Special Issue "Oxidative Stress and Oxygen Radicals"

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A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (31 December 2014)

Special Issue Editors

Guest Editor
Prof. Dr. Michael Breitenbach (Website)

Department of Cell Biology, University of Salzburg, Hellbrunnerstraße 34, A-5020 Salzburg, Austria
Interests: yeast; genetics; aging; oxidative stress; NADPH oxidase; metabolic regulation; mitochondria; respiration; apoptosis
Guest Editor
Prof. Dr. Peter Eckl (Website)

Department of Cell Biology, University of Salzburg, Hellbrunnerstrasse 34, A-5020 Salzburg, Austria
Interests: ; oxidative stress; lipid peroxidation; apoptosis; degenerative disease

Special Issue Information

Dear Colleagues,

In the following short description of our publication project we want to provide you with information regarding the progress with our work.

We have gathered a very representative panel of 20 authors (with their co-authors) who have agreed to write chapters for our public access online publication project, which will also lead to a book publication.

The following is a short outline of the contents:

Oxidative stress and disturbance of oxidative homeostasis is widely described in the literature as being one of the main causes of cell death, as well as creating detrimental processes in whole organisms including aging and various diseases such as cardiovascular disease, neurodegenerative diseases and cancer.

We are pleased to present the current list of contributions on the following subjects:

  • The basic biology of oxidative stress and oxidative stress defense;
  • Mass-spectrometry-based methods for detection of oxidized proteins in disease;
  • High-resolution respirometry and oxidative stress;
  • The proteomic and metabolomic signature of oxidative stress;
  • Metabolic re-configuration in oxidative stress;
  • Oxygen metabolism and oxidative stress in plants;
  • Physiological roles of NADPH oxidases in fungi;
  • Oxidative stress, ion channels and neurodegeneration;
  • Oxidative stress in autism;
  • ROS and inflammation: from oxidative stress to cell signaling;
  • Ferritin-induced oxidative stress;
  • Heme oxygenase in hypoxia and inflammation;
  • Muscle metabolism and oxidative stress;
  • Hypoxia, oxidative stress and therapy;
  • Oxidative stress and advanced glycation end products;
  • 4-Hydroxynonenal—A bioactive lipid peroxidation product;
  • Oxidative stress responses in Candida albicans;
  • Role of oxidative stress in extracellular trap formation;
  • The role of oxidative stress in aging;
  • Oxidative damage in the aging human skin.

The chapters of this upcoming thematic issue will be published immediately after peer review and acceptance online.

Yours sincerely,

Prof. Dr. Michael Breitenbach
Prof. Dr. Peter Eckl
Guest Editor

Submission

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed Open Access quarterly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 600 CHF (Swiss Francs). English correction and/or formatting fees of 250 CHF (Swiss Francs) will be charged in certain cases for those articles accepted for publication that require extensive additional formatting and/or English corrections.


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Published Papers (17 papers)

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Editorial

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Open AccessEditorial Introduction to Oxidative Stress in Biomedical and Biological Research
Biomolecules 2015, 5(2), 1169-1177; doi:10.3390/biom5021169
Received: 11 May 2015 / Revised: 1 June 2015 / Accepted: 4 June 2015 / Published: 9 June 2015
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Abstract
Oxidative stress is now a well-researched area with thousands of new articles appearing every year. We want to give the reader here an overview of the topics in biomedical and basic oxidative stress research which are covered by the authors of this [...] Read more.
Oxidative stress is now a well-researched area with thousands of new articles appearing every year. We want to give the reader here an overview of the topics in biomedical and basic oxidative stress research which are covered by the authors of this thematic issue. We also want to give the newcomer a short introduction into some of the basic concepts, definitions and analytical procedures used in this field. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available

