Radiation Induced Anemia in Rats Exposed Repeatedly to Mixed Gamma-Neutron Radiation

Baum, S. J.; Varon, Myron I.; Wyant, D. E.

doi:10.2307/3572838

Cited by 8 publications

(3 citation statements)

References 13 publications

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“…Delayed anemia as expression of a residual injury in bone marrow was first described in chronically irradiated guinea pigs (Lorenz, 1951), later confirmed in other rodents tBaum et al., 1970;Davis et al, 1971;Covelli and Metalli;1973), and then shown to be inducible by drugs as well (Morley and Blake, 1974). The defect was studied in experiments involving a bleeding challenge (Rugh and Wolff, 1957;Hochman et al, 1967;Gong et al, 1969) and quantified in experiments which determined animal resistance to a secondary radiation dose (Storer, 1964;Corp and Mole, 1966;Yuhas et al, 1969).…”

mentioning

confidence: 83%

Residual radiation injury exhibited in long‐term bone marrow cultures

Reincke

Hannon

Hellman

1982

Journal Cellular Physiology

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Residual radiation injury was demonstrated in long-term primary cultures of mouse bone marrow. Control cultures underwent three phases of hematopoietic activity as distinguished by initial establishment, steady high (plateau) production of granulocytes, and gradual decline. Irradiation with 50, 300, or 550 rads, given at the end of the initial phase, did not prevent any culture flasks from entering the plateau phase. However, actual production levels and the time they were maintained varied inversely with the radiation dose so that the accumulated postradiation cell production corresponded to an exponential dose-response relationship at any time after treatment. The accumulated cell productions were found to be similar in all groups when expressed by the number of stem cell doublings necessary to produce them. The findings cannot be explained by reproductive cell death and are consistent with the notion of a limited division capacity in hematopoietic stem cells.

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mentioning

confidence: 83%

Residual radiation injury exhibited in long‐term bone marrow cultures

Reincke

Hannon

Hellman

1982

Journal Cellular Physiology

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“…Permanent anemia and pancytopenia can be caused by the reduced capability for cellular proliferation due to the stem cells injury produced by radiation. [14,69,70,72,76]. Radiation induces an inflammatory response in the irradiated organs characterized by leukocyte infiltration and vascular permeability changes and vascular injury [90,99].…”

Section: Inflammation Induced By Radiationmentioning

confidence: 99%

Radiation Toxins - Effects of Radiation Toxicity, Molecular Mechanisms of Action, Radiomimetic Properties and Possible Countermeasures for Radiation Injury

Popov¹,

Jones²,

Maliev³

2012

Current Topics in Ionizing Radiation Research

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“…In addition, intracellular lesions are produced in surviving repopulating cells and can be observed even several months after irradiation [1,18]; these lesions can be quantified by a simple assay [11,12,22]. These effects may be partially compensated by increased cycling of the surviving CFU-S [10].…”

Section: Introductionmentioning

confidence: 99%

Proliferative compensation of residual radiation damage in the compartment of hematopoietic early progenitor cells of the mouse

Hübner

Wangenheim

Feinendegen

1984

Radiat Environ Biophys

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The rate of cell entry from the compartment of hematopoietic early progenitor cells into differentiation was determined in sublethally irradiated mice. By use of the criterion of repopulating ability, transplantation of 5-(125I) iodo-2'-deoxyuridine labeled bone marrow cells into fatally irradiated syngeneic recipients allows to measure the relative number of early progenitor cells lodging in the spleen and the turnover of these cells in the donors. Following 450 rad the relative number of transplantable early progenitor cells in S-phase recovers to normal within 2 weeks and stabilizes after 5 weeks. At this time, the labeled progenitors turn over with a half-time of 1.4-2.2 days; the respective times for unirradiated mice are 1.5-1.8 days. Thus, quantitative and qualitative residual radiation damage that is known to exist in the compartment of CFU-S, is disguised within 2-5 weeks after irradiation by proliferative compensation in the entirety of early hemopoietic precursor cells which are here defined by their capacity of self renewal and delivery of differentiated cells and of seeding to spleens of lethally irradiated recipients.

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Radiation Induced Anemia in Rats Exposed Repeatedly to Mixed Gamma-Neutron Radiation

Cited by 8 publications

References 13 publications

Residual radiation injury exhibited in long‐term bone marrow cultures

Residual radiation injury exhibited in long‐term bone marrow cultures

Radiation Toxins - Effects of Radiation Toxicity, Molecular Mechanisms of Action, Radiomimetic Properties and Possible Countermeasures for Radiation Injury

Proliferative compensation of residual radiation damage in the compartment of hematopoietic early progenitor cells of the mouse

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