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      Lifestyle, Oxidative Stress, and Antioxidants: Back and Forth in the Pathophysiology of Chronic Diseases


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          Oxidative stress plays an essential role in the pathogenesis of chronic diseases such as cardiovascular diseases, diabetes, neurodegenerative diseases, and cancer. Long term exposure to increased levels of pro-oxidant factors can cause structural defects at a mitochondrial DNA level, as well as functional alteration of several enzymes and cellular structures leading to aberrations in gene expression. The modern lifestyle associated with processed food, exposure to a wide range of chemicals and lack of exercise plays an important role in oxidative stress induction. However, the use of medicinal plants with antioxidant properties has been exploited for their ability to treat or prevent several human pathologies in which oxidative stress seems to be one of the causes. In this review we discuss the diseases in which oxidative stress is one of the triggers and the plant-derived antioxidant compounds with their mechanisms of antioxidant defenses that can help in the prevention of these diseases. Finally, both the beneficial and detrimental effects of antioxidant molecules that are used to reduce oxidative stress in several human conditions are discussed.

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          Free radicals and antioxidants in normal physiological functions and human disease.

          Reactive oxygen species (ROS) and reactive nitrogen species (RNS, e.g. nitric oxide, NO(*)) are well recognised for playing a dual role as both deleterious and beneficial species. ROS and RNS are normally generated by tightly regulated enzymes, such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively. Overproduction of ROS (arising either from mitochondrial electron-transport chain or excessive stimulation of NAD(P)H) results in oxidative stress, a deleterious process that can be an important mediator of damage to cell structures, including lipids and membranes, proteins, and DNA. In contrast, beneficial effects of ROS/RNS (e.g. superoxide radical and nitric oxide) occur at low/moderate concentrations and involve physiological roles in cellular responses to noxia, as for example in defence against infectious agents, in the function of a number of cellular signalling pathways, and the induction of a mitogenic response. Ironically, various ROS-mediated actions in fact protect cells against ROS-induced oxidative stress and re-establish or maintain "redox balance" termed also "redox homeostasis". The "two-faced" character of ROS is clearly substantiated. For example, a growing body of evidence shows that ROS within cells act as secondary messengers in intracellular signalling cascades which induce and maintain the oncogenic phenotype of cancer cells, however, ROS can also induce cellular senescence and apoptosis and can therefore function as anti-tumourigenic species. This review will describe the: (i) chemistry and biochemistry of ROS/RNS and sources of free radical generation; (ii) damage to DNA, to proteins, and to lipids by free radicals; (iii) role of antioxidants (e.g. glutathione) in the maintenance of cellular "redox homeostasis"; (iv) overview of ROS-induced signaling pathways; (v) role of ROS in redox regulation of normal physiological functions, as well as (vi) role of ROS in pathophysiological implications of altered redox regulation (human diseases and ageing). Attention is focussed on the ROS/RNS-linked pathogenesis of cancer, cardiovascular disease, atherosclerosis, hypertension, ischemia/reperfusion injury, diabetes mellitus, neurodegenerative diseases (Alzheimer's disease and Parkinson's disease), rheumatoid arthritis, and ageing. Topics of current debate are also reviewed such as the question whether excessive formation of free radicals is a primary cause or a downstream consequence of tissue injury.
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            Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal

            Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown.
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              The NOX family of ROS-generating NADPH oxidases: physiology and pathophysiology.

              For a long time, superoxide generation by an NADPH oxidase was considered as an oddity only found in professional phagocytes. Over the last years, six homologs of the cytochrome subunit of the phagocyte NADPH oxidase were found: NOX1, NOX3, NOX4, NOX5, DUOX1, and DUOX2. Together with the phagocyte NADPH oxidase itself (NOX2/gp91(phox)), the homologs are now referred to as the NOX family of NADPH oxidases. These enzymes share the capacity to transport electrons across the plasma membrane and to generate superoxide and other downstream reactive oxygen species (ROS). Activation mechanisms and tissue distribution of the different members of the family are markedly different. The physiological functions of NOX family enzymes include host defense, posttranlational processing of proteins, cellular signaling, regulation of gene expression, and cell differentiation. NOX enzymes also contribute to a wide range of pathological processes. NOX deficiency may lead to immunosuppresion, lack of otoconogenesis, or hypothyroidism. Increased NOX activity also contributes to a large number or pathologies, in particular cardiovascular diseases and neurodegeneration. This review summarizes the current state of knowledge of the functions of NOX enzymes in physiology and pathology.

