Enhanced Neoplastic Transformation in an Inhomogeneous Radiation Field: An Effect of the Presence of Heavily Damaged Cells

In the inhomogeneous radiation field surrounding small β-particle sources, nonlethally and heavily damaged cells are in proximity, permitting interaction via extracellular signals. This situation is typical of hot particles such as those released during the accident at Chernobyl. Beta-particle-emitt...

Full description

Saved in:
Bibliographic Details
Published in:Radiation research 1997-12, Vol.148 (6), p.543-547
Main Authors: Sigg, Martina, Nigel E. A. Crompton, Burkart, Werner
Format: Article
Language:English
Subjects:
Animals
Beta Particles
Biological and medical sciences
Carcinogenesis, carcinogens and anticarcinogens
Cell culture techniques
Cell Transformation, Neoplastic - radiation effects
Cells, Cultured
DNA Damage
Epidermal cells
Epithelial cells
Female
Irradiation
Medical sciences
Mice
Mice, Inbred C3H
Physical agents
Radiation damage
Radiation dosage
Radiotherapy
Solar X rays
Tumors
Yttrium
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:In the inhomogeneous radiation field surrounding small β-particle sources, nonlethally and heavily damaged cells are in proximity, permitting interaction via extracellular signals. This situation is typical of hot particles such as those released during the accident at Chernobyl. Beta-particle-emitting yttrium-90 wires (average energy 934 keV) were employed to investigate radiation-induced neoplastic transformation under these conditions. Integrated 24-h doses ranging from 0 to 750 Gy across the exposure field were applied. At equal levels of toxicity a 10-fold enhancement of neoplastic transformation frequency in C3H 10T1/2 cells was observed in the presence of heavily damaged cells. Homogeneous fields of low-dose-rate β-particle radiation produced neoplastic transformation frequencies typical for comparable photon exposures reported in the literature.
ISSN:0033-7587
1938-5404
DOI:10.2307/3579729