Research

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Open AccessArticle High-Resolution Respirometry for Simultaneous Measurement of Oxygen and Hydrogen Peroxide Fluxes in Permeabilized Cells, Tissue Homogenate and Isolated Mitochondria
Biomolecules 2015, 5(3), 1319-1338; doi:10.3390/biom5031319
Received: 7 April 2015 / Revised: 8 June 2015 / Accepted: 8 June 2015 / Published: 29 June 2015
Cited by 3 | PDF Full-text (6362 KB) | HTML Full-text | XML Full-text
Abstract
Whereas mitochondria are well established as the source of ATP in oxidative phosphorylation (OXPHOS), it is debated if they are also the major cellular sources of reactive oxygen species (ROS). Here we describe the novel approach of combining high-resolution respirometry and fluorometric [...] Read more.
Whereas mitochondria are well established as the source of ATP in oxidative phosphorylation (OXPHOS), it is debated if they are also the major cellular sources of reactive oxygen species (ROS). Here we describe the novel approach of combining high-resolution respirometry and fluorometric measurement of hydrogen peroxide (H2O2) production, applied to mitochondrial preparations (permeabilized cells, tissue homogenate, isolated mitochondria). The widely used H2O2 probe Amplex Red inhibited respiration in intact and permeabilized cells and should not be applied at concentrations above 10 µM. H2O2 fluxes were generally less than 1% of oxygen fluxes in physiological substrate and coupling states, specifically in permeabilized cells. H2O2 flux was consistently highest in the Complex II-linked LEAK state, reduced with CI&II-linked convergent electron flow and in mitochondria respiring at OXPHOS capacity, and were further diminished in uncoupled mitochondria respiring at electron transfer system capacity. Simultaneous measurement of mitochondrial respiration and H2O2 flux requires careful optimization of assay conditions and reveals information on mitochondrial function beyond separate analysis of ROS production. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available
Open AccessArticle Anti-Inflammatory Activity of Haskap Cultivars is Polyphenols-Dependent
Biomolecules 2015, 5(2), 1079-1098; doi:10.3390/biom5021079
Received: 19 January 2015 / Accepted: 22 May 2015 / Published: 2 June 2015
Cited by 4 | PDF Full-text (1761 KB) | HTML Full-text | XML Full-text
Abstract
Haskap (Lonicera caerulea L.) berries have long been used for their health promoting properties against chronic conditions. The current study investigated the effect of Canadian haskap berry extracts on pro-inflammatory cytokines using a human monocytic cell line THP-1 derived macrophages stimulated [...] Read more.
Haskap (Lonicera caerulea L.) berries have long been used for their health promoting properties against chronic conditions. The current study investigated the effect of Canadian haskap berry extracts on pro-inflammatory cytokines using a human monocytic cell line THP-1 derived macrophages stimulated by lipopolysaccharide. Methanol extracts of haskap from different growing locations in Canada were prepared and characterized for their total phenolic profile using colorimetric assays and liquid chromatography—Mass spectrometry (UPLC-MS/MS). Human THP-1 monocytes were seeded in 24-well plates (5 × 105/well) and treated with phorbol 12-myristate 13-acetate (PMA, 0.1 μg/mL) for 48 h to induce macrophage differentiation. After 48 h, the differentiated macrophages were washed with Hank’s buffer and treated with various concentrations