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Special Issue "The Role of Oxidant Stress in Disease"

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Immunology".

Deadline for manuscript submissions: closed (30 November 2016)

Special Issue Editor

Guest Editor
Dr. Francisco Dasí

Valencia Clinical Hospital Research Foundation (IIS INCLIVA), Avda. Menéndez y Pelayo 4, 46010 Valencia, Spain
Website | E-Mail
Interests: oxidative stress; pulmonary rare diseases; epigenetics

Special Issue Information

Dear Colleagues,

Oxidative stress refers to a condition caused by a persistent imbalance between antioxidants and oxidants, in favour of the latter. Under physiological conditions, reactive oxygen species (ROS) are constantly produced both by endogenous and exogenous sources in the organism where they are involved in physiological responses, such as signalling processes and defence mechanisms against infectious pathogens. However, its accumulation, either transitorily or chronically, leads to damage of the cellular components, producing changes in the cellular metabolism and its regulation, eventually leading to disease. Over the last 25 years, clinical and basic research has shown a relationship between oxidative stress and disease. In humans, oxidative stress is thought to be involved in the development of several diseases, such as cancer, cardiovascular and neurological diseases, rare diseases, and aging among many others. Once the implication of oxidative stress in a particular disease is demonstrated, the possibility of using antioxidant therapies in the clinical setting (both as antioxidant therapy and as prophylactics) is proposed. Therefore, the aim of these series of articles is to provide the reader with the latest knowledge on the biochemistry of oxidative stress and its role in the development of different human pathologies.

Dr. Francisco Dasí
Guest Editor

Manuscript Submission Information

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Keywords

  • Oxidative stress
  • reactive oxygen species
  • reactive nitrogen species
  • antioxidant therapies
  • glutathione
  • lipid peroxidation
  • protein oxidation
  • nucleic acid oxidation
  • malondialdehyde
  • 8-hydroxydeoxyguanosine

Published Papers (6 papers)

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Research

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Open AccessArticle
The Effects of Ascorbate, N-Acetylcysteine, and Resveratrol on Fibroblasts from Patients with Mitochondrial Disorders
J. Clin. Med. 2017, 6(1), 1; https://doi.org/10.3390/jcm6010001
Received: 21 October 2016 / Revised: 11 December 2016 / Accepted: 14 December 2016 / Published: 22 December 2016
Cited by 9 | PDF Full-text (1010 KB) | HTML Full-text | XML Full-text
Abstract
Reactive oxygen species (ROS) are assumed to be implicated in the pathogenesis of inborn mitochondrial diseases affecting oxidative phosphorylation (OXPHOS). In the current study, we characterized the effects of three small molecules with antioxidant properties (N-acetylcysteine, ascorbate, and resveratrol) on ROS [...] Read more.
Reactive oxygen species (ROS) are assumed to be implicated in the pathogenesis of inborn mitochondrial diseases affecting oxidative phosphorylation (OXPHOS). In the current study, we characterized the effects of three small molecules with antioxidant properties (N-acetylcysteine, ascorbate, and resveratrol) on ROS production and several OXPHOS parameters (growth in glucose free medium, ATP production, mitochondrial content and membrane potential (MMP)), in primary fibroblasts derived from seven patients with different molecularly defined and undefined mitochondrial diseases. N-acetylcysteine appeared to be the most beneficial compound, reducing ROS while increasing growth and ATP production in some patients’ cells. Ascorbate showed a variable positive or negative effect on ROS, ATP production, and mitochondrial content, while incubation with resveratrol disclosed either no effect or detrimental effect on ATP production and MMP in some cells. The individual responses highlight the importance of investigating multiple parameters in addition to ROS to obtain a more balanced view of the overall effect on OXPHOS when evaluating antioxidant treatment options for mitochondrial diseases. Full article
(This article belongs to the Special Issue The Role of Oxidant Stress in Disease)
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Open AccessArticle
Modulation of Vascular ACE by Oxidative Stress in Young Syrian Cardiomyopathic Hamsters: Therapeutic Implications
J. Clin. Med. 2016, 5(7), 64; https://doi.org/10.3390/jcm5070064
Received: 18 May 2016 / Revised: 5 July 2016 / Accepted: 7 July 2016 / Published: 13 July 2016
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Abstract
Increased vascular angiotensin-converting enzyme (ACE) activity and oxidative stress are present in young Syrian cardiomyopathic hamsters (SCH) before the clinical manifestation of heart failure (HF). The developmental time-course of these alterations and their potential interactions, however, are still unknown. We evaluated mRNA and [...] Read more.
Increased vascular angiotensin-converting enzyme (ACE) activity and oxidative stress are present in young Syrian cardiomyopathic hamsters (SCH) before the clinical manifestation of heart failure (HF). The developmental time-course of these alterations and their potential interactions, however, are still unknown. We evaluated mRNA and protein levels of ACE, endothelial nitric oxide synthase (eNOS), and inducible nitric oxide synthase (iNOS) in the vasculature of SCH from one to four months of age. Total RNA and proteins were quantified with real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot, respectively. The role of nitric oxide (NO) on vascular ACE activity was also assessed. ACE mRNA and protein levels were up-regulated in SCH at two months of age compared with controls (CT) (p < 0.05). At this two-month stage, eNOS protein levels were lower in SCH (87%) than in CT (100%) (p < 0.05), although iNOS protein levels increased significantly (482%) compared to CT (100%; p < 0.05). In addition, ACE mRNA expression and activity were modulated by NO at two months of age. Thus, the combination of low eNOS and high iNOS protein levels may underlie vascular renin-angiotensin system (RAS) over-activation. Altogether, these factors may contribute to the development of endothelial dysfunction and vascular hyper-reactivity in the early stages of heart failure, and eventually trigger cardiac deterioration in this animal model of HF. Full article
(This article belongs to the Special Issue The Role of Oxidant Stress in Disease)
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Review

