Hematopoietic responses under protracted exposures to low daily dose gamma irradiation

Seed, Thomas M.; Fritz, T.E.; Tolle, D.V.; Jackson, William E.

doi:10.1016/s0273-1177(02)00159-x

Cited by 31 publications

(35 citation statements)

References 8 publications

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“…8a). With these assumptions, the level of depressed granulocyte at a rate of 37.5 mGy d Ϫ1 is predicted to be about 37% of normal, which is also consistent with the experimental report (Seed et al 2002).…”

Section: Low Dose Rate Chronic Irradiationsupporting

confidence: 87%

“…At levels of 3.0, 7.5, and 18.8 mGy d Ϫ1 of total body irradiation, they found the granulocyte concentrations in dogs were reduced to about 65%, 51%, and 41%, respectively, of the normal value (Fliedner et al 1996). A threshold of dose rate between 37.5 and 75.0 mGy d Ϫ1 , beyond which the hematopoietic system may fail, was also identified experimentally (Seed et al 2002).…”

Section: Low Dose Rate Chronic Irradiationmentioning

confidence: 85%

“…Researchers at Argonne National Laboratory have conducted a series of chronic irradiation studies with beagle dogs (Seed et al 2002). The granulocyte concentrations over long-term chronic gamma irradiation at various levels were well documented.…”

Section: Low Dose Rate Chronic Irradiationmentioning

confidence: 99%

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Characterization of the Radiation-Damaged Precursor Cells in Bone Marrow Based on Modeling of the Peripheral Blood Granulocytes Response

Cucinotta²

2011

Health Physics

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Bone marrow failure is the major cause of radiation lethality in mammals. Since bone marrow is distributed heterogeneously within trabecular spongiosa encased in a cortex of cortical bone, it is very difficult to measure the extent of the radiation damage directly. However, indirect consequences of damage to marrow, such as reductions in peripheral blood cell counts, are easily measured. In this paper, the authors investgate a mathematical model of the granulopoiesis system that provides quantitative relationships between reductions in peripheral blood cells and the bone marrow precursor cells following radiation exposure. A coarse-grained architecture of cellular replication and production as well as a mechanism for implicit regulation used in this model are discussed. The model is based on previous investigations of rodents. The authors test how well the model matches, in the principal dynamic regime of hematopoiesis, experimental data on large animals as well as empirical data on humans following radiation exposure. Due to its ability to infer, albeit indirectly, radiation damage to bone marrow, this model will provide a useful computational tool in radiation accident management, military operations involving nuclear warfare, radiation therapy, and space radiation risk assessment.

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Section: Low Dose Rate Chronic Irradiationsupporting

confidence: 87%

Section: Low Dose Rate Chronic Irradiationmentioning

confidence: 85%

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Characterization of the Radiation-Damaged Precursor Cells in Bone Marrow Based on Modeling of the Peripheral Blood Granulocytes Response

Cucinotta²

2011

Health Physics

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“…Present risk assessment of high and low dose radiation is extrapolated from epidemiological studies of atomic bomb survivors in Hiroshima and Nagasaki; however, there is some uncertainty in the assessment of risks at lower doses (11,85). Full body low dose radiation is known to induce apoptotic and immunological responses in the organ tissues, including the bone marrow (18,86,87). Full body low dose radiation in mice has been found to enhance the function of macrophages (and CD8ϩ T cells) in several studies (18 -20).…”

Section: Tnfr2/p75 Regulate Ir-induced Nontargeted Effectsmentioning

confidence: 99%

TNF-TNFR2/p75 Signaling Inhibits Early and Increases Delayed Nontargeted Effects in Bone Marrow-derived Endothelial Progenitor Cells

Sasi¹,

Song²,

Park³

et al. 2014

Journal of Biological Chemistry

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Background: Ionizing radiation can induce DNA damage in nonirradiated (N-IR) cells via nontargeted effects (NTE). Results: TNF-␣ and IL-1␣ mediate NTE in N-IR bone marrow-derived EPCs, and neutralizing TNF-␣ diminishes NTE in WT and p55 knock-out BM-EPCs. Conclusion: TNF-TNFR2/p75 signaling alters accumulation of inflammatory cytokines that attenuate NTE in N-IR EPCs. Significance: TNFR2/p75 may represent a gene target for mitigation of delayed RBR in BM-EPCs.

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“…Hematopoiesis can maintain a sufficient level of blood cell functioning due to increased cell production associated with shortening of cell cycle and maturation period (Grygoryev et al 1986), intensification of proliferation activity of early cell forms (stem and progenitor cells) (Muksinova and Mushkacheva 1990), and development of extramedular hematopoiesis (Fliedner et al 2002b). Besides, radioadapted animals have displayed an increased repair of sublethal damage in bone marrow progenitors (Seed et al 2002b).…”

Section: Introductionmentioning

confidence: 99%

Early Hematopoietic Effects of Chronic Radiation Exposure in Humans

Akleyev

Akushevich²,

Dimov³

et al. 2010

Health Physics

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The major goal of this study was to identify and quantitatively describe the association between the characteristics of chronic (low-dose rate) exposure to (low LET) ionizing radiation and cellularity of peripheral blood cell lines. About 3,200 hemograms (i.e., spectra of blood counts) obtained over the years of maximal exposure to ionizing radiation (1950)(1951)(1952)(1953)(1954)(1955)(1956)) for inhabitants of the Techa River were used in analyses. The mean cumulative red bone marrow dose (with standard errors), calculated using Techa River Dosimetry System-2000, was 333.6 ± 4.6 mGy (SD = 259.9 mGy, max = 1151 mGy) to the year 1956. The statistical approach included both empirical methods for estimating frequencies of cytopenic states of the investigated blood cell lines (e.g. neutrophile, platelets, erythrocyte, etc.), and regression methods, including generalized linear models and logistic regressions which allowed taking into account confounding factors (e.g., attained age, age at maximal exposure, presence of concomitant diseases, and demographic characteristics). The results of the analyses demonstrated hematopoiesis inhibition manifested by a decrease in peripheral blood cellularity and an increase in the frequency of cytopenia in all blood cell lines (leukocytes, including lymphocytes, monocytes, neutrophiles, as well as platelets and erythrocytes). The intensity of hematopoiesis inhibition in the period of maximal exposures is determined by the combined influence of the dose rate and cumulative dose. The contribution of specific confounding factors was quantified and shown to be much less important than dose characteristics. The best predictor among dose characteristics was identified for each blood cell line. A 2-fold increase in dose rate is assumed to be a characteristic of radiosensitivity and a quantitative characteristic of the effect.

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Hematopoietic responses under protracted exposures to low daily dose gamma irradiation

Cited by 31 publications

References 8 publications

Characterization of the Radiation-Damaged Precursor Cells in Bone Marrow Based on Modeling of the Peripheral Blood Granulocytes Response

Characterization of the Radiation-Damaged Precursor Cells in Bone Marrow Based on Modeling of the Peripheral Blood Granulocytes Response

TNF-TNFR2/p75 Signaling Inhibits Early and Increases Delayed Nontargeted Effects in Bone Marrow-derived Endothelial Progenitor Cells

Early Hematopoietic Effects of Chronic Radiation Exposure in Humans

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