of test compounds for 4 h, followed by the lipopolysaccharide (LPS)-stimulation (18 h). Borealis cultivar showed the highest phenolic content, flavonoid content and anthocyanin content (p < 0.05). A negative correlation existed between the polyphenol concentration of the extracts and pro-inflammatory cytokines: Interleukin-6 (IL-6), tumour necrosis factor-alpha (TNF-α), prostaglandin (PGE2), and cyclooxygenase-2 (COX-2) enzyme. Borealis exhibited comparable anti-inflammatory effects to COX inhibitory drug, diclofenac. The results showed that haskap berry polyphenols has the potential to act as an effective inflammation inhibitor. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available
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Open AccessArticle Heme Degradation by Heme Oxygenase Protects Mitochondria but Induces ER Stress via Formed Bilirubin
Biomolecules 2015, 5(2), 679-701; doi:10.3390/biom5020679
Received: 3 February 2015 / Revised: 8 April 2015 / Accepted: 16 April 2015 / Published: 30 April 2015
Cited by 2 | PDF Full-text (4686 KB) | HTML Full-text | XML Full-text
Abstract
Heme oxygenase (HO), in conjunction with biliverdin reductase, degrades heme to carbon monoxide, ferrous iron and bilirubin (BR); the latter is a potent antioxidant. The induced isoform HO-1 has evoked intense research interest, especially because it manifests anti-inflammatory and anti-apoptotic effects relieving [...] Read more.
Heme oxygenase (HO), in conjunction with biliverdin reductase, degrades heme to carbon monoxide, ferrous iron and bilirubin (BR); the latter is a potent antioxidant. The induced isoform HO-1 has evoked intense research interest, especially because it manifests anti-inflammatory and anti-apoptotic effects relieving acute cell stress. The mechanisms by which HO mediates the described effects are not completely clear. However, the degradation of heme, a strong pro-oxidant, and the generation of BR are considered to play key roles. The aim of this study was to determine the effects of BR on vital functions of hepatocytes focusing on mitochondria and the endoplasmic reticulum (ER). The affinity of BR to proteins is a known challenge for its exact quantification. We consider two major consequences of this affinity, namely possible analytical errors in the determination of HO activity, and biological effects of BR due to direct interaction with protein function. In order to overcome analytical bias we applied a polynomial correction accounting for the loss of BR due to its adsorption to proteins. To identify potential intracellular targets of BR we used an in vitro approach involving hepatocytes and isolated mitochondria. After verification that the hepatocytes possess HO activity at a similar level as liver tissue by using our improved post-extraction spectroscopic assay, we elucidated the effects of increased HO activity and the formed BR on mitochondrial function and the ER stress response. Our data show that BR may compromise cellular metabolism and proliferation via induction of ER stress. ER and mitochondria respond differently to elevated levels of BR and HO-activity. Mitochondria are susceptible to hemin, but active HO protects them against hemin-induced toxicity. BR at slightly elevated levels induces a stress response at the ER, resulting in a decreased proliferative and metabolic activity of hepatocytes. However, the proteins that are targeted by BR still have to be identified. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available

