Response of V79 cells to low doses of X-rays and negative-mesons: clonogenic survival and DNA strand breaks

Marples, Brian; Adomat, Hans; Koch, Cameron J.; Skov, Kirsten A.

doi:10.1080/095530096144905

Cited by 28 publications

(2 citation statements)

References 25 publications

(14 reference statements)

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“…Firstly, the fact that HRS occurring at the low dose range 100-300 mGy followed by the induction of radioresistance (IRR) was interpreted as being linked to a low-dose adaptive phenomenon: the initial very low dose subsequently induced the repair of IR induced DNA strand breaks yielding radiation resistance (IRR) [153,[161][162][163].…”

Section: Irrmentioning

confidence: 99%

Low-Dose Non-Targeted Effects and Mitochondrial Control

Averbeck

2023

IJMS

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Non-targeted effects (NTE) have been generally regarded as a low-dose ionizing radiation (IR) phenomenon. Recently, regarding long distant abscopal effects have also been observed at high doses of IR) relevant to antitumor radiation therapy. IR is inducing NTE involving intracellular and extracellular signaling, which may lead to short-ranging bystander effects and distant long-ranging extracellular signaling abscopal effects. Internal and “spontaneous” cellular stress is mostly due to metabolic oxidative stress involving mitochondrial energy production (ATP) through oxidative phosphorylation and/or anaerobic pathways accompanied by the leakage of O2− and other radicals from mitochondria during normal or increased cellular energy requirements or to mitochondrial dysfunction. Among external stressors, ionizing radiation (IR) has been shown to very rapidly perturb mitochondrial functions, leading to increased energy supply demands and to ROS/NOS production. Depending on the dose, this affects all types of cell constituents, including DNA, RNA, amino acids, proteins, and membranes, perturbing normal inner cell organization and function, and forcing cells to reorganize the intracellular metabolism and the network of organelles. The reorganization implies intracellular cytoplasmic-nuclear shuttling of important proteins, activation of autophagy, and mitophagy, as well as induction of cell cycle arrest, DNA repair, apoptosis, and senescence. It also includes reprogramming of mitochondrial metabolism as well as genetic and epigenetic control of the expression of genes and proteins in order to ensure cell and tissue survival. At low doses of IR, directly irradiated cells may already exert non-targeted effects (NTE) involving the release of molecular mediators, such as radicals, cytokines, DNA fragments, small RNAs, and proteins (sometimes in the form of extracellular vehicles or exosomes), which can induce damage of unirradiated neighboring bystander or distant (abscopal) cells as well as immune responses. Such non-targeted effects (NTE) are contributing to low-dose phenomena, such as hormesis, adaptive responses, low-dose hypersensitivity, and genomic instability, and they are also promoting suppression and/or activation of immune cells. All of these are parts of the main defense systems of cells and tissues, including IR-induced innate and adaptive immune responses. The present review is focused on the prominent role of mitochondria in these processes, which are determinants of cell survival and anti-tumor RT.

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Section: Irrmentioning

confidence: 99%

Low-Dose Non-Targeted Effects and Mitochondrial Control

Averbeck

2023

IJMS

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“…HRS has been observed in cells given acute proton and pi-meson irradiation ( Marples et al . 1994 ; Marples et al . 1996 ; Schettino et al .…”

Section: Introductionmentioning

confidence: 99%

TGF-B3 Dependent Modification of Radiosensitivity in Reporter Cells Exposed to Serum from Whole-Body Low Dose-Rate Irradiated Mice

Edin¹,

Altaner²,

Altanerova³

et al. 2014

Dose-Response

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Prior findings in vitro of a TGF-β3 dependent mechanism induced by low dose-rate irradiation and resulting in increased radioresistance and removal of low dose hyper-radiosensitivity (HRS) was tested in an in vivo model. DBA/2 mice were given whole-body irradiation for 1 h at low dose-rates (LDR) of 0.3 or 0.03 Gy/h. Serum was harvested and added to RPMI (4% mouse serum and 6% bovine serum).This medium was transferred to reporter cells (T-47D breast cancer cells or T98G glioblastoma cells). The response to subsequent challenge irradiation of the reporter cells was measured by the colony assay. While serum from unirradiated control mice had no effect on the radiosensitivity in the reporter cells, serum from mice given 0.3 Gy/h or 0.03 Gy/h for 1 h removed HRS and also increased survival in response to doses up to 5 Gy. The effect lasted for at least 15 months after irradiation. TGF-β3 neutralizer added to the medium containing mouse serum inhibited the effect. Serum from mice given irradiation of 0.3 Gy/h for 1 h and subsequently treated with iNOS inhibitor 1400W did not affect radiosensitivity in reporter cells; neither did serum from the unirradiated progeny of mice given 1h LDR whole-body irradiation.

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Combinations of Topoisomerase Inhibitors and Ionizing Radiation

Bastasch

Choy

Multimodal Concepts for Integration of Cytotoxic Drugs

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Response of V79 cells to low doses of X-rays and negative-mesons: clonogenic survival and DNA strand breaks

Cited by 28 publications

References 25 publications

Low-Dose Non-Targeted Effects and Mitochondrial Control

Low-Dose Non-Targeted Effects and Mitochondrial Control

TGF-B3 Dependent Modification of Radiosensitivity in Reporter Cells Exposed to Serum from Whole-Body Low Dose-Rate Irradiated Mice

Combinations of Topoisomerase Inhibitors and Ionizing Radiation

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