Advances in Molecular Toxicology Vol 11

 
 
Elsevier (Verlag)
  • 1. Auflage
  • |
  • erschienen am 2. Oktober 2017
  • |
  • 290 Seiten
 
E-Book | ePUB mit Adobe DRM | Systemvoraussetzungen
978-0-12-812523-6 (ISBN)
 

Advances in Molecular Toxicology, Volume 11, features the latest advances in the subspecialties of the broad area of molecular toxicology. This series details the study of the molecular basis of toxicology by which a vast array of agents encountered in the human environment, and produced by the human body, manifest themselves as toxins.

The book is not strictly limited to documenting these examples, but also covers the complex web of chemical and biological events that give rise to toxin-induced symptoms and disease. The new technologies that are being harnessed to analyze and understand these events are also reviewed by leading experts in the field.

  • Provides cutting-edge reviews by leading workers in the discipline
  • Includes in-depth dissection of the molecular aspects that are of interest to a broad range of scientists, physicians and any student in the allied disciplines
  • Presents leading-edge applications of technological innovations in chemistry, biochemistry and molecular medicine
1872-0854
  • Englisch
  • Saint Louis
  • |
  • Niederlande
  • 11,27 MB
978-0-12-812523-6 (9780128125236)
weitere Ausgaben werden ermittelt
  • Front Cover
  • Advances in Molecular Toxicology
  • Copyright
  • Contents
  • Contributors
  • Preface
  • Chapter One: Toxicity of Naturally Occurring Anthraquinones
  • 1. Introduction
  • 1.1. Biosynthesis of AQs
  • 1.1.1. The polyketide pathway
  • 1.1.2. The chorismate/o-succinylbenzoic acid pathway
  • 1.2. Biosynthesis of ring A and B or shikimate pathway
  • 1.3. Biosynthesis of ring C
  • 1.3.1. The MVA pathway
  • 1.3.2. The MEP pathway
  • 2. Toxicological Effects of Plants Containing Anthraquinones
  • 2.1. Rhamnus alaternus
  • 2.1.1. AQs profiling of R. alaternus
  • 2.1.2. Toxicity of R. alaternus
  • 2.2. Rhamnus frangula
  • 2.2.1. AQs profiling of R. frangula
  • 2.2.2. Toxicity of R. frangula
  • 2.3. Rhamnus cathartica
  • 2.3.1. AQs profiling of Rhamnus cathartica
  • 2.3.2. Toxicity of Rhamnus cathartica
  • 2.4. Rhamnus purshiana
  • 2.4.1. AQs profiling of R. purshiana
  • 2.4.2. Toxicity of R. purshiana
  • 2.5. Aloe vera
  • 2.5.1. AQs profiling of A. vera
  • 2.5.2. Toxicity of A. vera
  • 2.6. Polygonum multiflorum
  • 2.6.1. AQs profiling of P. multiflorum
  • 2.6.2. Toxicity of P. multiflorum
  • 2.7. Cassia obtusifolia
  • 2.7.1. AQs profiling of C. obtusifolia
  • 2.7.2. Toxicity of C. obtusifolia
  • 2.8. Rheum palmatum
  • 2.8.1. AQs profiling of R. palmatum
  • 2.8.2. Toxicity of R. palmatum
  • 2.9. Cassia acutifolia
  • 2.9.1. AQs profiling of C. acutifolia
  • 2.9.2. Toxicity of C. acutifolia
  • 2.10. Rubia tinctorum
  • 2.10.1. AQs profiling of R. tinctorum
  • 2.10.2. Toxicity of R. tinctorum
  • 2.11. Hypericum perforatum
  • 2.11.1. AQs profiling of H. perforatum
  • 2.11.2. Toxicity of H. perforatum
