Special Issue "Redox Stress and Redox Homeostatic Response to Trauma and Injury"

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A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (30 November 2014)

Special Issue Editor

Guest Editor
Dr. Nikolai V. Gorbunov (Website)

The Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc., Bethesda, MD 20817, USA
Interests: trauma; radiation injury; bacteria and host interaction; microvascular remodeling; redox signaling; autophagy; mitochondrial remodeling; interaction

Special Issue Information

Dear Colleagues,

Prompt response to major trauma and injury includes a massive recruitment of numerous mesenchymal, reticuloendotelial, and endothelial precursor cells, along with inflammatory cells from the peripheral blood and the bone marrow in order to sustain the damage recovery. The pathogenesis of trauma/injury is also associated with numerous systemic abnormalities caused by (i) cardiopulmonary, vascular, and neurogenic shock; (ii) the rupturing, hemorrhaging, and edema of internal organs; (iii) progressive systemic hypotension and hypoxia; and (iv) the massive release of paracrine and autocrine factors (e.g., alarmins, DAMPs, nitric oxide, inflammatory cytokines, neurohumoral mediators), and the constituents of damaged cells that drive aseptic inflammation. These events can result in the redox stress, affect redox homeostasis, and suppress cell differentiation and proliferation; thus, these events can exacerbate tissue damage, promote the multiple organ dysfunction syndrome, and/or extend recuperation period in sequelae of the acute diseases.

The Special Issue’s aims and objectives are:

(i) to cover the assessment and integration of the following subjects:

  • the interplay between the redox metabolome, redox signaling, and aseptic inflammation that is due to trauma/injury damage to organs and systems
  • the advantages and limitations of experimental techniques (including in vitro models) and of the arrays of redox molecular sensors that are employed for assessing traumatic redox stress

(ii) to elucidate the role of “free radical” and “radical-free” mechanisms of redox stress and redox signaling, as well as the effects of antioxidants and other dietary factors in the pathogenesis of aseptic inflammation and post-traumatic recovery.

Prof. Dr. Nikolai V. Gorbunov
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. Antioxidants 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 300 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.


Keywords

  • trauma/injury
  • redox/oxidative stress
  • redox metabolome
  • redox sensors
  • inflammation
  • antioxidants

Published Papers (5 papers)