Review

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Open AccessReview 4-Hydroxy-nonenal—A Bioactive Lipid Peroxidation Product
Biomolecules 2015, 5(4), 2247-2337; doi:10.3390/biom5042247
Received: 2 June 2015 / Revised: 24 July 2015 / Accepted: 29 July 2015 / Published: 30 September 2015
Cited by 6 | PDF Full-text (1594 KB) | HTML Full-text | XML Full-text
Abstract
This review on recent research advances of the lipid peroxidation product 4-hydroxy-nonenal (HNE) has four major topics: I. the formation of HNE in various organs and tissues, II. the diverse biochemical reactions with Michael adduct formation as the most prominent one, III. [...] Read more.
This review on recent research advances of the lipid peroxidation product 4-hydroxy-nonenal (HNE) has four major topics: I. the formation of HNE in various organs and tissues, II. the diverse biochemical reactions with Michael adduct formation as the most prominent one, III. the endogenous targets of HNE, primarily peptides and proteins (here the mechanisms of covalent adduct formation are described and the (patho-) physiological consequences discussed), and IV. the metabolism of HNE leading to a great number of degradation products, some of which are excreted in urine and may serve as non-invasive biomarkers of oxidative stress. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available
Open AccessReview The Impact of Non-Enzymatic Reactions and Enzyme Promiscuity on Cellular Metabolism during (Oxidative) Stress Conditions
Biomolecules 2015, 5(3), 2101-2122; doi:10.3390/biom5032101
Received: 6 May 2015 / Revised: 3 August 2015 / Accepted: 31 August 2015 / Published: 10 September 2015
Cited by 4 | PDF Full-text (1507 KB) | HTML Full-text | XML Full-text
Abstract
Cellular metabolism assembles in a structurally highly conserved, but functionally dynamic system, known as the metabolic network. This network involves highly active, enzyme-catalyzed metabolic pathways that provide the building blocks for cell growth. In parallel, however, chemical reactivity of metabolites and unspecific [...] Read more.
Cellular metabolism assembles in a structurally highly conserved, but functionally dynamic system, known as the metabolic network. This network involves highly active, enzyme-catalyzed metabolic pathways that provide the building blocks for cell growth. In parallel, however, chemical reactivity of metabolites and unspecific enzyme function give rise to a number of side products that are not part of canonical metabolic pathways. It is increasingly acknowledged that these molecules are important for the evolution of metabolism, affect metabolic efficiency, and that they play a potential role in human disease—age-related disorders and cancer in particular. In this review we discuss the impact of oxidative and other cellular stressors on the formation of metabolic side products, which originate as a consequence of: (i) chemical reactivity or modification of regular metabolites; (ii) through modifications in substrate specificity of damaged enzymes; and (iii) through altered metabolic flux that protects cells in stress conditions. In particular, oxidative and heat stress conditions are causative of metabolite and enzymatic damage and thus promote the non-canonical metabolic activity of the cells through an increased repertoire of side products. On the basis of selected examples, we discuss the consequences of non-canonical metabolic reactivity on evolution, function and repair of the metabolic network. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available
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Open AccessReview Oxidative Stress and Maxi Calcium-Activated Potassium (BK) Channels
Biomolecules 2015, 5(3), 1870-1911; doi:10.3390/biom5031870
Received: 8 May 2015 / Revised: 17 July 2015 / Accepted: 20 July 2015 / Published: 17 August 2015
Cited by 3 | PDF Full-text (939 KB) | HTML Full-text | XML Full-text
Abstract
All cells contain ion channels in their outer (plasma) and inner (organelle) membranes. Ion channels, similar to other proteins, are targets of oxidative impact, which modulates ion fluxes across membranes. Subsequently, these ion currents affect electrical excitability, such as action potential discharge [...] Read more.
All cells contain ion channels in their outer (plasma) and inner (organelle) membranes. Ion channels, similar to other proteins, are targets of oxidative impact, which modulates ion fluxes across membranes. Subsequently, these ion currents affect electrical excitability, such as action potential discharge (in neurons, muscle, and receptor cells), alteration of the membrane resting potential, synaptic transmission, hormone secretion, muscle contraction or coordination of the cell cycle. In this chapter we summarize effects of oxidative stress and redox mechanisms on some ion channels, in particular on maxi calcium-activated potassium (BK) channels which play an outstanding role in a plethora of physiological and pathophysiological functions in almost all cells and tissues. We first elaborate on some general features of ion channel structure and function and then summarize effects of oxidative alterations of ion channels and their functional consequences. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available
