Basal levels of glutathione peroxidase correlate with onset of radiation induced lung disease in inbred mouse strains

Kunwar, Amit; Haston, Christina K.

doi:10.1152/ajplung.00088.2014

Cited by 8 publications

(4 citation statements)

References 35 publications

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“…Correlation tests were performed using the cor.test function in R ( http://cran.r-project.org ). Gene expression data were analysed as in refs 59 , 61 .…”

Section: Methodsmentioning

confidence: 99%

The Th1/Th17 balance dictates the fibrosis response in murine radiation-induced lung disease

Paun

Bergeron

Haston

2017

Sci Rep

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Radiotherapy can result in lung diseases pneumonitis or fibrosis dependent on patient susceptibility. Herein we used inbred and genetically altered mice to investigate whether the tissue adaptive immune response to radiation injury influences the development of radiation-induced lung disease. Six inbred mouse strains were exposed to 18 Gy whole thorax irradiation and upon respiratory distress strains prone to pneumonitis with fibrosis presented an increased pulmonary frequency of Thelper (Th)17 cells which was not evident in strains prone solely to pneumonitis. The contribution of Th17 cells to fibrosis development was supported as the known enhanced fibrosis of toll-like receptor 2&4 deficient mice, compared to C57BL/6J mice, occurred with earlier onset neutrophilia, and with increased levels of pulmonary Th17, but not Th1, cells following irradiation. Irradiated Il17−/− mice lacked Th17 cells, and were spared both fibrosis and pneumonitis, as they survived to the end of the experiment with a significantly increased pulmonary Th1 cell frequency, only. Interferon-γ−/− mice, deficient in Th1 cells, developed a significantly enhanced fibrosis response compared to that of C57BL/6J mice. The tissue adaptive immune response influences the pulmonary disease response to radiotherapy, as an increased Th17 cell frequency enhanced and a Th1 response spared, fibrosis in mice.

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“…Correlation tests were performed using the cor.test function in R ( http://cran.r-project.org ). Gene expression data were analysed as in refs 59 , 61 .…”

Section: Methodsmentioning

confidence: 99%

The Th1/Th17 balance dictates the fibrosis response in murine radiation-induced lung disease

Paun

Bergeron

Haston

2017

Sci Rep

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“…In comparison with wild type, GPx2-deficient mice showed greater levels of oxidative damage, airway inflammation and airway hyperresponsiveness in ovalbumininduced asthma mouse model [219]. Basal levels of GPx in lungs were shown to be a key determinant of severity of pulmonary fibrosis in mouse models [220]. Peroxiredoxins are the family of peroxidase enzymes, which play a dominant role in detoxification of hydrogen peroxide within the cells.…”

Section: Enzymatic Antioxidant System In Lungsmentioning

confidence: 99%

Oxidative Stress Mechanisms in the Pathogenesis of Environmental Lung Diseases

Thimmulappa

Chattopadhyay

Rajasekaran

2019

Oxidative Stress in Lung Diseases

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Globally, respiratory diseases are major cause of disability and mortality, and more alarmingly, it disproportionately affects developing countries, which is largely attributed to poor quality of air. Tobacco smoke and emissions from combustion of fossil fuel and biomass fuel are the major airborne pollutants affecting human lung health. Oxidative stress is the dominant driving force by which the airborne pollutants exert their toxicity in lungs and cause respiratory diseases. Most airborne pollutants are associated with intrinsic oxidative potential and, additionally, stimulate endogenous production of reactive oxygen species (ROS) and reactive nitrogen species (RNS). Elevated ROS and RNS in lungs modulate redox signals and cause irreversible damage to critical biomolecules (lipids, proteins and DNA) and initiate various pathogenic cellular process. This chapter provides an insight into oxidative stress-linked pathogenic cellular process such as lipid peroxidation, inflammation, cell death, mitochondrial dysfunction, endoplasmic reticulum stress, epigenetic changes, profibrotic signals and mucus hypersecretion, which drive the development and progression of lung diseases. Lungs are associated with robust enzymatic and non-enzymatic (GSH, ascorbic acid, uric acid, vitamin E) antioxidant defences. However, sustained production of free radicals due to continuous exposures to airborne pollutants overwhelms lung antioxidant defences and causes oxidative injury.

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“…Radiation biomarkers can fall into several categorizations as mentioned above. For instance, radiation-induced cytogenetic changes can serve as diagnostic biomarkers (6); radionuclide body burdens can be used to monitor the efficacy of decorporation agents (7); absolute neutrophil counts after radiation exposure and growth factor treatment have been used as pharmacodynamic markers (8); procalcitonin, a marker of total-body irradiation (TBI), can predict radiation lethality at 10 days postirradiation (9), and glutathione peroxidase can predict lethality from radiationinduced lung disease in mice (10); DNA damage in cells from Fanconi anemia patients is a prognostic marker for radiation sensitivity (11); cardiovascular biomarkers such as troponin T can be used as safety biomarker for patients undergoing left-sided irradiation for breast cancer (12); and biomarkers detected as part of retrospective radiation biodosimetry can indicate an increased susceptibility/risk of later cancer development (13). Because biomarkers represent surrogates of an outcome, one cannot assume that correlations are meaningful.…”

Section: Introductionmentioning

confidence: 99%

Development of Biomarkers for Radiation Biodosimetry and Medical Countermeasures Research: Current Status, Utility, and Regulatory Pathways

et al. 2021

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Biomarkers are important indicators of biological processes in health or disease. For this reason, they play a critical role in advanced development of radiation biodosimetry tools and medical countermeasures (MCMs). They can aid in the assessment of radiation exposure level, extent of radiation-induced injury, and/or efficacy of an MCM. This meeting report summarizes the presentations and discussions from the 2020 workshop titled, “Biomarkers in Radiation Biodosimetry and Medical Countermeasures,” sponsored by the Radiation and Nuclear Countermeasures Program (RNCP) at the National Institute of Allergy and Infectious Diseases (NIAID). The main goals of this meeting were to: 1. Provide an overview on biomarkers and to focus on the state of science with regards to biomarkers specific to radiation biodosimetry and MCMs; 2. Understand developmental challenges unique to the role of biomarkers in the fields of radiation biodosimetry and MCM development; and 3. Identify existing gaps and needs for translational application.

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Basal levels of glutathione peroxidase correlate with onset of radiation induced lung disease in inbred mouse strains

Abstract: Kunwar A, Haston CK. Basal levels of glutathione peroxidase correlate with onset of radiation induced lung disease in inbred mouse strains.

Cited by 8 publications

References 35 publications

The Th1/Th17 balance dictates the fibrosis response in murine radiation-induced lung disease

The Th1/Th17 balance dictates the fibrosis response in murine radiation-induced lung disease

Oxidative Stress Mechanisms in the Pathogenesis of Environmental Lung Diseases

Development of Biomarkers for Radiation Biodosimetry and Medical Countermeasures Research: Current Status, Utility, and Regulatory Pathways

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