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Research

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Open AccessArticle Ceruloplasmin and Hypoferremia: Studies in Burn and Non-Burn Trauma Patients
Antioxidants 2015, 4(1), 153-169; doi:10.3390/antiox4010153
Received: 26 November 2014 / Revised: 25 February 2015 / Accepted: 28 February 2015 / Published: 6 March 2015
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Abstract
Objective: Normal iron handling appears to be disrupted in critically ill patients leading to hypoferremia that may contribute to systemic inflammation. Ceruloplasmin (Cp), an acute phase reactant protein that can convert ferrous iron to its less reactive ferric form facilitating binding [...] Read more.
Objective: Normal iron handling appears to be disrupted in critically ill patients leading to hypoferremia that may contribute to systemic inflammation. Ceruloplasmin (Cp), an acute phase reactant protein that can convert ferrous iron to its less reactive ferric form facilitating binding to ferritin, has ferroxidase activity that is important to iron handling. Genetic absence of Cp decreases iron export resulting in iron accumulation in many organs. The objective of this study was to characterize iron metabolism and Cp activity in burn and non-burn trauma patients to determine if changes in Cp activity are a potential contributor to the observed hypoferremia. Material and Methods: Under Brooke Army Medical Center Institutional Review Board approved protocols, serum or plasma was collected from burn and non-burn trauma patients on admission to the ICU and at times up to 14 days and measured for indices of iron status, Cp protein and oxidase activity and cytokines. Results: Burn patients showed evidence of anemia and normal or elevated ferritin levels. Plasma Cp oxidase activity in burn and trauma patients were markedly lower than controls on admission and increased to control levels by day 3, particularly in burn patients. Plasma cytokines were elevated throughout the 14 days study along with evidence of an oxidative stress. No significant differences in soluble transferrin receptor were noted among groups on admission, but levels in burn patients were lower than controls for the first 5 days after injury. Conclusion: This study further established the hypoferremia and inflammation associated with burns and trauma. To our knowledge, this is the first study to show an early decrease in Cp oxidase activity in burn and non-burn trauma patients. The results support the hypothesis that transient loss of Cp activity contributes to hypoferremia and inflammation. Further studies are warranted to determine if decreased Cp activity increases the risk of iron-induced injury following therapeutic interventions such as transfusions with blood that has undergone prolonged storage in trauma resuscitation. Full article
(This article belongs to the Special Issue Redox Stress and Redox Homeostatic Response to Trauma and Injury)
Open AccessArticle Antioxidant Approaches to Management of Ionizing Irradiation Injury
Antioxidants 2015, 4(1), 82-101; doi:10.3390/antiox4010082
Received: 5 December 2014 / Accepted: 12 January 2015 / Published: 23 January 2015
Cited by 1 | PDF Full-text (687 KB) | HTML Full-text | XML Full-text
Abstract
Ionizing irradiation induces acute and chronic injury to tissues and organs. Applications of antioxidant therapies for the management of ionizing irradiation injury fall into three categories: (1) radiation counter measures against total or partial body irradiation; (2) normal tissue protection against acute [...] Read more.
Ionizing irradiation induces acute and chronic injury to tissues and organs. Applications of antioxidant therapies for the management of ionizing irradiation injury fall into three categories: (1) radiation counter measures against total or partial body irradiation; (2) normal tissue protection against acute organ specific ionizing irradiation injury; and (3) prevention of chronic/late radiation tissue and organ injury. The development of antioxidant therapies to ameliorate ionizing irradiation injury began with initial studies on gene therapy using Manganese Superoxide Dismutase (MnSOD) transgene approaches and evolved into applications of small molecule radiation protectors and mitigators. The understanding of the multiple steps in ionizing radiation-induced cellular, tissue, and organ injury, as well as total body effects is required to optimize the use of antioxidant therapies, and to sequence such approaches with targeted therapies for the multiple steps in the irradiation damage response. Full article
(This article belongs to the Special Issue Redox Stress and Redox Homeostatic Response to Trauma and Injury)
Open AccessArticle Curcumin Stimulates the Antioxidant Mechanisms in Mouse Skin Exposed to Fractionated γ-Irradiation
Antioxidants 2015, 4(1), 25-41; doi:10.3390/antiox4010025
Received: 9 December 2014 / Accepted: 6 January 2015 / Published: 13 January 2015
Cited by 1 | PDF Full-text (553 KB) | HTML Full-text | XML Full-text
Abstract
Fractionated irradiation is one of the important radiotherapy regimens to treat different types of neoplasia. Despite of the immense therapeutic gains accrued by delivering fractionated irradiation to tumors, the radiation burden on skin increases significantly. Low doses of irradiation to skin adversely [...] Read more.
Fractionated irradiation is one of the important radiotherapy regimens to treat different types of neoplasia. Despite of the immense therapeutic gains accrued by delivering fractionated irradiation to tumors, the radiation burden on skin increases significantly. Low doses of irradiation to skin adversely affect its molecular and metabolic status. The use of antioxidant/s may help to alleviate the radiation-induced changes in the skin and allow delivering a higher dose of radiation to attain better therapeutic gains. Curcumin is an antioxidant and a free radical scavenging dietary supplement, commonly used as a flavoring agent in curries. Therefore, the effect of 100 mg/kg body weight curcumin was studied on the antioxidant status of mice skin exposed to a total dose of 10, 20 and 40 Gy γ-radiation below the rib cage delivered as a single fraction of 2 Gy per day for 5, 10 or 20 days. Skin biopsies from both the curcumin treated or untreated irradiated groups were collected for the biochemical estimations at various post-irradiation times. The irradiation of animals caused a dose dependent decline in the glutathione concentration, glutathione peroxidase, and superoxide dismutase activities and increased the lipid peroxidation in the irradiated skin. Curcumin treatment before irradiation resulted in a significant rise in the glutathione concentration and activities of both the glutathione peroxidase and superoxide dismutase enzymes in mouse skin, whereas lipid peroxidation declined significantly. The present study indicates that curcumin treatment increased the antioxidant status of mouse exposed to different doses of fractionated γ-radiation. Full article
(This article belongs to the Special Issue Redox Stress and Redox Homeostatic Response to Trauma and Injury)

