Neoplastic Transformation<i>In Vitro</i>after Exposure to Low Doses of Mammographic-Energy X Rays: Quantitative and Mechanistic Aspects

Sj, Ko; Xy, Liao; Molloi, Sabee; Elmore, Eugene; Jl, Redpath

doi:10.1667/rr3277

Cited by 48 publications

(92 citation statements)

References 48 publications

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“…is the undefined dose dissipation function developed further in Section 2.9, applied to the Ko et al (2004) tion and fading, is that the data indicates the AR protection persisting up to 38 hours and fading does not begin until this "threshold" time, t 0 = 38 hours, as shown in the Figure 1C of Leonard (2007b). We have premised that the fading stems from two causes, i.e.…”

Section: 1a the F(d T P ) Protection Activation Fading And Dose mentioning

confidence: 84%

“…Perhaps even more significant are the AR radio-protection from the low energy mammogram (Ko et al 2004) and diagnostic (Redpath et al 2003) X-rays that has led to conclusions that the low energy mammography X-rays do not result in excessive cancer risk as premised by others (Heyes et al 2004 but conversely provides potential protection from breast cancer (Redpath andMitchel 2006, Redpath 2007). For analysis purposes, the Koana et al (2004) provides only several data points of chromosome mutation frequencies and not sufficient for detailed microdosimetry model analysis.…”

Section: B E Leonardmentioning

confidence: 99%

“…We will show a protective Bystander Effect behavior, which can be modeled in Equations (35) and (35a) by setting negative values to the parameter σ, the fraction of cells that are hypersensitive, providing for them to be hypersensitive to protective Bystander signaling. We will examine, in Sections 3.4 and 4.1.c, the data of Ko et al (2004) that shows conclusive protective Bystander Effect behavior by using a negative value for σ.…”

Section: 8e Protective and Deleterious Bystander Effectsmentioning

confidence: 99%

“…Figure 6, used for the microdose analysis of the Hooker et al (2004) data has illustrated the three dose response regions in the case of a protective Bystander behavior. As Figure 8B, we show the possible three regions, Bystander Region, Adaptive Response Region and the Direct Damage Region, for the Ko et al (2004) data. Using Equations (35) and (35a), we have fit the composite AR-BE Micro-dose Model to the Ko et al (2004) data.…”

Section: 4b Composite Microdose Model Fit To Ko Et Al Mammogram Xmentioning

confidence: 99%

“…Many investigators have preferred to study in vitro AR effects from the large challenge doses since chromosome aberration levels produced for scoring purposes are much larger, and better accuracy can be achieved, than that obtained solely from the low spontaneous cell damage (Wiencke et al 1986, Wolff et al 1989, Shadley and Wiencke 1989, Broome et al 2002, Wang et al 2003, Iyer and Lehnert 2002, Day et al 2006. However, some investigators have measured the ability of cells to undergo AR protection (from only low-LET priming dose radiation) of only the natural spontaneous aberrations continually occurring in cells from endogenic toxic damage to chromosomes (Pohl-Ruling et al 1983, Azzam et al 1996, Redpath and Antoniono 1998, Redpath et al 2001, Ko et al 2004, Hooker et al 2004, Elmore et al 2006, Koana et al 2007.…”

mentioning

confidence: 99%

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A Review: Development of a Microdose Model for Analysis of Adaptive Response and Bystander Dose Response Behavior

Leonard¹

2008

Dose-Response

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Prior work has provided incremental phases to a microdosimetry modeling program to describe the dose response behavior of the radio-protective adaptive response effect. We have here consolidated these prior works (Leonard 2000, 2005, 2007a, 2007b, 2007c) to provide a composite, comprehensive Microdose Model that is also herein modified to include the bystander effect. The nomenclature for the model is also standardized for the benefit of the experimental cellular radio-biologist. It extends the prior work to explicitly encompass separately the analysis of experimental data that is 1.) only dose dependent and reflecting only adaptive response radio-protection, 2.) both dose and dose-rate dependent data and reflecting only adaptive response radio-protection for spontaneous and challenge dose damage, 3.) only dose dependent data and reflecting both bystander deleterious damage and adaptive response radio-protection (AR-BE model). The Appendix cites the various applications of the model. Here we have used the Microdose Model to analyze the, much more human risk significant, Elmore et al (2006) data for the dose and dose rate influence on the adaptive response radio-protective behavior of HeLa x Skin cells for naturally occurring, spontaneous chromosome damage from a Brachytherapy type 125 I photon radiation source. We have also applied the AR-BE Microdose Model to the Chromosome inversion data of Hooker et al (2004) reflecting both low LET bystander and adaptive response effects. The micro-beam facility data of Miller et al (1999), Nagasawa and Little (1999) and Zhou et al (2003) is also examined. For the Zhou et al (2003) data, we use the AR-BE model to estimate the threshold for adaptive response reduction of the bystander effect. The mammogram and diagnostic Xray induction of AR and protective BE are observed. We show that bystander damage is reduced in the similar manner as spontaneous and challenge dose damage as shown by the Azzam et al (1996) data. We cite primary unresolved questions regarding adaptive response behavior and bystander behavior. The five features of major significance provided by the Microdose Model so far are 1.) Single Specific Energy Hits initiate Adaptive Response, 2.) Mammogram and diagnostic X-rays induce a protective Bystander Effect as well as Adaptive Response radio-protection. 3.) For mammogram X-rays the Adaptive Response protection is retained at high primer dose levels. 4.) The dose range of the AR protection depends on the value of the Specific Energy per Hit, . 5.) Alpha particle induced deleterious Bystander damage is modulated by low LET radiation.