Open AccessReview Hypoxia, Oxidative Stress and Fat
Biomolecules 2015, 5(2), 1143-1150; doi:10.3390/biom5021143
Received: 18 April 2015 / Revised: 19 May 2015 / Accepted: 19 May 2015 / Published: 8 June 2015
Cited by 6 | PDF Full-text (539 KB) | HTML Full-text | XML Full-text
Abstract
Metabolic disturbances in white adipose tissue in obese individuals contribute to the pathogenesis of insulin resistance and the development of type 2 diabetes mellitus. Impaired insulin action in adipocytes is associated with elevated lipolysis and increased free fatty acids leading to ectopic [...] Read more.
Metabolic disturbances in white adipose tissue in obese individuals contribute to the pathogenesis of insulin resistance and the development of type 2 diabetes mellitus. Impaired insulin action in adipocytes is associated with elevated lipolysis and increased free fatty acids leading to ectopic fat deposition in liver and skeletal muscle. Chronic adipose tissue hypoxia has been suggested to be part of pathomechanisms causing dysfunction of adipocytes. Hypoxia can provoke oxidative stress in human and animal adipocytes and reduce the production of beneficial adipokines, such as adiponectin. However, time-dose responses to hypoxia relativize the effects of hypoxic stress. Long-term exposure of fat cells to hypoxia can lead to the production of beneficial substances such as leptin. Knowledge of time-dose responses of hypoxia on white adipose tissue and the time course of generation of oxidative stress in adipocytes is still scarce. This paper reviews the potential links between adipose tissue hypoxia, oxidative stress, mitochondrial dysfunction, and low-grade inflammation caused by adipocyte hypertrophy, macrophage infiltration and production of inflammatory mediators. Full article
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Open AccessReview Oxidative Stress and the Homeodynamics of Iron Metabolism
Biomolecules 2015, 5(2), 808-847; doi:10.3390/biom5020808
Received: 31 December 2014 / Revised: 21 April 2015 / Accepted: 22 April 2015 / Published: 11 May 2015
Cited by 6 | PDF Full-text (1198 KB) | HTML Full-text | XML Full-text
Abstract
Iron and oxygen share a delicate partnership since both are indispensable for survival, but if the partnership becomes inadequate, this may rapidly terminate life. Virtually all cell components are directly or indirectly affected by cellular iron metabolism, which represents a complex, redox-based [...] Read more.
Iron and oxygen share a delicate partnership since both are indispensable for survival, but if the partnership becomes inadequate, this may rapidly terminate life. Virtually all cell components are directly or indirectly affected by cellular iron metabolism, which represents a complex, redox-based machinery that is controlled by, and essential to, metabolic requirements. Under conditions of increased oxidative stress—i.e., enhanced formation of reactive oxygen species (ROS)—however, this machinery may turn into a potential threat, the continued requirement for iron promoting adverse reactions such as the iron/H2O2-based formation of hydroxyl radicals, which exacerbate the initial pro-oxidant condition. This review will discuss the multifaceted homeodynamics of cellular iron management under normal conditions as well as in the context of oxidative stress. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available
Open AccessReview The Role of Reactive Oxygen Species (ROS) in the Formation of Extracellular Traps (ETs) in Humans
Biomolecules 2015, 5(2), 702-723; doi:10.3390/biom5020702
Received: 21 November 2014 / Revised: 22 April 2015 / Accepted: 24 April 2015 / Published: 4 May 2015
Cited by 9 | PDF Full-text (1233 KB) | HTML Full-text | XML Full-text
Abstract
Extracellular traps (ETs) are reticulate structures of extracellular DNA associated with antimicrobial molecules. Their formation by phagocytes (mainly by neutrophils: NETs) has been identified as an essential element of vertebrate innate immune defense. However, as ETs are also toxic to host cells [...] Read more.
