targeted Drug Delivery.

Affiliations and Expertise

Chemistry Department, Faculty of Science, Al Baha University, Saudi Arabia

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