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Title: Repair of radiation damage in mammalian cells

Conference ·
OSTI ID:5993638

The responses, such as survival, mutation, and carcinogenesis, of mammalian cells and tissues to radiation are dependent not only on the magnitude of the damage to macromolecular structures - DNA, RNA, protein, and membranes - but on the rates of macromolecular syntheses of cells relative to the half-lives of the damages. Cells possess a number of mechanisms for repairing damage to DNA. If the repair systems are rapid and error free, cells can tolerate much larger doses than if repair is slow or error prone. It is important to understand the effects of radiation and the repair of radiation damage because there exist reasonable amounts of epidemiological data that permits the construction of dose-response curves for humans. The shapes of such curves or the magnitude of the response will depend on repair. Radiation damage is emphasized because: (a) radiation dosimetry, with all its uncertainties for populations, is excellent compared to chemical dosimetry; (b) a number of cancer-prone diseases are known in which there are defects in DNA repair and radiation results in more chromosomal damage in cells from such individuals than in cells from normal individuals; (c) in some cases, specific radiation products in DNA have been correlated with biological effects, and (d) many chemical effects seem to mimic radiation effects. A further reason for emphasizing damage to DNA is the wealth of experimental evidence indicating that damages to DNA can be initiating events in carcinogenesis.

Research Organization:
Brookhaven National Lab., Upton, NY (USA)
DOE Contract Number:
AC02-76CH00016
OSTI ID:
5993638
Report Number(s):
BNL-30056; BIO-3766; CONF-810873-2; ON: DE81030824; TRN: 81-017435
Resource Relation:
Conference: NATO CNEN conference, Rome, Italy, 24 Aug 1981
Country of Publication:
United States
Language:
English