Extracellular traps (ETs) are reticulate structures of extracellular DNA associated with antimicrobial molecules. Their formation by phagocytes (mainly by neutrophils: NETs) has been identified as an essential element of vertebrate innate immune defense. However, as ETs are also toxic to host cells and potent triggers of autoimmunity, their role between pathogen defense and human pathogenesis is ambiguous, and they contribute to a variety of acute and chronic inflammatory diseases. Since the discovery of ET formation (ETosis) a decade ago, evidence has accumulated that most reaction cascades leading to ET release involve ROS. An important new facet was added when it became apparent that ETosis might be directly linked to, or be a variant of, the autophagy cell death pathway. The present review analyzes the evidence to date on the interplay between ROS, autophagy and ETosis, and highlights and discusses several further aspects of the ROS-ET relationship that are incompletely understood. These aspects include the role of NADPH oxidase-derived ROS, the molecular requirements of NADPH oxidase-dependent ETosis, the roles of NADPH oxidase subtypes, extracellular ROS and of ROS from sources other than NADPH oxidase, and the present evidence for ROS-independent ETosis. We conclude that ROS interact with ETosis in a multidimensional manner, with influence on whether ETosis shows beneficial or detrimental effects. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available
Open AccessReview Oxidative Stress in Aging Human Skin
Biomolecules 2015, 5(2), 545-589; doi:10.3390/biom5020545
Received: 12 January 2015 / Revised: 18 March 2015 / Accepted: 9 April 2015 / Published: 21 April 2015
Cited by 14 | PDF Full-text (712 KB) | HTML Full-text | XML Full-text
Abstract
Oxidative stress in skin plays a major role in the aging process. This is true for intrinsic aging and even more for extrinsic aging. Although the results are quite different in dermis and epidermis, extrinsic aging is driven to a large extent [...] Read more.
Oxidative stress in skin plays a major role in the aging process. This is true for intrinsic aging and even more for extrinsic aging. Although the results are quite different in dermis and epidermis, extrinsic aging is driven to a large extent by oxidative stress caused by UV irradiation. In this review the overall effects of oxidative stress are discussed as well as the sources of ROS including the mitochondrial ETC, peroxisomal and ER localized proteins, the Fenton reaction, and such enzymes as cyclooxygenases, lipoxygenases, xanthine oxidases, and NADPH oxidases. Furthermore, the defense mechanisms against oxidative stress ranging from enzymes like superoxide dismutases, catalases, peroxiredoxins, and GSH peroxidases to organic compounds such as L-ascorbate, α-tocopherol, beta-carotene, uric acid, CoQ10, and glutathione are described in more detail. In addition the oxidative stress induced modifications caused to proteins, lipids and DNA are discussed. Finally age-related changes of the skin are also a topic of this review. They include a disruption of the epidermal calcium gradient in old skin with an accompanying change in the composition of the cornified envelope. This modified cornified envelope also leads to an altered anti-oxidative capacity and a reduced barrier function of the epidermis. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available
Open AccessReview Biological Activities of Reactive Oxygen and Nitrogen Species: Oxidative Stress versus Signal Transduction
Biomolecules 2015, 5(2), 472-484; doi:10.3390/biom5020472
Received: 3 February 2015 / Revised: 30 March 2015 / Accepted: 2 April 2015 / Published: 15 April 2015
Cited by 24 | PDF Full-text (242 KB) | HTML Full-text | XML Full-text
Abstract
In the past, reactive oxygen and nitrogen species (RONS) were shown to cause oxidative damage to biomolecules, contributing to the development of a variety of diseases. However, recent evidence has suggested that intracellular RONS are an important component of intracellular signaling cascades. [...] Read more.
In the past, reactive oxygen and nitrogen species (RONS) were shown to cause oxidative damage to biomolecules, contributing to the development of a variety of diseases. However, recent evidence has suggested that intracellular RONS are an important component of intracellular signaling cascades. The aim of this review was to consolidate old and new ideas on the chemical, physiological and pathological role of RONS for a better understanding of their properties and specific activities. Critical consideration of the literature reveals that deleterious effects do not appear if only one primary species (superoxide radical, nitric oxide) is present in a biological system, even at high concentrations. The prerequisite of deleterious effects is the formation of highly reactive secondary species (hydroxyl radical, peroxynitrite), emerging exclusively upon reaction with another primary species or a transition metal. The secondary species are toxic, not well controlled, causing irreversible damage to all classes of biomolecules. In contrast, primary RONS are well controlled (superoxide dismutase, catalase), and their reactions with biomolecules are reversible, making them ideal for physiological/pathophysiological intracellular signaling. We assume that whether RONS have a signal transducing or damaging effect is primarily defined by their quality, being primary or secondary RONS, and only secondly by their quantity. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available
