scholarly journals Cellular Adaptive Response and Regulation of HIF after Low Dose Gamma-radiation Exposure

2018 ◽  
Author(s):  
Nitin Motilal Gandhi
Keyword(s):  
Radiation Exposure ◽  
Adaptive Response ◽  
Low Dose ◽  
Lower Amount ◽  
Induced Response ◽  
Priming Dose ◽  
Γ Radiation ◽  
Radiation Induced ◽  
Challenging Dose

AbstractPurposeCellular damage due to low dose of γ-radiation (≤0.1 Gy) is generally extrapolated from observing the effects at higher doses. These estimations are not accurate. This has led to uncertainties while assessing the radiation risk factors at low doses. Although there are reports on the radiation induced adaptive response, the mechanism of action is not fully elucidated, leading to the uncertainties. One of the outcomes of low dose radiation exposure is believed to be adaptive response. The mechanism of adaptive response is not fully understood. Therefore, the study was undertaken to understand the role of hypoxia inducible factor (HIF) on radiation induced adaptive response.Materials and methodsMCF-7 cells pre-exposed to low dose γ-radiation (0.1 Gy; Priming dose) were exposed to 2 Gy (challenging dose) 8 hrs after the priming dose and studied for the adaptive response. Cell death was measured by MTT assay, and apoptosis was measured by FACS analysis. DNA damage was measures by alkaline comet assay. HIF transcription activity was assayed using transiently transfected plasmid having HIF consensus sequence and luciferase as the reporter gene.ResultsCells when exposed to 0.1 Gy priming dose 8 hrs prior to the higher dose (2 Gy; Challenging dose) results in lower amount of radiation induced damages compared to the cells exposed to 2 Gy alone. Cobalt chloride treatment in place of priming dose also results in the protection to cells when exposed to challenging dose. There was up-regulation of HIF activity when cells were exposed to priming dose, indicating the role of HIF in radiation induced response.ConclusionResults indicate the γ-radiation induced adaptive response. One of the mechanism proposed is up-regulation of HIF after low dose exposure, which protects the cells from damages when they are exposed to challenging dose of 2 Gy radiation dose.

Reactive oxygen species in cell responses to toxic agents

2002 ◽  
Vol 21 (2) ◽  
pp. 85-90 ◽  
Author(s):  
L E Feinendegen
Keyword(s):  
Radiation Exposure ◽  
Mammalian Cells ◽  
Low Dose ◽  
X Rays ◽  
Low Dose Radiation ◽  
Cell Responses ◽  
Toxic Agents ◽  
Particle Tracks ◽  
Dose Radiation

This review first summarizes experimental data on biological effects of different concentrations of ROS in mammalian cells and on their potential role in modifying cell responses to toxic agents. It then attempts to link the role of steadily produced metabolic ROS at various concentrations in mammalian cells to that of environmentally derived ROS bursts from exposure to ionizing radiation. The ROS from both sources are known to both cause biological damage and change cellular signaling, depending on their concentration at a given time. At low concentrations signaling effects of ROS appear to protect cellular survival and dominate over damage, and the reverse occurs at high ROS concentrations. Background radiation generates suprabasal ROS bursts along charged particle tracks several times a year in each nanogram of tissue, i.e., average mass of a mammalian cell. For instance, a burst of about 200 ROS occurs within less than a microsecond from low-LET irradiation such as X-rays along the track of a Compton electron (about 6 keV, ranging about 1 μm). One such track per nanogram tissue gives about 1 mGy to this mass. The number of instantaneous ROS per burst along the track of a 4-meV ¬-particle in 1 ng tissue reaches some 70000. The sizes, types and sites of these bursts, and the time intervals between them directly in and around cells appear essential for understanding low-dose and low dose-rate effects on top of effects from endogenous ROS. At background and low-dose radiation exposure, a major role of ROS bursts along particle tracks focuses on ROS-induced apoptosis of damage-carrying cells, and also on prevention and removal of DNA damage from endogenous sources by way of temporarily protective, i.e., adaptive, cellular responses. A conclusion is to consider low-dose radiation exposure as a provider of physiological mechanisms for tissue homoeostasis.

scholarly journals Adaptive Response in Zebrafish Embryos Induced Using Microbeam Protons as Priming Dose and X-ray Photons as Challenging Dose

