"Reactive oxygen species (ROS) play an essential role in different biological functions, including physiological regulatory mechanisms to damaging alterations involved in the pathogenesis of an increasing number of human diseases. ROS are metabolic products from numerous cells, but two vital cellular organelles are intimately involved in their production and metabolism, i.e. the endoplasmic reticulum and the mitochondria. Excess cellular levels of ROS may cause damage to proteins, nucleic acids, lipids, membranes, and organelles, which may lead to the activation of cell death processes such as apoptosis. Apoptosis is a highly regulated process that is essential for the development and survival of multicellular organisms. These organisms often need to discard superfluous or potentially harmful cells, have accumulated mutations, or become infected by pathogens. Apoptosis features a characteristic set of morphological and biochemical features whereby cells undergo a cascade of self-destruction. Thus, proper regulation of apoptosis is essential for maintaining normal cellular homeostasis. Mitochondrial ROS (mtROS) play a central role in cell signaling and regulating the main pathways of apoptosis, mediated by mitochondria, death receptors, and the endoplasmic reticulum (ER) stress. This book focuses on the current understanding of the role of ROS in each of these three main pathways of apoptosis related to different human diseases, with particular emphasis on Metabolic, Inflammatory, Neurodegenerative, and Neoplastic diseases. It's promise and limitations are also discussed by targeting ROS with different antioxidants in preventing non-communicable diseases. The role of mtROS in the complex interplay and crosstalk between these different signaling pathways of apoptosis related to different human diseases remains to be unraveled further in future research"--

Oxygen represents only 20% of the Earth's atmosphere, yet it is vital for the survival of aerobic organisms. There is a dark part of the use of oxygen that consists in generating reactive species that are potentially harmful to living organisms. Moreover, reactive oxygen species can combine with nitrogen derivatives and generate many other reactive species. Thus, living organisms are continuously assaulted by reactive species from external or internal sources. However, the real danger comes in the case of high concentrations and prolonged exposure to these species. This book presents an image of the mechanisms of action of reactive species and emphasizes their involvement in diseases. Inflammation and cancer are examined to determine when and how reactive species turn the evolution of a benign process to a malignant one. Some answers may come from recent studies indicating that reactive species are responsible for epigenetic changes.

ROS occur continuously in all the cells as a part of normal cellular function and are a potential double -edged sword in diseases prevention and promotion. When ROS present in high enough concentration, can damage cellular proteins, lipids and nucleic acids that may promote various diseases. Advances in research have shown that low to moderate concentrations of ROS play crucial roles in normal physiological processes, such as through redox regulation of protein phosphorylation, ion channels and transcription factors etc. and are also required for biosynthetic processes, including thyroid hormone production and cross linking of extracellular matrix. ROS induced disease, can be either due to a lack of ROS (chronic granulomatous disease, certain autoimmune disorders) or a surplus of ROS (CV & neurodegenerative diseases). The human body has several mechanisms to counteract the ROS by producing antioxidants, which are either naturally produced in situ or externally supplied through foods and /or supplements. Antioxidant supplementation has proven largely ineffective in clinical studies, most probably because their action is too late, too little and too non-specific.

Unlike other narrowly focused books, Reactive Oxygen Species in Biology and Human Health provides a comprehensive overview of ROS. It covers the current status of research and provides pointers to future research goals. Additionally, it authoritatively reviews the impact of reactive oxygen species with respect to various human diseases and discusses antioxidants and other compounds that counteract oxidative stress. Comprised of seven sections, the first section describes the introduction, detection, and production of ROS, emphasizing phenolic compounds and vitamin E for their abilities to act as antioxidants. This section also highlights the role of lipoprotein-associated oxidative stress. Section two addresses the importance of iron accumulation in the brain resulting in the development of a group of neurodegenerative disorders (NDs) and identifies several causative genes for neurodegeneration with brain iron accumulation (NBIA) associated with Parkinsonism-related disorders. The third section discusses a number of NDs, including amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), Huntington's disease (HD), epilepsy, and multiple sclerosis (MS). Section four addresses autoimmune diseases caused by ROS, including asthma, autoimmune liver diseases, rheumatoid arthritis, thyroid disease, primary biliary cirrhosis, and systemic lupus. Section five analyzes a number of different cancers, including lung cancer, breast cancer, and melanoma, along with possible treatment regimens. Section six discusses cardiovascular diseases (CVDs) induced by ROS, presents the ROS-associated complex biochemical processes inducing inflammation as an important cause of CVDs, and explains the roles carotenoids play in preventing CVDs. The final section addresses other human diseases induced by oxidative stress, including sickle cell disease, nonalcoholic steatohepatitis, retinopathy, fibromyalgia, chronic obstructive pulmonary disease, asthma, pulmonary hypertension, infertility, and aging of human skin.

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