Oxidative Stress And Inflammation As Targets For Novel Preventive And Therapeutic Approaches In Non Communicable Diseases Ii

Non-communicable diseases are chronic non-infectious pathologies that represent the leading cause of death and disability for the general population. Oxidative stress and inflammation induce and modulate several signaling pathways that play a crucial role in the pathophysiology and progression of these diseases. Therefore, they represent a good target for the development of different therapeutic strategies and open new strategies for assessment and intervention. This book focuses on different approaches to investigate the underlying pathogenesis and treatment mechanisms of conditions related to oxidative stress and inflammation. Particular attention is given to biomarkers specific to these features that can detail the pathogenesis and evolution of kidney disease, cardiovascular disease, obesity, breast cancer, and idiopathic pulmonary fibrosis. In addition, the potential medicinal and beneficial effects of plant compounds such as oleuropein, columbianadin, and rebaudioside A are addressed.

Non-communicable diseases (NCDs) are chronic diseases that include most ageing-related diseases, representing the main cause of death and disability in the general population. Inflammation and oxidative stress are common features in NCDs, responsible for the cell, tissue, and organ damage that contributes to the progression of these diseases. They may be also key targets for the development of novel preventive and therapeutic strategies. This Special Issue includes 14 peer-reviewed papers, including 12 original research papers and 2 reviews. Together, they represent the most recent progress in the field of several degenerative disorders, aiming to establish specific biomarkers, detailing the pathogenesis and the evolution of these diseases, making a correct diagnosis, and opening up new therapeutic strategies. Of relevance, many studies report the beneficial effects of natural compounds, derived from several plants, leaves, and fruits; their antioxidant and anti-inflammatory properties suggest their use as a dietary supplement for prevention and/or complement to standard therapies.

Non-communicable diseases (NCDs) are chronic diseases that include most ageing-related diseases, representing the main cause of death and disability in the general population. Inflammation and oxidative stress are common features in NCDs, responsible for the cell, tissue, and organ damage that contributes to the progression of these diseases. They may be also key targets for the development of novel preventive and therapeutic strategies. This Special Issue includes 14 peer-reviewed papers, including 12 original research papers and 2 reviews. Together, they represent the most recent progress in the field of several degenerative disorders, aiming to establish specific biomarkers, detailing the pathogenesis and the evolution of these diseases, making a correct diagnosis, and opening up new therapeutic strategies. Of relevance, many studies report the beneficial effects of natural compounds, derived from several plants, leaves, and fruits; their antioxidant and anti-inflammatory properties suggest their use as a dietary supplement for prevention and/or complement to standard therapies. Special thanks to all authors and reviewers for their valuable contributions and constructive suggestions and to the publishing team of Antioxidants for their help in compiling this Special Issue.

Oxidative stress and inflammation underpin most diseases; their mechanisms are inextricably linked. For example, chronic inflammation is associated with oxidation, anti-inflammatory cascades are linked to decreased oxidation, increased oxidative stress triggers inflammation and redox balance inhibits the inflammatory cellular response. Whether or not oxidative stress and inflammation represent the causes or the consequences of cellular pathology, they contribute significantly to the pathogenesis of non-communicable diseases. The incidence of obesity and other related metabolic disturbances are rising, as are age-related diseases due to progressively aging populations. Interrelations between the mechanisms of oxidative stress and of inflammatory signaling and metabolism are, in the broad sense of energy transformation, being increasingly recognized as part of the problem in non-communicable diseases. The book Oxidative Stress and Inflammation in Non-communicable Diseases: Molecular Mechanisms and Perspectives in Therapeutics is an update on the latest research on the molecular basis of non-communicable diseases and the search for possible therapeutic alternatives. The authors of this monograph are experts in their field and the book as a whole, provides an overview of the biochemical alterations underlying diseases such as cardiovascular disease, cancer, obesity, renal disease, neurological diseases and diabetes, emphasizing those aspects that they share in common. We hope that this book will be useful for researchers in biomedicine and also for physicians interested in finding the root causes of the disease, as well as for post-graduate students in biochemistry, molecular biology, nutrition or medicine.

Novel Therapeutic Approaches Targeting Oxidative Stress investigates the role of oxidative stress in disease and explores the latest methods and approaches to targeting oxidative stress for treatment and diagnosis. The book begins with an introduction to oxidative stress and its significance. Subsequent sections cover biochemical methods for detecting free radicals and novel therapeutic approaches for targeting oxidative stress in a number of different diseases. This includes age-related illnesses, neuropsychiatric disorders such as schizophrenia and bipolar disorder, and neurodegenerative diseases like Alzheimer’s and Parkinson’s disease. Novel approaches for targeting oxidative stress in cancer and cardiovascular diseases are also explored. The book then moves on to discuss advances in drug delivery systems and detecting oxidative stress biomarkers using biosensors. It concludes with case studies that illustrate the targeting of oxidative stress and future perspectives. Explores oxidative stress in a variety of diseases, including neurological disorders, cardiovascular diseases, age-related diseases, and cancer Covers a range of therapeutic approaches to target oxidative stress Includes chapters on the application of novel drug delivery systems and diagnostic biosensors to oxidative stress Features case studies illustrating the targeting of oxidative stress

