No Lengthening of Life Span in Mice Continuously Exposed to Gamma Rays at Very Low Dose Rates

Tanaka, Satoshi; Tanaka, Ignacia Braga; Sasagawa, Sumiko; Ichinohe, Kazuaki; Tsuruo, Takashi; Matsushita, Satoru; Matsumoto, Tsuneya; Otsu, Hiroshi; Sato, Fumiaki

doi:10.1667/rr3042

Cited by 90 publications

(49 citation statements)

References 24 publications

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“…Similar studies on mice irradiated with 414 mGy at a dose rate of 0.86 mGy/d (0.65 µGy/min) showed no detectable change. These characteristics correspond roughly to that observed for life-shortening (Tanaka, Tanaka, Sasagawa, Ichinohe, Takabatake, Matsushita, et al, 2003) and cancer-induction (Tanaka, Tanaka, Ichinohe, Matsushita, Matsumoto, Otsu, et al, 2007), suggesting a role of genomic alteration in radiation-induced cancer and/or life shortening.…”

Section: Resultssupporting

confidence: 80%

“…These dose responses look similar to the effects on life shortening and cancer induction elucidated before under comparable conditions in B6C3 F1 mice (Tanaka, Tanaka, Sasagawa, Ichinohe, Takabatake, Matsushita, et al, 2003;Tanaka, Tanaka, Ichinohe, Matsushita, Matsumoto, Otsu, et al, 2007). It suggests a possible association between genomic alteration and life shortening and/or cancer induction.…”

Section: Data Science Journal Volume 8 24 September 2009supporting

confidence: 85%

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Alteration of Genome Structure Induced by Very Low Dose-Rate Irradiation in Mouse Tissues

Ono¹,

Uehara²,

Okudaira

et al. 2009

Data Sci. J.

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Section: Resultssupporting

confidence: 80%

Section: Data Science Journal Volume 8 24 September 2009supporting

confidence: 85%

Alteration of Genome Structure Induced by Very Low Dose-Rate Irradiation in Mouse Tissues

Ono¹,

Uehara²,

Okudaira

et al. 2009

Data Sci. J.

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“…Although some research groups have recently reported the effects of low doses of radiation on longevity and senescence (17,32,33), the underlying molecular mechanisms remained unknown. We thus focused on the mechanisms by which low doses of ionizing radiation inhibit cellular senescence.…”

Section: Discussionmentioning

confidence: 99%

Low doses of ionizing radiation suppress doxorubicin-induced senescence-like phenotypes by activation of ERK1/2 and suppression of p38 kinase in MCF7 human breast cancer cells

Shin

Woo²,

Lee³

et al. 2010

Int J Oncol

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Abstract. Low-dose radiation has a variety of effects on cellular activities, including the cell division cycle, apoptosis, proliferation and senescence. However, the effects of low doses of radiation remain controversial. In this study, we examined the effects of low-dose radiation on cellular senescence. We treated MCF7 cells with 0.01 μg/ml doxorubicin to induce replicative senescence, 2 h after exposure to low doses of ionizing radiation of 0.05, 0.1, or 0.2 Gy. The status of p53, senescence-associated ß-galactosidase activity, p38 kinase levels, H2AX levels and ERK/MAPK levels were examined. Low doses of ionizing radiation inhibit doxorubicininduced senescence in human breast cancer MCF7 cells. The phosphorylations of both p38 MAP kinase and p53 induced by doxorubicin were suppressed by low doses of ionizing radiation. The senescence was inhibited without genomic damage, because the level of Á-H2AX protein was not changed. Moreover, low doses of ionizing radiation inhibited senescence through the activation of ERK1/2. The results thus suggest that low doses of radiation suppress doxorubicin-induced replicative senescence through the inhibition of p38-dependent phosphorylation of p53 and by activation of ERK1/2, without genomic damage. Overall, our results suggest that low doses of ionizing radiation may have a protective role against replicative senescence induced by doxorubicin.

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“…When the average t x was longer than about 1 day, no tumors appeared and no life shortening was observed. On the other hand, a recent life-span study on specific-pathogen-free B6C3F1 mice used chronic exposure to 137 Cs γ -radiation at 0.05, 1.1, and 21 mGy per day beginning at 8 weeks for 400 days (Tanaka et al, 2003). No lengthening of life span was found.…”

Section: Microdoses At Low Dose Ratementioning

confidence: 98%

Responses to Low Doses of Ionizing Radiation in Biological Systems

Feinendegen

Pollycove

Sondhaus

2004

Nonlinearity in Biology, Toxicology, Medicine

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Biological tissues operate through cells that act together within signaling networks. These assure coordinated cell function in the face of constant exposure to an array of potentially toxic agents, externally from the environment and endogenously from metabolism. Living tissues are indeed complex adaptive systems.To examine tissue effects specific for low-dose radiation, (1) absorbed dose in tissue is replaced by the sum of the energies deposited by each track event, or hit, in a cell-equivalent tissue micromass (1 ng) in all micromasses exposed, that is, by the mean energy delivered by all microdose hits in the exposed micromasses, with cell dose expressing the total energy per micromass from multiple microdoses; and (2) tissue effects are related to cell damage and protective cellular responses per average microdose hit from a given radiation quality for all such hits in the exposed micromasses.The probability of immediate DNA damage per low-linear-energy-transfer (LET) average micro-dose hit is extremely small, increasing over a certain dose range in proportion to the number of hits. Delayed temporary adaptive protection (AP) involves (a) induced detoxification of reactive oxygen species, (b) enhanced rate of DNA repair, (c) induced removal of damaged cells by apoptosis followed by normal cell replacement and by cell differentiation, and (d) stimulated immune response, all with corresponding changes in gene expression. These AP categories may last from less than a day to weeks and be tested by cell responses against renewed irradiation. They operate physiologically against nonradiogenic, largely endogenous DNA damage, which occurs abundantly and continually. Background radiation damage caused by rare microdose hits per micromass is many orders of magnitude less frequent. Except for apoptosis, AP increasingly fails above about 200 mGy of low-LET radiation, corresponding to about 200 microdose hits per exposed micromass. This ratio appears to exceed approximately 1 per day for protracted exposure. The balance between damage and protection favors protection at low cell doses and damage at high cell doses. Bystander effects from high-dosed cells to nonirradiated neighboring cells appear to include both damage and protection.Regarding oncogenesis, a model based on the aforementioned dual response pattern at low doses and dose rates is consistant with the nonlinear reponse data and contradicts the linear no-threshold dose-risk hypothesis for radiation-induced cancer. Indeed, a dose-cancer risk function should include both linear and nonlinear terms.

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No Lengthening of Life Span in Mice Continuously Exposed to Gamma Rays at Very Low Dose Rates

Cited by 90 publications

References 24 publications

Alteration of Genome Structure Induced by Very Low Dose-Rate Irradiation in Mouse Tissues

Alteration of Genome Structure Induced by Very Low Dose-Rate Irradiation in Mouse Tissues

Low doses of ionizing radiation suppress doxorubicin-induced senescence-like phenotypes by activation of ERK1/2 and suppression of p38 kinase in MCF7 human breast cancer cells

Responses to Low Doses of Ionizing Radiation in Biological Systems

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