Open AccessReview Mass Spectrometry-Based Methods for Identifying Oxidized Proteins in Disease: Advances and Challenges
Biomolecules 2015, 5(2), 378-411; doi:10.3390/biom5020378
Received: 2 February 2015 / Revised: 20 March 2015 / Accepted: 23 March 2015 / Published: 14 April 2015
Cited by 5 | PDF Full-text (1315 KB) | HTML Full-text | XML Full-text
Abstract
Many inflammatory diseases have an oxidative aetiology, which leads to oxidative damage to biomolecules, including proteins. It is now increasingly recognized that oxidative post-translational modifications (oxPTMs) of proteins affect cell signalling and behaviour, and can contribute to pathology. Moreover, oxidized proteins have [...] Read more.
Many inflammatory diseases have an oxidative aetiology, which leads to oxidative damage to biomolecules, including proteins. It is now increasingly recognized that oxidative post-translational modifications (oxPTMs) of proteins affect cell signalling and behaviour, and can contribute to pathology. Moreover, oxidized proteins have potential as biomarkers for inflammatory diseases. Although many assays for generic protein oxidation and breakdown products of protein oxidation are available, only advanced tandem mass spectrometry approaches have the power to localize specific oxPTMs in identified proteins. While much work has been carried out using untargeted or discovery mass spectrometry approaches, identification of oxPTMs in disease has benefitted from the development of sophisticated targeted or semi-targeted scanning routines, combined with chemical labeling and enrichment approaches. Nevertheless, many potential pitfalls exist which can result in incorrect identifications. This review explains the limitations, advantages and challenges of all of these approaches to detecting oxidatively modified proteins, and provides an update on recent literature in which they have been used to detect and quantify protein oxidation in disease. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available
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Open AccessReview Impact of Oxidative Stress on Exercising Skeletal Muscle
Biomolecules 2015, 5(2), 356-377; doi:10.3390/biom5020356
Received: 13 January 2015 / Revised: 24 March 2015 / Accepted: 30 March 2015 / Published: 10 April 2015
Cited by 7 | PDF Full-text (585 KB) | HTML Full-text | XML Full-text
Abstract
It is well established that muscle contractions during exercise lead to elevated levels of reactive oxygen species (ROS) in skeletal muscle. These highly reactive molecules have many deleterious effects, such as a reduction of force generation and increased muscle atrophy. Since the [...] Read more.
It is well established that muscle contractions during exercise lead to elevated levels of reactive oxygen species (ROS) in skeletal muscle. These highly reactive molecules have many deleterious effects, such as a reduction of force generation and increased muscle atrophy. Since the discovery of exercise-induced oxidative stress several decades ago, evidence has accumulated that ROS produced during exercise also have positive effects by influencing cellular processes that lead to increased expression of antioxidants. These molecules are particularly elevated in regularly exercising muscle to prevent the negative effects of ROS by neutralizing the free radicals. In addition, ROS also seem to be involved in the exercise-induced adaptation of the muscle phenotype. This review provides an overview of the evidences to date on the effects of ROS in exercising muscle. These aspects include the sources of ROS, their positive and negative cellular effects, the role of antioxidants, and the present evidence on ROS-dependent adaptations of muscle cells in response to physical exercise. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available
Open AccessReview Oxidative Stress in Fungi: Its Function in Signal Transduction, Interaction with Plant Hosts, and Lignocellulose Degradation
Biomolecules 2015, 5(2), 318-342; doi:10.3390/biom5020318
Received: 23 December 2014 / Revised: 19 March 2015 / Accepted: 23 March 2015 / Published: 3 April 2015
Cited by 3 | PDF Full-text (2340 KB) | HTML Full-text | XML Full-text
Abstract
In this review article, we want to present an overview of oxidative stress in fungal cells in relation to signal transduction, interaction of fungi with plant hosts, and lignocellulose degradation. We will discuss external oxidative stress which may occur through the interaction [...] Read more.
