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

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