  • 2.12. Cassia occidentalis
  • 2.12.1. AQs profiling of C. occidentalis
  • 2.12.2. Toxicity of C. occidentalis
  • 2.13. Morinda citrifolia
  • 2.13.1. AQs profiling of M. citrifolia
  • 2.13.2. Toxicity of M. citrifolia
  • 3. Inference
  • Acknowledgments
  • References
  • Chapter Two: Advances in TCE Toxicology
  • 1. Introduction
  • 2. Carcinogenicity of TCE
  • 2.1. Kidney cancer
  • 2.1.1. Epidemiological data
  • 2.1.2. Animal experiments
  • 2.1.3. Modes of action
  • 2.1.3.1. Mutagenicity
  • 2.1.3.2. Nongenotoxic mechanisms
  • 2.2. Liver cancer
  • 2.2.1. Epidemiological data
  • 2.2.2. Animal experiments
  • 2.2.3. Modes of action for hepatocarcinogenicity
  • 2.2.3.1. Mutagenicity
  • 2.2.3.2. Cell proliferation
  • 2.2.3.3. Peroxisome proliferator-activated receptor alpha (PPARα) activation
  • 2.2.3.4. Epigenetic mechanisms
  • 3. Cardiac Developmental Toxicity of TCE
  • 3.1. Epidemiological data
  • 3.2. Animal experiments
  • 3.3. In vitro model
  • 3.4. Modes of action
  • 3.4.1. Epithelial-mesenchymal cell transformation
  • 3.4.2. Ca2+ fluxes
  • 3.4.3. Epigenetic mechanisms
  • 4. Immunotoxicity of TCE
  • 4.1. Systemic sclerosis
  • 4.1.1. Epidemiological data
  • 4.1.2. Animal experiments
  • 4.2. Generalized hypersensitivity syndrome
  • 4.2.1. Epidemiological data
  • 4.2.2. Animal experiments
  • 4.3. Immunosuppression
  • 4.3.1. Epidemiological data
  • 4.3.2. Animal experiments
  • 4.4. Modes of action
  • 4.5. Conclusion
  • References
  • Chapter Three: Current Status, Gaps, and Weaknesses of the Mechanism of Selective Dopaminergic Toxicity of MPTP/MPP+
  • 1. Introduction
  • 2. MPTP
  • 2.1. Discovery
  • 2.2. Animal models
  • 2.3. In vitro cell models
  • 2.4. Mechanism of selective dopaminergic toxicity
  • 2.5. Mitochondrial complex I inhibition hypothesis
  • 3. Dopaminergic Toxins Structurally Similar to MPTP/MPP+
  • 3.1. MPTP/MPP+ derivatives
  • 3.2. Endogenous dopaminergic toxins structurally similar to MPTP
  • 3.2.1. TIQ derivatives
  • 3.2.1.1. Salsolinol
  • 3.2.1.2. THP
  • 3.2.2. ß-Caroline derivatives
  • 4. Gaps and the Weaknesses of the Mechanism of MPTP/MPP+ Model
  • 4.1. Oxidation of MPTP by MAO-B
  • 4.2. Role of DAT and OCT-3 in the toxicity of MPTP/MPP+
  • 4.3. Is efficient cellular uptake itself sufficient for the MPP+ toxicity?
  • 4.4. VMAT2 and detoxification mechanism
  • 5. Mechanism of Mitochondrial Uptake of MPP+
  • 5.1. Effect of Ca2+ on the mitochondrial accumulation of MPP+
  • 6. Possible Role of DA in MPTP/MPP+ Dopaminergic Toxicity
  • 7. Conclusions
  • Acknowledgments
  • References
  • Chapter Four: Adult Stem Cells and Anticancer Therapy
  • 1. Biopharmaceutical Stem Cell Potential
  • 2. Stem Cells
  • 2.1. Pluripotent stem cells
  • 2.2. Adult stem cells
  • 2.2.1. Mesenchymal stem cells
  • 2.2.2. Developmentally early stem cells in adult tissues
  • 2.2.3. Muscle-derived stem cells
  • 2.2.4. Hematopoietic stem cells
  • 2.3. Transdifferentiation
  • 2.4. Normal stem cells in the control of a tumor
