Possible damage of repair systems by Pi-mesons of different LET spectra.
Pi-meson experiments with repair-deficient spermatides and oocytes of Drosophila melanogaster have permitted a study of the LET dependence of the repair of different types of chromosomal lesions. The data show a distinction between primary events connected with fusion modalities (repair or misrepair) and those associated with no fusion. Repair deficiency increases the induction of chromosomal loss and dominant lethality (early damage) and decreases the induction of translocations (misrepair), perhaps responsible for late effects. The induction of nonfusion events is higher for pions compared to X rays and increases with mean lineal energy spectra, whereas the production of translocations is maximal at intermediate ionization density. The direct damage of repair systems by high-LET pions is postulated to explain these observations.
D000818:Animals; D002470:Cell Survival / Q000528:radiation effects; D002869:Chromosome Aberrations / Q000528:radiation effects*; D004260:DNA Repair / Q000528:radiation effects*; D004307:Dose-Response Relationship, Radiation; D004331:Drosophila melanogaster / Q000528:radiation effects; D004601:Elementary Particles; D004735:Energy Transfer; D005260:Female; D008297:Male; D008651:Mesons; D009865:Oocytes / Q000528:radiation effects / Q000648:ultrastructure; D011829:Radiation Dosage; D012062:Relative Biological Effectiveness; D013087:Spermatids / Q000528:radiation effects / Q000648:ultrastructure; D014960:X Chromosome / Q000528:radiation effects