Cytogenetic and survival adaptive responses in G1 phase human lymphocytes

Shadley, Jeff D.; Dai, Guoqiang

doi:10.1016/0027-5107(92)90056-8

Cited by 71 publications

(24 citation statements)

References 19 publications

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“…1984, Wiencke et al . 1986, Ikushima 1987, Wolff et al 1988, Sankaranarayanan et al 1989, Shadley and Dai 1992 and cell survival (Lambin et al . 1993, Marples andjoiner 1993) as endpoints .…”

Section: Introductionmentioning

confidence: 98%

Hypersensitive Response of Normal Human Lung Epithelial Cells at Low Radiation Doses

Singh

Arrand

Joiner

1994

International Journal of Radiation Biology

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The effect of very low single X-ray doses (0.05-4 Gy) was investigated in a human lung epithelial cell line (L132). Cell survival measurements were made using a Dynamic Microscopic Imaging Processing Scanner (DMIPS), which allowed single cells to be located accurately, their positions recorded and these positions revisited after an appropriate incubation period at 37 degrees C; surviving cells were identified by their ability to produce a colony > or = 50 cells. The survival data at doses > or = 2 Gy were well-fitted by a linear-quadratic (LQ) model. For doses < 1 Gy, increased X-ray effectiveness was observed with cell survival below the prediction from the fit of the LQ model to the higher dose data, extrapolated into the low dose region. This is the first evidence for the existence of a hypersensitive survival response to very low doses in normal human cells. The transition between the low dose hypersensitive region and greater resistance at higher doses, could result from induced radioresistance which requires a threshold of radiation-induced damage before being triggered.

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Section: Introductionmentioning

confidence: 98%

Hypersensitive Response of Normal Human Lung Epithelial Cells at Low Radiation Doses

Singh

Arrand

Joiner

1994

International Journal of Radiation Biology

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“…This phenomenon, first reported in 1984, has been identified as a radio-adaptive response characterized by either an elevation in cell survival and/or a reduction in genomic damage as measured by markers of genomic instability [1–3]. While this phenomenon has not been universally observed in all cell systems or even in similar cell types from different individuals, it has been demonstrated to occur in sufficient frequency in cultured cells, as well as rodent and human cell systems to be identified as an important consequence of low dose radiation exposure.…”

Section: Introductionmentioning

confidence: 99%

SOD2-mediated adaptive responses induced by low-dose ionizing radiation via TNF signaling and amifostine

Murley

Baker

Miller

et al. 2011

Free Radical Biology and Medicine

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Manganese superoxide dismutase (SOD2)-mediated adaptive processes that protect against radiation-induced micronuclei formation can be induced in cells following a 2 Gy exposure by previously exposing them to either low dose ionizing radiation (10 cGy) or WR1065 (40 µM), the active thiol form of amifostine. While both adaptive processes culminate with elevated levels of SOD2 enzymatic activities, the underlying pathways differ in complexity, with the tumor necrosis factor α (TNFα) signaling pathway implicated in the low dose radiation-induced response, but not in the thiol-induced pathway. The goal of this study was the characterization of the effects of TNFα receptors1 and 2 (TNFR1, 2) on the adaptive responses induced by low dose irradiation or thiol exposures using micronuclei formation as an endpoint. BFS-1 wild type (WT) cells with functional TNFR1 and 2 were exposed 24 h prior to a 2 Gy dose of ionizing radiation to either 10 cGy or a 40 µM dose of WR1065. BFS2C-SH02 cells defective in TNFR1 and BFS2C-SH22 cells defective in both TNFR1 and 2, generated from BFS2C-SH02 cells by transfection with a murine TNFR2 targeting vector and confirmed to be TNFR2 defective by quantitative PCR, were also exposed under similar conditions for comparison. A 10 cGy dose of radiation induced a significant elevation of SOD2 activity in BFS-1 (P < 0.001) and BFS2C-SH02 (P = 0.005) but not BFS2C-SH22 cells (P = 0.433) as compared to their respective untreated controls. In contrast, WR1065 significantly induced elevations in SOD2 activity in all three cell lines (P = 0.001; P = 0.007; P = 0.020; respectively). A significant reduction in the frequency of radiation-induced micronuclei was observed in each cell line when exposure to a 2 Gy challenge dose of radiation occurred during the period of maximal elevation in SOD2 activity. However, this adaptive effect was completely inhibited if the cells were transfected 24 h prior to low dose radiation or thiol exposure with SOD2 siRNA. Under the conditions tested, TNFR1,2 inhibition negatively impacted the low dose radiation-induced but not the thiol-induced adaptive responses observed to be mediated by elevations in SOD2 activity.

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“…Although we have not carried out any statistical analysis of the individual experiments because the very high number of degrees of freedom obtained would cause even a minor difference to be highly significant, the enhanced UV-light-induced UDS levels could be interpreted as evidence for the existence of a heterogeneity within the mouse population with respect to the ability to express an adaptive response. Such a heterogeneity has been reported by several authors in human lymphocytes (Bosi and Olivieri 1989;Sankaranarayanan et al 1989;Shadley and Dai 1992). However, several experiments also yielded a reduced level of UVlight-induced UDS in adapted cells, implying that the differences are rather a result of a variability inherent to this endpoint, than of some induced cellular processes.…”

Section: Discussionmentioning

confidence: 77%

No indications of an enhanced UV-light-induced unscheduled DNA synthesis in splenocytes of mice following a low-dose irradiation in vivo or in vitro

Wójcik

Seemayer

Müller

et al. 1995

Radiat Environ Biophys

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One of the open questions regarding the adaptive response to ionizing radiation is whether it can be induced in G0 lymphocytes. In the majority of experiments in which an adaptive response in G0 lymphocytes was observed, the adapting dose was applied in vivo. In order to investigate whether there is some in vivo component of adaptive response, mouse splenocytes of the C57BL/6 strain were irradiated with 0.1 Gy x-rays either in vivo or in vitro, and their UV-light-induced unscheduled DNA synthesis (UDS) levels were determined autoradiographically. An augmented UV-light-induced UDS following an adapting dose applied in vivo has previously been described by several authors in splenocytes of C57BL/6 mice, indicating that the adapting dose enhanced the DNA repair capacity of lymphocytes. In the present investigation, however, no evidence of an adaptive response could be seen regardless of whether the adapting dose was given in vivo or in vitro. Those results present a further indication for the fact that the adaptive response to ionizing radiation is not always inducible, even in lymphocytes of an inbred mouse strain in which its existence has been reported before.

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Cytogenetic and survival adaptive responses in G1 phase human lymphocytes

Cited by 71 publications

References 19 publications

Hypersensitive Response of Normal Human Lung Epithelial Cells at Low Radiation Doses

Hypersensitive Response of Normal Human Lung Epithelial Cells at Low Radiation Doses

SOD2-mediated adaptive responses induced by low-dose ionizing radiation via TNF signaling and amifostine

No indications of an enhanced UV-light-induced unscheduled DNA synthesis in splenocytes of mice following a low-dose irradiation in vivo or in vitro

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