The Elimination of Low-Dose Hypersensitivity in Chinese Hamster V79-379A Cells by Pretreatment with X Rays or Hydrogen Peroxide

1995 ◽  
Vol 141 (2) ◽  
pp. 160 ◽  
Author(s):  
B. Marples ◽  
M. C. Joiner
Keyword(s):  
Hydrogen Peroxide ◽  
Low Dose ◽  
Chinese Hamster ◽  
X Rays

scholarly journals Modeling cell survival and change in amount of DNA during protracted irradiation

2016 ◽  
Vol 58 (3) ◽  
pp. 302-312 ◽  
Author(s):  
Yusuke Matsuya ◽  
Kaori Tsutsumi ◽  
Kohei Sasaki ◽  
Yuji Yoshii ◽  
Takaaki Kimura ◽  
...  
Keyword(s):  
Low Dose ◽  
Dose Range ◽  
Flow Cytometric Analysis ◽  
Chinese Hamster ◽  
Clonogenic Survival ◽  
High Dose ◽  
X Rays ◽  
Theoretical Evaluation ◽  
Flow Cytometric ◽  
M Phase

Abstract Hyper-radiosensitivity (HRS) is a well-known bioresponse under low-dose or low-dose-rate exposures. Although disorder of the DNA repair function, non-targeted effects and accumulation of cells in G2 have been experimentally observed, the mechanism for inducing HRS by long-term irradiation is still unclear. On the basis of biological experiments and a theoretical study, we have shown that change in the amount of DNA associated with accumulation of cells in G2 enhances radiosensitivity. To demonstrate continuous irradiation with 250 kVp X-rays, we adopted a fractionated regimen of 0.186 or 1.00 Gy per fraction at intervals of 1 h (i.e. 0.186 Gy/h, 1.00 Gy/h on average) to Chinese Hamster Ovary (CHO)-K1 cells. The change in the amount of DNA during irradiation was quantified by flow cytometric analysis with propidium iodide (PI). Concurrently, we attempted a theoretical evaluation of the DNA damage by using a microdosimetric-kinetic (MK) model that was modified to incorporate the change in the amount of DNA. Our experimental results showed that the fraction of the cells in G2/M phase increased by 6.7% with 0.186 Gy/h and by 22.1% with 1.00 Gy/h after the 12th irradiation. The MK model considering the change in amount of DNA during the irradiation exhibited a higher radiosensitivity at a high dose range, which could account for the experimental clonogenic survival. The theoretical results suggest that HRS in the high dose range is associated with an increase in the total amount of DNA during irradiation.

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 Cromoglycate and nedocromil enhanced the reactive oxygen species-dependent suppressions with, but not without, dexamethasone in ischaemic and histamine paw oedema of mice

1997 ◽  
Vol 6 (5-6) ◽  
pp. 369-374
Author(s):  
Y. Oyanagui
Keyword(s):  
Reactive Oxygen Species ◽  
Hydrogen Peroxide ◽  
Superoxide Dismutase ◽  
Glucocorticoid Receptor ◽  
Low Dose ◽  
Natural Antioxidant ◽  
Target Cells ◽  
Oxygen Species ◽  
Paw Oedema ◽  
Β Carotene

Anti-inflammatory actions of two anti-allergic drugs, alone or with dexamethasone (Dex) were examined in two models, because inflammation is claimed to be important for allergic events, especially for asthma. Cromoglycate and nedocromil were tested in ischaemic- and histamineinduced paw oedema models of mice. These antiallergic drugs (1–100 mg/kg, i.p.) failed to suppress these oedemata, but enhanced the suppressions by a low dose of dexamethasone (0.1 mg/kg, s.c.) at 3–8 h after Dex injection. The mode of effects by anti-allergic drugs resembled that of a natural antioxidant (α-tocopherol, β-carotene etc.), and was different from that of an immunosuppressant like FK506. The enhancing potencies of the two anti-allergic drugs were similar at 6 h after Dex in both oedemata, and were diminished by superoxide dismutase (SOD) or catalase (i.p.). Cycloheximide completely abolished suppressions. Nedocromil, but not cromoglycate, inhibits inflammatory events. Therefore, there are common unknown actions by which the two anti-allergics enhance suppression by Dex. A possible mechanism of this action was supposed to enhance the superoxide and/or hydrogen peroxide-dependent glucocorticoid receptor (GR) signalling in the target cells.

scholarly journals Low-Dose Radiation Activates Akt and Nrf2 in the Kidney of Diabetic Mice: A Potential Mechanism to Prevent Diabetic Nephropathy

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Xiao Xing ◽  
Chi Zhang ◽  
Minglong Shao ◽  
Qingyue Tong ◽  
Guirong Zhang ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Low Dose ◽  
X Rays ◽  
Diabetic Mice ◽  
Low Dose Radiation ◽  
Single Exposure ◽  
Akt Phosphorylation ◽  
And Function ◽  
Nrf2 Expression ◽  
Dose Radiation

Repetitive exposure of diabetic mice to low-dose radiation (LDR) at 25 mGy could significantly attenuate diabetes-induced renal inflammation, oxidative damage, remodeling, and dysfunction, for which, however, the underlying mechanism remained unknown. The present study explored the effects of LDR on the expression and function of Akt and Nrf2 in the kidney of diabetic mice. C57BL/6J mice were used to induce type 1 diabetes with multiple low-dose streptozotocin. Diabetic and age-matched control mice were irradiated with whole body X-rays at either single 25 mGy and 75 mGy or accumulated 75 mGy (25 mGy daily for 3 days) and then sacrificed at 1–12 h for examining renal Akt phosphorylation and Nrf2 expression and function. We found that 75 mGy of X-rays can stimulate Akt signaling pathway and upregulate Nrf2 expression and function in diabetic kidneys; single exposure of 25 mGy did not, but three exposures to 25 mGy of X-rays could offer a similar effect as single exposure to 75 mGy on the stimulation of Akt phosphorylation and the upregulation of Nrf2 expression and transcription function. These results suggest that single 75 mGy or multiple 25 mGy of X-rays can stimulate Akt phosphorylation and upregulate Nrf2 expression and function, which may explain the prevention of LDR against the diabetic nephropathy mentioned above.

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