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Open AccessFeature PaperReview
The Role of Interleukin-18, Oxidative Stress and Metabolic Syndrome in Alzheimer’s Disease
J. Clin. Med. 2017, 6(5), 55; https://doi.org/10.3390/jcm6050055
Received: 29 November 2016 / Revised: 6 May 2017 / Accepted: 18 May 2017 / Published: 21 May 2017
Cited by 11 | PDF Full-text (3594 KB) | HTML Full-text | XML Full-text
Abstract
The role of interleukins (ILs) and oxidative stress (OS) in precipitating neurodegenerative diseases including sporadic Alzheimer’s disease (AD), requires further clarification. In addition to neuropathological hallmarks—extracellular neuritic amyloid-β (Aβ) plaques, neurofibrillary tangles (NFT) containing hyperphosphorylated tau and neuronal loss—chronic inflammation, as well as [...] Read more.
The role of interleukins (ILs) and oxidative stress (OS) in precipitating neurodegenerative diseases including sporadic Alzheimer’s disease (AD), requires further clarification. In addition to neuropathological hallmarks—extracellular neuritic amyloid-β (Aβ) plaques, neurofibrillary tangles (NFT) containing hyperphosphorylated tau and neuronal loss—chronic inflammation, as well as oxidative and excitotoxic damage, are present in the AD brain. The pathological sequelae and the interaction of these events during the course of AD need further investigation. The brain is particularly sensitive to OS, due to the richness of its peroxidation-sensitive fatty acids, coupled with its high oxygen demand. At the same time, the brain lack robust antioxidant systems. Among the multiple mechanisms and triggers by which OS can accumulate, inflammatory cytokines can sustain oxidative and nitrosative stress, leading eventually to cellular damage. Understanding the consequences of inflammation and OS may clarify the initial events underlying AD, including in interaction with genetic factors. Inflammatory cytokines are potential inducers of aberrant gene expression through transcription factors. Susceptibility disorders for AD, including obesity, type-2 diabetes, cardiovascular diseases and metabolic syndrome have been linked to increases in the proinflammatory cytokine, IL-18, which also regulates multiple AD related proteins. The association of IL-18 with AD and AD-linked medical conditions are reviewed in the article. Such data indicates that an active lifestyle, coupled to a healthy diet can ameliorate inflammation and reduce the risk of sporadic AD. Full article
(This article belongs to the Special Issue The Role of Oxidant Stress in Disease)
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Open AccessReview
Oxidative Stress: A New Target for Pancreatic Cancer Prognosis and Treatment
J. Clin. Med. 2017, 6(3), 29; https://doi.org/10.3390/jcm6030029
Received: 29 November 2016 / Revised: 15 February 2017 / Accepted: 6 March 2017 / Published: 9 March 2017
Cited by 21 | PDF Full-text (542 KB) | HTML Full-text | XML Full-text
Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal types of tumors, and its incidence is rising worldwide. Survival can be improved when tumors are detected at an early stage; however, this cancer is usually asymptomatic, and the disease only becomes apparent [...] Read more.
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal types of tumors, and its incidence is rising worldwide. Survival can be improved when tumors are detected at an early stage; however, this cancer is usually asymptomatic, and the disease only becomes apparent after metastasis. Several risk factors are associated to this disease. Chronic pancreatitis, diabetes, and some infectious disease are the most relevant risk factors. Incidence of PDAC has increased in the last decades. It is hypothesized it could be due to other acquired risk habits, like smoking, high alcohol intake, and obesity. Indeed, adipose tissue is a dynamic endocrine organ that secretes different pro-inflammatory cytokines, enzymes, and other factors that activate oxidative stress. Reactive oxygen species caused by oxidative stress, damage DNA, proteins, and lipids, and produce several toxic and high mutagenic metabolites that could modify tumor behavior, turning it into a malignant phenotype. Anti-oxidant compounds, like vitamins, are considered protective factors against cancer. Here, we review the literature on oxidative stress, the molecular pathways that activate or counteract oxidative stress, and potential treatment strategies that target reactive oxygen species suitable for this kind of cancer. Full article
