Effects of LET, Fluence and Particle Energy on Inactivation, Chromosomal Aberrations and DNA Strand Breaks

Kraft, Gerhard

doi:10.1007/978-1-4613-1567-4_11

Cited by 7 publications

(1 citation statement)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1989 . This is consistent with the classic RBE-LET relationship (Hall 1978, Kraft 1988, ICRP 1963 . In this study, when viewed 64 weeks post-exposure the MN frequency remained dependent on radiation dose (Figure 3 a) .…”

Section: 2 Nuclear Fragmentation(fn)supporting

confidence: 87%

Accelerated Heavy Ions and the Lens. IX. Late Effects of LET and Dose on Cellular Parameters in the Murine Lens

Tao

Medvedovsky

David

et al. 1993

International Journal of Radiation Biology

View full text Add to dashboard Cite

Lenses of mice irradiated with 250 MeV protons, 670 MeV/amu 20Ne, 600 MeV/amu 56Fe, 350 MeV/amu 56Fe, 600 MeV/amu 93Nb or 593 MeV/amu 139La ions were evaluated by analysing cytopathological indicators which have been implicated in the cataractogenic process. The LETs ranged from 0.39 to 953 keV/microns and the fluences from 1.31 x 10(3)/mm2 to 5.12 x 10(7)/mm2. The lenses were assessed 64 weeks post-irradiation in order to observe the late effects of LET and dose on the target cell population of the lens' epithelium. Our studies showed that growth-dependent pathological changes occurred at the cellular level as a function of dose and LET. For a given particle dose, as the LET rose, the number of abnormal mitotic figures, micronuclei frequency, and the disorganization of meridional rows increased to a maximum and then reached a plateau or decreased. For particles of the same LET, the severity of meridional rows disorganization and micronuclei frequency increased with increasing dose. The numbers of cells surviving at late times post-irradiation were comparable with those of controls. In addition, the cellular density was similarly unaffected. These observations are consistent with the current theory of the mechanism of radiation cataractogenesis which posits that genomic damage to the epithelial cells surviving the exposure is responsible for opacification.

show abstract

Section: 2 Nuclear Fragmentation(fn)supporting

confidence: 87%