2010 ◽  
Vol 51 (6) ◽  
pp. 657-664 ◽  
Author(s):  
Viann Wing Yan CHOI ◽  
Teruaki KONISHI ◽  
Masakazu OIKAWA ◽  
Hiroyuki ISO ◽  
Shuk Han CHENG ◽  
...  
Keyword(s):  
Adaptive Response ◽  
Zebrafish Embryos ◽  
Priming Dose ◽  
X Ray ◽  
Challenging Dose

scholarly journals Oxidized Cell-Free DNA Is a Factor of Stress Signaling in Radiation-Induced Bystander Effects in Different Types of Human Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Marina S. Konkova ◽  
Andrew A. Kaliyanov ◽  
Vasilina A. Sergeeva ◽  
Margarita S. Abramova ◽  
Svetlana V. Kostyuk
Keyword(s):  
Low Dose ◽  
Bystander Effect ◽  
Biological Properties ◽  
Stress Signaling ◽  
Cell Free Dna ◽  
Free Dna ◽  
Cytokine Levels ◽  
Different Types ◽  
Radiation Induced

In pathology or under damaging conditions, the properties of cell-free DNA (cfDNA) change. An example of such change is GC enrichment, which drastically alters the biological properties of cfDNA. GC-rich cfDNA is a factor of stress signaling, whereas genomic cfDNA is biologically inactive. GC-rich cfDNA stimulates TLR9-MyD88-NF-κB signaling cascade, leading to an increase in proinflammatory cytokine levels in the organism. In addition, GC-rich DNA is prone to oxidation and oxidized cfDNA can stimulate secondary oxidative stress. This article is a review of works dedicated to the investigation of a low-dose ionizing radiation effect, a bystander effect, and the role of cfDNA in both of these processes.

Low Doses of Very Low-Dose-Rate Low-LET Radiation Suppress Radiation-Induced Neoplastic TransformationIn Vitroand Induce an Adaptive Response

2008 ◽  
Vol 169 (3) ◽  
pp. 311-318 ◽  
Author(s):  
E. Elmore ◽  
X-Y. Lao ◽  
R. Kapadia ◽  
E. Giedzinski ◽  
C. Limoli ◽  
...  
Keyword(s):  
Dose Rate ◽  
Adaptive Response ◽  
Low Dose ◽  
Low Doses ◽  
Low Dose Rate ◽  
Radiation Induced

scholarly journals Modeling of Molecular Mechanisms of Radiation Adaptive Response Formation

2021 ◽  
Keyword(s):  
Adaptive Response ◽  
Molecular Mechanisms ◽  
Low Dose ◽  
Low Doses ◽  
Radiation Hormesis ◽  
Biological Objects ◽  
Mechanisms Of Formation ◽  
Radiation Induced ◽  
High Doses ◽  
Lnt Model

The phenomenon of adaptive response is expressed in the increase of resistance of a biological object to high doses of mutagens under the conditions of previous exposure to these (or other) mutagens in low doses. Low doses of mutagen activate a number of protective mechanisms in a living object, which are called hormetic. Thus, the adaptive response and hormesis are links in the same chain. Radiation hormesis refers to the generally positive effect of low doses of low LET radiation on biological objects. The phenomenology of radiation-induced adaptive response and radiation hormesis for biological objects of different levels of organization is considered; the review of existing theories describing the dose-effect relationship has been reviewed. The hypothesis proposing one of the mechanisms of formation of radiation adaptive response of cells taking into account the conformational structure of chromatin has been submitted. The analysis of modern concepts of the phenomenon of hormesis on the basis of modeling of molecular mechanisms of formation of hormetic reactions to low-dose low LET radiation has been carried out. The parameters that can be used for quantitative and graphical evaluation of the phenomenon of hormesis was considered, and a formula for calculating the coefficient of radiation-induced adaptive response has been proposed. A review of mathematical models describing the radiation relative risk of gene mutations and neoplastic transformations at low-dose irradiation of cohorts has been performed. The following conclusions have been made: radiation hormesis and adaptive response are generally recognized as real and reproducible biological phenomena, which should be considered as very important phenomena of evolutionarily formed biological protection of living organisms from ionizing radiation. The hormesis model of dose-response relationship makes much more accurate predictions of a living object's response to radiation (or other stressors) in the low-dose range than the linear threshold (LNT) model does. The LNT model can adequately describe reactions only in the region of high doses of radiation, and, therefore, extrapolation modeling of biological object’s reactions from the zone of high doses to low doses is not correct.

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