(This article belongs to the Special Issue The Role of Oxidant Stress in Disease)
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Open AccessReview
CVD and Oxidative Stress
J. Clin. Med. 2017, 6(2), 22; https://doi.org/10.3390/jcm6020022
Received: 1 December 2016 / Revised: 12 February 2017 / Accepted: 14 February 2017 / Published: 20 February 2017
Cited by 23 | PDF Full-text (1341 KB) | HTML Full-text | XML Full-text
Abstract
Nowadays, it is known that oxidative stress plays at least two roles within the cell, the generation of cellular damage and the involvement in several signaling pathways in its balanced normal state. So far, a substantial amount of time and effort has been [...] Read more.
Nowadays, it is known that oxidative stress plays at least two roles within the cell, the generation of cellular damage and the involvement in several signaling pathways in its balanced normal state. So far, a substantial amount of time and effort has been expended in the search for a clear link between cardiovascular disease (CVD) and the effects of oxidative stress. Here, we present an overview of the different sources and types of reactive oxygen species in CVD, highlight the relationship between CVD and oxidative stress and discuss the most prominent molecules that play an important role in CVD pathophysiology. Details are given regarding common pharmacological treatments used for cardiovascular distress and how some of them are acting upon ROS-related pathways and molecules. Novel therapies, recently proposed ROS biomarkers, as well as future challenges in the field are addressed. It is apparent that the search for a better understanding of how ROS are contributing to the pathophysiology of CVD is far from over, and new approaches and more suitable biomarkers are needed for the latter to be accomplished. Full article
(This article belongs to the Special Issue The Role of Oxidant Stress in Disease)
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Open AccessFeature PaperReview
Oxidative Stress in COPD: Sources, Markers, and Potential Mechanisms
J. Clin. Med. 2017, 6(2), 21; https://doi.org/10.3390/jcm6020021
Received: 16 December 2016 / Revised: 1 February 2017 / Accepted: 5 February 2017 / Published: 15 February 2017
Cited by 29 | PDF Full-text (1203 KB) | HTML Full-text | XML Full-text
Abstract
Markers of oxidative stress are increased in chronic obstructive pulmonary disease (COPD) and reactive oxygen species (ROS) are able to alter biological molecules, signaling pathways and antioxidant molecule function, many of which have been implicated in the pathogenesis of COPD. However, the involvement [...] Read more.
Markers of oxidative stress are increased in chronic obstructive pulmonary disease (COPD) and reactive oxygen species (ROS) are able to alter biological molecules, signaling pathways and antioxidant molecule function, many of which have been implicated in the pathogenesis of COPD. However, the involvement of ROS in the development and progression of COPD is not proven. Here, we discuss the sources of ROS, and the defences that have evolved to protect against their harmful effects. We address the role that ROS may have in the development and progression of COPD, as well as current therapeutic attempts at limiting the damage they cause. Evidence has indicated that the function of several key cells appears altered in COPD patients, and expression levels of important oxidant and antioxidant molecules may be abnormal. Therapeutic trials attempting to restore equilibrium to these molecules have not impacted upon all facets of disease and whilst the theory behind ROS influence in COPD appears sound, current models testing relevant pathways to tissue damage are limited. The heterogeneity seen in COPD patients presents a challenge to our understanding, and further research is essential to identify potential targets and stratified COPD patient populations where ROS therapies may be maximally efficacious. Full article
(This article belongs to the Special Issue The Role of Oxidant Stress in Disease)
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J. Clin. Med. EISSN 2077-0383 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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