  • 3. Anticancer Drugs-Current Directions, Advances, and Challenges
  • 3.1. Conventional cytotoxic agents
  • 3.2. Targeted therapy
  • 3.2.1. Anti-CSC-targeted therapy
  • 3.2.2. Targeting tumor heterogeneity
  • 3.2.3. Targeting cancer cell plasticity
  • 3.3. Anticancer drug toxicity problem
  • 4. Assessment of Drug Toxicity
  • 4.1. Methods for toxicity evaluation
  • 4.1.1. Plasma membrane-dependent accumulation of dyes inside a cell
  • 4.1.2. Mitochondria-associated dyes
  • 4.1.3. Redox-based assays
  • 4.1.4. ATP level measurement
  • 4.1.5. Other enzymatic activity in a cytoplasm
  • 4.1.6. Protein release
  • 4.1.7. Clonogenic assay
  • 4.1.8. Cell counting/detachment
  • 4.1.9. Protein staining
  • 4.1.10. Phosphatidylserine detection with annexin V
  • 4.2. Cellular models for anticancer drug testing
  • 4.2.1. Single-cell models
  • 4.2.2. 2D cell cultures
  • 4.2.3. 3D drug testing models
  • 4.2.3.1. Scaffold-based 3D culture systems
  • 4.2.3.2. Tissue slices
  • 4.2.3.3. 3D cellular spheroids
  • 4.2.3.4. Organoid model
  • 4.2.3.5. Organs on chips
  • 4.2.4. Toward cell monitoring in situ
  • 4.3. Effect of anticancer drugs on HSCs
  • 4.4. Effect of anticancer drugs on stem cells from solid tissues
  • 5. Concluding Remarks
  • References
  • Chapter Five: Inhibitors and Poisons of Mammalian Type II Topoisomerases
  • 1. Introduction to Topoisomerases
  • 2. Clinically Approved Poisons and Their Derivatives
  • 2.1. Podophyllotoxin derivatives
  • 2.2. Anthracyclines
  • 2.3. Acridines
  • 2.4. Ellipticines
  • 3. Catalytic Inhibitors and Derivatives
  • 3.1. Bisdioxopiperazines
  • 3.2. Merbarone
  • 3.3. Novobiocin
  • 4. Recent Updates in Novel Analogs and Drug Metabolites
  • 4.1. Etoposide metabolites and analogs
  • 4.2. Acridine analogs
  • 4.3. Anthracyclines
  • 4.4. Salicylate
  • 5. Recent Updates in Natural Products and Dietary Compounds
  • 5.1. A berberine derivative
  • 5.2. Curcumin
  • 5.3. Eusynstyelamide B
  • 5.4. HU-331
  • 5.5. Resveratrol
  • 5.6. Xanthones
  • 6. Recent Updates in Synthetic Compounds
  • 6.1. Benzo[a]phenazine derivatives
  • 6.2. Naphthalimide derivatives and conjugates
  • 6.3. Phenanthriplatin
  • 6.4. Pyridine
  • 6.5. 1,3-Benzoazolyl-substituted pyrrolo[2,3-b]pyrazine
  • 6.6. Quinoline aminopurine compound 1
  • 6.7. Quinolone-based anticancer agent: Vosaroxin
  • 6.8. Quinoxaline analogs
  • 6.9. Thiadiazoles
  • 6.10. Thiochromanone
  • 6.11. Thiosemicarbazones
  • 6.12. Triazines
  • 7. The Path Forward: Strategies for Targeting Topoisomerase II
  • Acknowledgments
  • References
  • Chapter Six: Metabolic Activation and Toxicities of bis-Benzylisoquinoline Alkaloids
  • 1. Introduction
  • 2. bis-Benzylisoquinoline Alkaloids
  • 2.1. Dauricine
  • 2.2. Tetrandrine
  • 2.3. Neferine
  • 2.4. Berbamine
  • 3. Detection of Reactive Metabolites Generated From para-Methylene Phenol Moiety
  • 4. Conclusion
  • References
  • Index
  • Back Cover

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