Specifically focusing on the redox regulation of cell signaling responsible for oxidative stress and inflammatory tissue damage, this reference provides a comprehensive overview of cutting-edge research on the intracellular events mediating or preventing oxidative stress and pro-inflammatory processes induced by endogenous and xenobiotic factors-an

We are faced with a metabolic disease pandemic. The prevalence of obesity-related metabolic diseases has increased exponentially in the last 50 years, in large part from a sedentary lifestyle and consumption of a diet high in fat (HFD) and simple sugars. Many diet-induced metabolic diseases, such as type 2 diabetes, atherosclerosis and non-alcoholic fatty liver disease, are associated with obesity. The direct connection between metabolic diseases and obesity is in part related to the development of low grade inflammation and disruption of metabolic regulation caused by oxidative stress. Using mouse models, we demonstrate the therapeutic potential of antioxidants and over-the-counter anti-inflammatory drugs in targeting and preventing diet-induced metabolic disease, and conclude that oxidative stress and inflammation provide common etiological mechanisms and potential therapeutic targets for prevention or reversal of diet-induced metabolic diseases. Consumption of a HFD causes dramatic changes in physiology of an individual. In particular, dyslipidemia induced by consumption of a high-fat or unbalanced diet can cause alterations in the structure and function of adipose, vasculature, liver, and muscle. Chronic imbalance in plasma lipids can cause an oxidative response in these tissues through the induction of the NADPH oxidase (NOX) complex, producing superoxide anion (O2) in the cytoplasm. Chronic activation of NOX results in overproduction of reactive oxygen, which can alter expression of adipose tissue-derived cytokines and inflammatory mediators such as adiponectin, leptin, visfatin, resistin, TNF[alpha], IL-6, and IL-1[beta]. Disruption of these signals cause global modulation of metabolism, resulting in accumulation of lipid in muscle and liver, elevation of blood pressure, and insulin resistance. Treating mice with antioxidants and anti-inflammatory drugs prevents the development of obesity, insulin resistance, and dyslipidemia, suggesting that ablation of this common etiological factor in metabolic disease may prove a useful therapeutic strategy for disease prevention or reversal. The analgesic drug, acetaminophen (APAP), demonstrated the greatest effect in preventing HFD-induced metabolic disease in mice, likely through its combined anti-inflammatory and antioxidant potential. Other over-the-counter analgesic drugs and antioxidants were tested yielding similar results. One potentially important mechanism for APAPs protective effects is the inhibition of NOX activity in white adipose tissue, which may help to maintain normal adipose homeostasis. We have also examined the protective effects of endogenous antioxidant systems in preventing diet-induced metabolic disease. Mice lacking the modifier subunit [Gclm ( -/- )] of glutamate cysteine ligase (GCL) were fed a HFD for 10 weeks and compared to wildtype [Gclm (+/+)] mice. We found that Gclm ( -/- ) mice were resistant to diet-induced obesity and hepatic lipid accumulation. Gclm ( -/- ) mice also appeared to have higher basal metabolic rate, indicated by increased systemic oxygen consumption.Combined, these findings highlight the importance of oxidative stress in the development of diet-induced metabolic disease, and provide a common etiological target for development of new therapeutic strategies. Further characterization of the effects of oxidative stress in development of these diseases may provide more specific targets for prevention or reversal of HFD-induced metabolic diseases.

Oxidative stress plays a crucial role in the pathophysiology of various diseases when there is a disruption of the intracellular redox balance and the homeostatic balance between cellular oxidants and antioxidants. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) react with molecular targets including proteins, lipids, and nucleic acids contributing to mitochondrial injury and cellular dysfunction. This book intends to provide the readers with an extensive overview of the novel approaches and prospects based on oxidative and nitrosative stress in the pathophysiology of various diseases and in the current treatment strategies with antioxidants.

The book starts with the editors' preface summarizing the contributions of each of the following thirteen articles dealing with chemical and pharmacological aspects of the molecular modulators of the oxidative stress in regard to various therapeutic approaches in cardiovascular and neurodegenerative diseases, cancer, and diabetes. The seven articles present data from original research studies enlightening the roles and mechanisms of action of small molecular weight compounds (natural and synthetic; ascorbic acid/vitamin C, deferoxamine, N-acetylcysteine, MitoVitE, α-tocopherol, trolox, and ezetimibe) or proteins (SIRT3) in modulation of oxidative stress. In the six review papers, the authors present and discuss the possible therapeutic potential of novel approaches and compounds that are promising and deserve further investigation, in modulation of oxidative stress.

In the 1980s, biochemists and biologists were attracted by the role of reactive oxygen species in the irreversible damage or modification of the structure of biological molecules. However, in the 1990s, reactive oxygen species have been recognized to be involved in reversible structural alterations of molecules: The homeostatic modulation of oxidant levels is a highly efficient mechanism that allows all cells to tightly control their redox status within a very narrow range. Especially the activity of the Rel/NF-kB family of transcriptional factors that regulate responses in inflammation, reperfusion injury and apoptosis is controlled by intracellular reactive oxygen species levels. Our understanding of how these transcriptional factors are negatively or positively regulated by oxidative stress has since greatly increased. Questions for future investigation center on the modulation of oxidative stress by personal genome information for the prevention of several pathologic states.