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The aim was to evaluate the effect of modelled microgravity on radiation-induced chromosome aberrations (CAs). G(0) peripheral blood lymphocytes were exposed to 60 MeV protons or 250 kV(p) X-rays in the dose range 0 - 6 Gy, and allowed to repair DNA damage for 24 h under either normal gravity or microgravity modelled by the NASA-designed rotating-wall bioreactor. Cells were then stimulated to proliferate by phytohaemagglutinin (PHA) under normal gravity conditions and prematurely condensed chromosomes were harvested after 48 h. CAs were scored in chromosomes 1 and 2 by fluorescence in-situ hybridization. Proliferation gravisensitivity was examined by cell growth curves and by morphological evaluation of mitogen-induced activation. Cell replication rounds were monitored by bromodeoxyuridine labelling. Modelled microgravity markedly reduced PHA-mediated lymphocyte blastogenesis and cell growth. However, no significant differences between normal gravity and modelled microgravity were found in the dose - response curves for the induction of aberrant cells or total interchromosomal exchange frequency. Rotating-wall bioreactor-based microgravity reproduced space-related alterations of mitogen stimulation in human lymphocytes but did not affect the yield of CAs induced by low-linear energy transfer radiation.

Purpose: The relationship between different forms of persistent radiation damage in irradiated cells was investigated in order to identify a common underlying mechanism. Material and methods: V-79 Chinese hamster cells were irradiated with different doses of X-rays, neutrons and alpha -particles. In the progeny of surviving cells, up to 4 weeks after irradiation, delayed reproductive death, delayed micronuclei, delayed appearance of dicentric chromosomes and delayed apoptosis were investigated in parallel. Results: A similar dose-response relationship was found for all endpoints, with a steep rise at low doses to a plateau at doses 3Gy. The target for inducing genomic instability by alpha -particles is larger than the nucleus. All chromosomes are equally involved in delayed breakage reunion events. Conclusion: The results indicate that non-lethal radiation damage to an extranuclear target leads to a persistent increase in clastogenic activity in the surviving irradiated cells.