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PubMed2002

Molecular targets in cellular response to ionizing radiation and implications in space radiation protection.

DNA repair systems and cell cycle checkpoints closely co-operate in the attempt of maintaining the genomic integrity of cells damaged by ionizing radiation. DNA double-strand breaks (DSB) are considered as the most biologically important radiation-induced damage. Their spatial distribution and association with other types of damage depend on radiation quality. It is believed these features affect damage reparability, thus explaining the higher efficiency for cellular effects of densely ionizing radiation with respect to gamma-rays. DSB repair systems identified in mammalian cells are homologous recombination (HR), single-strand annealing (SSA) and non-homologous end-joining (NHEJ). Some enzymes may participate in more than one of these repair systems. DNA damage also triggers biochemical signals activating checkpoints responsible for delay in cell cycle progression that allows more time for repair. Those at G1/S and S phases prevent replication of damaged DNA and those at G2/M phase prevent segregation of changed chromosomes. Individuals with lack or alterations of genes involved in DNA DSB repair and cell cycle checkpoints exhibit syndromes characterized by genome instability and predisposition to cancer. Information reviewed in this paper on the basic mechanisms of cellular response to ionizing radiation indicates their importance for a number of issues relevant to protection of astronauts from space radiation.

Animals↗
PubMed1997

Radiation protection of radiosensitive populations.

Radiosensitive populations (defined as subpopulations with increased radiogenic risk for cancer) may include individuals with known genetic predispositions for cancer (e.g., breast cancer), and persons with certain diseases, such as ataxia telangiectasia, which are characterized by enhanced radiation sensitivity and increased risk for cancer. Although approximately 10% of the population may be radiosensitive, current radiological protection limits, based on the "average" individual, should be retained. Radiation is a weak environmental carcinogen. Diet and cigarette smoking each account for 15-18 times more cancer deaths. Radiosensitivity is a much less important host factor than age and genetic predisposition. Workers should be allowed to "declare" a predisposition for cancer. Workers who have declared radiosensitivities should be provided with additional information regarding job-related risks and strategies to reduce dose. "Declared" employees should not be subjected to different terms and conditions of employment.

Ataxia Telangiectasia↗