Review

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Open AccessReview Protracted Oxidative Alterations in the Mechanism of Hematopoietic Acute Radiation Syndrome
Antioxidants 2015, 4(1), 134-152; doi:10.3390/antiox4010134
Received: 19 September 2014 / Revised: 7 January 2015 / Accepted: 2 February 2015 / Published: 27 February 2015
Cited by 1 | PDF Full-text (894 KB) | HTML Full-text | XML Full-text
Abstract
The biological effects of high-dose total body ionizing irradiation [(thereafter, irradiation (IR)] are attributed to primary oxidative breakage of biomolecule targets, mitotic, apoptotic and necrotic cell death in the dose-limiting tissues, clastogenic and epigenetic effects, and cascades of functional and reactive responses [...] Read more.
The biological effects of high-dose total body ionizing irradiation [(thereafter, irradiation (IR)] are attributed to primary oxidative breakage of biomolecule targets, mitotic, apoptotic and necrotic cell death in the dose-limiting tissues, clastogenic and epigenetic effects, and cascades of functional and reactive responses leading to radiation sickness defined as the acute radiation syndrome (ARS). The range of remaining and protracted injuries at any given radiation dose as well as the dynamics of post-IR alterations is tissue-specific. Therefore, functional integrity of the homeostatic tissue barriers may decline gradually within weeks in the post-IR period culminating with sepsis and failure of organs and systems. Multiple organ failure (MOF) leading to moribundity is a common sequela of the hemotapoietic form of ARS (hARS). Onset of MOF in hARS can be presented as “two-hit phenomenon” where the “first hit” is the underlying consequences of the IR-induced radiolysis in cells and biofluids, non-septic inflammation, metabolic up-regulation of pro-oxidative metabolic reactions, suppression of the radiosensitive hematopoietic and lymphoid tissues and the damage to gut mucosa and vascular endothelium. While the “second hit” derives from bacterial translocation and spread of the bacterial pathogens and inflammagens through the vascular system leading to septic inflammatory, metabolic responses and a cascade of redox pro-oxidative and adaptive reactions. This sequence of events can create a ground for development of prolonged metabolic, inflammatory, oxidative, nitrative, and carbonyl, electrophilic stress in crucial tissues and thus exacerbate the hARS outcomes. With this perspective, the redox mechanisms, which can mediate the IR-induced protracted oxidative post-translational modification of proteins, oxidation of lipids and carbohydrates and their countermeasures in hARS are subjects of the current review. Potential role of ubiquitous, radioresistant mesenchymal stromal cells in the protracted responses to IR and IR-related septicemia is also discussed. Full article
(This article belongs to the Special Issue Redox Stress and Redox Homeostatic Response to Trauma and Injury)
Open AccessReview Modulation of Radiation Response by the Tetrahydrobiopterin Pathway
Antioxidants 2015, 4(1), 68-81; doi:10.3390/antiox4010068
Received: 18 November 2014 / Revised: 7 January 2015 / Accepted: 13 January 2015 / Published: 22 January 2015
Cited by 1 | PDF Full-text (192 KB) | HTML Full-text | XML Full-text
Abstract
Ionizing radiation (IR) is an integral component of our lives due to highly prevalent sources such as medical, environmental, and/or accidental. Thus, understanding of the mechanisms by which radiation toxicity develops is crucial to address acute and chronic health problems that occur [...] Read more.
Ionizing radiation (IR) is an integral component of our lives due to highly prevalent sources such as medical, environmental, and/or accidental. Thus, understanding of the mechanisms by which radiation toxicity develops is crucial to address acute and chronic health problems that occur following IR exposure. Immediate formation of IR-induced free radicals as well as their persistent effects on metabolism through subsequent alterations in redox mediated inter- and intracellular processes are globally accepted as significant contributors to early and late effects of IR exposure. This includes but is not limited to cytotoxicity, genomic instability, fibrosis and inflammation. Damage to the critical biomolecules leading to detrimental long-term alterations in metabolic redox homeostasis following IR exposure has been the focus of various independent investigations over last several decades. The growth of the “omics” technologies during the past decade has enabled integration of “data from traditional radiobiology research”, with data from metabolomics studies. This review will focus on the role of tetrahydrobiopterin (BH4), an understudied redox-sensitive metabolite, plays in the pathogenesis of post-irradiation normal tissue injury as well as how the metabolomic readout of BH4 metabolism fits in the overall picture of disrupted oxidative metabolism following IR exposure. Full article
(This article belongs to the Special Issue Redox Stress and Redox Homeostatic Response to Trauma and Injury)

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