                Author and article information

                Front Physiol
                Front Physiol
                Front. Physiol.
                Frontiers in Physiology
                Frontiers Media S.A.
                02 July 2020
                : 11
                : 694
                [1] 1Department of Medical Parasitology, Faculty of Medicine, Kerman University of Medical Sciences , Kerman, Iran
                [2] 2Department of Chemistry, Manipal Institute of Technology, Manipal Academy of Higher Education , Manipal, India
                [3] 3Department of Biomedical Sciences, University of Cagliari , Cagliari, Italy
                [4] 4Department of Biomedical, Surgical and Dental Sciences, Milan State University , Milan, Italy
                [5] 5Department of Biological and Environmental Sciences and Technologies (Di.S.Te.B.A.), University of Salento , Lecce, Italy
                [6] 6Medical Faculty, Institute of Pharmacology, Clinical Pharmacology and Toxicology, University of Belgrade , Belgrade, Serbia
                [7] 7Department of Biochemistry, Faculty of Science, University of Bamenda , Bambili, Cameroon
                [8] 8CREA – Research Centre for Food and Nutrition , Rome, Italy
                [9] 9Department of Pharmaceutical Chemistry, H.N.B. Garhwal (A Central) University , Srinagar, India
                [10] 10Department of Biochemistry, Hemvati Nandan Bahuguna Garhwal University (A Central University) , Srinagar, India
                [11] 11Department of Agriculture and Food Engineering, School of Engineering, Holy Spirit University of Kaslik , Jounieh, Lebanon
                [12] 12General Pathology Section, Department of Experimental, Diagnostic and Specialty Medicine – DIMES , Bologna, Italy
                [13] 13Department of Agricultural and Environmental Sciences, Milan State University , Milan, Italy
                [14] 14Faculty of Medicine, University of Porto , Porto, Portugal
                [15] 15Institute for Research and Innovation in Health (i3S), University of Porto , Porto, Portugal
                [16] 16Department of Nutrition and Dietetics, Faculty of Pharmacy, University of Concepcion , Concepcion, Chile
                [17] 17Unidad de Desarrollo Tecnológico, Universidad de Concepción UDT , Concepcion, Chile
                [18] 18Department of Clinical Pharmacy, University of Medicine and Pharmacy of Craiova , Craiova, Romania
                [19] 19Department of Chemistry, The University of Alabama in Huntsville , Huntsville, AL, United States
                [20] 20Department of Clinical Pharmacy, University of Medicine and Pharmacy of Craiova , Craiova, Romania
                [21] 21Department of Clinical Oncology, Queen Elizabeth Hospital , Hong Kong, China
                [22] 22Phytochemistry Research Center, Shahid Beheshti University of Medical Sciences , Tehran, Iran
                Author notes

                Edited by: Chengxing Shen, Shanghai Sixth People’s Hospital, China

                Reviewed by: Kai Hu, University Hospital Würzburg, Germany; Jun Ren, University of Washington, United States

                *Correspondence: Miquel Martorell, mmartorell@ 123456udec.cl

                This article was submitted to Oxidant Physiology, a section of the journal Frontiers in Physiology

                Copyright © 2020 Sharifi-Rad, Anil Kumar, Zucca, Varoni, Dini, Panzarini, Rajkovic, Tsouh Fokou, Azzini, Peluso, Prakash Mishra, Nigam, El Rayess, Beyrouthy, Polito, Iriti, Martins, Martorell, Docea, Setzer, Calina, Cho and Sharifi-Rad.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                : 16 April 2020
                : 27 May 2020
                Page count
                Figures: 6, Tables: 0, Equations: 9, References: 204, Pages: 21, Words: 0

                Anatomy & Physiology
                reactive oxygen species,oxidative stress,natural antioxidants,neurological disorders,cardiovascular diseases,cancer,aging,antioxidant defense


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