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Section: 1a the F(d T P ) Protection Activation Fading And Dose mentioning

confidence: 84%

Section: B E Leonardmentioning

confidence: 99%

Section: 8e Protective and Deleterious Bystander Effectsmentioning

confidence: 99%

Section: 4b Composite Microdose Model Fit To Ko Et Al Mammogram Xmentioning

confidence: 99%

mentioning

confidence: 99%

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A Review: Development of a Microdose Model for Analysis of Adaptive Response and Bystander Dose Response Behavior

Leonard¹

2008

Dose-Response

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Activation of NF-κB in bone marrow cells of BALB/cJ mice following exposure in vivo to low doses of 137Cs γ-rays

Rithidech

Tungjai

Arbab

et al. 2005

Radiat Environ Biophys

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We measured levels of NF-kappaB activation in bone marrow (BM) cells collected at 1 and 4 h from male BALB/cJ mice (10-12 weeks old) given a whole body dose of 0, 0.05, 0.1 and 1 Gy of (137)Cs gamma-rays (at the dose rate of 0.75 Gy/min). At each harvest time-point, BM cells were collected from five mice per dose of radiation. We used two methods for detecting NF-kappaB activation (1) the NF-kappaB/p65 transcription factor enzyme-linked immunosorbance assay (ELISA) and (2) immunofluorescence staining with NF-kappaB/p65 antibody. Results from ELISA indicated 2.0 and 2.8-fold increases in NF-kappaB activation in BM cells isolated at 1 h post-exposure of mice to 0.1 or 1.0 Gy. The immunofluorescence staining method showed similar results. In samples isolated 4 h post-irradiation, however, no activated NF-kappaB signal was found, regardless of the method of detection. The data also demonstrated that NF-kappaB was not activated in bone marrow cells collected either at 1 or 4 h from BALB/cJ mice exposed to a single dose of 0.05 Gy (137)Cs gamma-rays. Taken together, the results from our in vivo study indicate the involvement of NF-kappaB activation in early response to 0.1 and 1.0 Gy (but not 0.05 Gy) of (137)Cs gamma-rays.

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Influence of the bystander phenomenon on the chromosome aberration pattern in human lymphocytes induced by in vitro α-particle exposure

Schmid¹,

Roos²

2008

Radiat Environ Biophys

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A recent publication on both chromosome-type and chromatid-type aberrations in lymphocytes of patients during treatment with radium-224 for ankylosing spondilitis has revived the question of whether the chromatid-type aberrations may be the consequence of factors released by irradiated cells. Therefore, the aim of the present study was to investigate the influence of such a bystander phenomenon on the chromosome aberration pattern of lymphocytes. Monolayers of human lymphocytes were irradiated with 1 Gy of alpha-particles from an americium-241 source in the absence or presence of whole blood, autologous plasma or culture medium. In the presence of any liquid covering the monolayer during irradiation, the chromatid-type aberrations were, contrary to expectation, elevated. Whereas the intercellular distribution of dicentrics was significantly overdispersed, the chromatid-type aberrations showed a regular dispersion. It can be concluded that the enhanced frequency of chromatid aberrations is the result of a damage signal or a bystander phenomenon released by irradiated cells.

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Neoplastic TransformationIn Vitroafter Exposure to Low Doses of Mammographic-Energy X Rays: Quantitative and Mechanistic Aspects

Cited by 48 publications

References 48 publications

A Review: Development of a Microdose Model for Analysis of Adaptive Response and Bystander Dose Response Behavior

A Review: Development of a Microdose Model for Analysis of Adaptive Response and Bystander Dose Response Behavior

Activation of NF-κB in bone marrow cells of BALB/cJ mice following exposure in vivo to low doses of 137Cs γ-rays

Influence of the bystander phenomenon on the chromosome aberration pattern in human lymphocytes induced by in vitro α-particle exposure

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