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

  • Book

  • June 2020
  • Elsevier Science and Technology
  • ID: 4991150

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.

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Table of Contents

1. Pathophysiological, toxicological and immunoregulatory roles of reactive oxygen and nitrogen species (RONS)2. Biological mechanisms of reactive oxygen species (ROS)3. Cellular signaling pathways with reactive oxygen species (ROS)4. Manganese as the essential element in oxidative stress, and metabolic diseases5. Affected energy metabolism is primal cause of manganese toxicity6. Heavy metals and free radicals-induced cell death mechanisms7. Cytotoxic mechanisms of xenobiotic heavy metals on oxidative stress8. Oxidative stress and oxidative damage-induced cell death9. Cell death mechanisms-apoptosis pathways and their implications in toxicology10. Programmed cell death mechanisms and nanoparticles toxicity11. Endoplasmic reticulum stress (ERS) and associated ROS in disease pathophysiology applications12. Endoplasmic reticulum (ER) stress-induced cell death mechanism 13.Modulation of endoplasmic reticulum (ER) stress of nanotoxicology for nanoparticles (NPs)14. Nanoparticle cellular uptake and intracellular targeting on reactive oxygen species (ROS) in biological activities 15. Metal nanoparticles (MNPs) and particulate matter (PM) induce toxicity16. Mechanisms for nanoparticles-mediated oxidative stress17. Nanotechnological modifications of nanoparticles on reactive oxygen and nitrogen species (RONS)18. Medical imaging the complexity of nanoparticles and ROS dynamics in vivo for clinical diagnosis application19.Titanium dioxide nanoparticles induced cytotoxicity, genotoxicity-generation of reactive oxygen species and cell damage20. Toxicity of ZnO nanoparticles induced reactive oxygen species and cancer cells21. Silver nanoparticles induce cellular cytotoxicity, genotoxicity, DNA damage and cell death22.Correlations between oxidative stress and aligning nanoparticles safety assessments 23. Effects of interactions between antioxidant defenses therapy and ROS24. FDA breakthrough (BT)- - drug therapy designations for clinical evidence Appendix: List of abbreviations

Authors

Loutfy H. Madkour Chemistry Department, Faculty of Science, Al Baha University, Saudi Arabia. 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.