In this review article, we want to present an overview of oxidative stress in fungal cells in relation to signal transduction, interaction of fungi with plant hosts, and lignocellulose degradation. We will discuss external oxidative stress which may occur through the interaction with other microorganisms or plant hosts as well as internally generated oxidative stress, which can for instance originate from NADPH oxidases or “leaky” mitochondria and may be modulated by the peroxiredoxin system or by protein disulfide isomerases thus contributing to redox signaling. Analyzing redox signaling in fungi with the tools of molecular genetics is presently only in its beginning. However, it is already clear that redox signaling in fungal cells often is linked to cell differentiation (like the formation of perithecia), virulence (in plant pathogens), hyphal growth and the successful passage through the stationary phase. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available
Open AccessReview Advanced Glycation End Products and Oxidative Stress in Type 2 Diabetes Mellitus
Biomolecules 2015, 5(1), 194-222; doi:10.3390/biom5010194
Received: 29 December 2014 / Revised: 6 February 2015 / Accepted: 2 March 2015 / Published: 16 March 2015
Cited by 31 | PDF Full-text (5403 KB) | HTML Full-text | XML Full-text
Abstract
Type 2 diabetes mellitus (T2DM) is a very complex and multifactorial metabolic disease characterized by insulin resistance and β cell failure leading to elevated blood glucose levels. Hyperglycemia is suggested to be the main cause of diabetic complications, which not only decrease [...] Read more.
Type 2 diabetes mellitus (T2DM) is a very complex and multifactorial metabolic disease characterized by insulin resistance and β cell failure leading to elevated blood glucose levels. Hyperglycemia is suggested to be the main cause of diabetic complications, which not only decrease life quality and expectancy, but are also becoming a problem regarding the financial burden for health care systems. Therefore, and to counteract the continually increasing prevalence of diabetes, understanding the pathogenesis, the main risk factors, and the underlying molecular mechanisms may establish a basis for prevention and therapy. In this regard, research was performed revealing further evidence that oxidative stress has an important role in hyperglycemia-induced tissue injury as well as in early events relevant for the development of T2DM. The formation of advanced glycation end products (AGEs), a group of modified proteins and/or lipids with damaging potential, is one contributing factor. On the one hand it has been reported that AGEs increase reactive oxygen species formation and impair antioxidant systems, on the other hand the formation of some AGEs is induced per se under oxidative conditions. Thus, AGEs contribute at least partly to chronic stress conditions in diabetes. As AGEs are not only formed endogenously, but also derive from exogenous sources, i.e., food, they have been assumed as risk factors for T2DM. However, the role of AGEs in the pathogenesis of T2DM and diabetic complications—if they are causal or simply an effect—is only partly understood. This review will highlight the involvement of AGEs in the development and progression of T2DM and their role in diabetic complications. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available
Open AccessReview Oxidative Stress Responses in the Human Fungal Pathogen, Candida albicans
Biomolecules 2015, 5(1), 142-165; doi:10.3390/biom5010142
Received: 12 January 2015 / Revised: 11 February 2015 / Accepted: 12 February 2015 / Published: 25 February 2015
Cited by 11 | PDF Full-text (13640 KB) | HTML Full-text | XML Full-text
Abstract
Candida albicans is a major fungal pathogen of humans, causing approximately 400,000 life-threatening systemic infections world-wide each year in severely immunocompromised patients. An important fungicidal mechanism employed by innate immune cells involves the generation of toxic reactive oxygen species (ROS), such as [...] Read more.
Candida albicans is a major fungal pathogen of humans, causing approximately 400,000 life-threatening systemic infections world-wide each year in severely immunocompromised patients. An important fungicidal mechanism employed by innate immune cells involves the generation of toxic reactive oxygen species (ROS), such as superoxide and hydrogen peroxide. Consequently, there is much interest in the strategies employed by C. albicans to evade the oxidative killing by macrophages and neutrophils. Our understanding of how C. albicans senses and responds to ROS has significantly increased in recent years. Key findings include the observations that hydrogen peroxide triggers the filamentation of this polymorphic fungus and that a superoxide dismutase enzyme with a novel mode of action is expressed at the cell surface of C. albicans. Furthermore, recent studies have indicated that combinations of the chemical stresses generated by phagocytes can actively prevent C. albicans oxidative stress responses through a mechanism termed the stress pathway interference. In this review, we present an up-date of our current understanding of the role and regulation of oxidative stress responses in this important human fungal pathogen. Full article
(This article belongs to the Special Issue Oxidative Stress and Oxygen Radicals) Print Edition available

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