Residual activation events functional after irradiation of mouse splenic lymphocytes

Journal Article · Tue Jan 01 04:00:00 EST 1991 · Radiation Research; (USA)

DOI:https://doi.org/10.2307/3577975· OSTI ID:6144899

Duncan, D D; Lawrence, D A ^[1]

---

1. Albany Medical College, New York, NY (USA)

We have sought to identify the radiosensitivity of lymphocytes by determining the extent of activation of mitogen-stimulated lymphocytes previously exposed to growth-inhibiting doses of radiation. Mouse splenic lymphocytes were exposed to 0-15 Gy 137Cs radiation, and structural and functional damage were assayed. Although damage to cellular thiols and nonprotein thiols was modest, there was a significant loss of viability by 6 h as determined by uptake of propidium iodide (PI). Since cells did not die immediately after irradiation, the activation events which remained were evaluated. Growth-inhibiting doses of radiation left cells partially responsive to mitogen, in that cells were able to exit G0 phase, but they could progress no further into the cell cycle than G1a phase. It is important to note that assessment of viability by uptake of PI indicated substantial cell death after 15 Gy (45%, 6 h; 90%, 24 h); however, cell cycle analysis at 24 h indicated no significant decrease in progression from G0 to G1a phase. The LPS-stimulated response of B cells was more radiosensitive than the Con A-stimulated response of T cells. Further analysis of the Con A response indicated that production of interleukin-2 (IL-2) was unaffected, but expression of the IL-2 receptor was inhibited. Inhibition of poly-ADP-ribosylation and damage to lipids did not prevent the lack of mitogen responsiveness, since neither the ADP-ribose transferase inhibitor 3-aminobenzamide nor lipid radical scavengers had restorative effects on the mitogenic response. Nor was Con A-stimulated incorporation of (3H)thymidine restored with inhibitors of prostaglandin or leukotriene synthesis, suggesting that inhibition was due to direct effects on the Con A responders, and not indirect effects mediated by arachidonate metabolites.

• OSTI ID: 6144899
• Journal Information: Radiation Research; (USA), Journal Name: Radiation Research; (USA) Vol. 125:1; ISSN 0033-7587; ISSN RAREA
• Country of Publication: United States
• Language: English

Related Subjects

550201 -- Biochemistry-- Tracer Techniques
560120* -- Radiation Effects on Biochemicals
Cells
& Tissue Culture
59 BASIC BIOLOGICAL SCIENCES
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
AGGLUTININS
ALKALI METAL ISOTOPES
ANIMAL CELLS
ANIMALS
ANTIBODIES
AZINES
BETA DECAY RADIOISOTOPES
BETA-MINUS DECAY RADIOISOTOPES
BIOLOGICAL EFFECTS
BIOLOGICAL MATERIALS
BIOLOGICAL RADIATION EFFECTS
BLOOD
BLOOD CELLS
BODY FLUIDS
CELL CYCLE
CESIUM 137
CESIUM ISOTOPES
CONCANAVALIN A
CONNECTIVE TISSUE CELLS
ENZYME INHIBITORS
GROWTH FACTORS
HEMAGGLUTININS
HETEROCYCLIC COMPOUNDS
HYDROGEN COMPOUNDS
ISOTOPE APPLICATIONS
ISOTOPES
LECTINS
LEUKOCYTES
LYMPHOCYTES
LYMPHOKINES
MAMMALS
MATERIALS
MICE
MITOGENS
NUCLEI
NUCLEOSIDES
NUCLEOTIDES
ODD-EVEN NUCLEI
ORGANIC COMPOUNDS
ORGANIC NITROGEN COMPOUNDS
PROTEINS
PYRIMIDINES
RADIATION EFFECTS
RADIOISOTOPES
RADIOSENSITIVITY
RIBOSIDES
RODENTS
SOMATIC CELLS
SPLEEN CELLS
THYMIDINE
TRACER TECHNIQUES
TRITIUM COMPOUNDS
VERTEBRATES
VIABILITY
YEARS LIVING RADIOISOTOPES