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S Pazzaglia

Publications and source records attributed to S Pazzaglia.

21 records · Page 2Linked to original sources
PubMed1991

Absence of a dose-fractionation effect on neoplastic transformation induced by fission-spectrum neutrons in C3H 10T1/2 cells.

We have investigated the effect of fission-spectrum neutron dose fractionation on neoplastic transformation of exponentially growing C3H 10T1/2 cells. Total doses of 10.8, 27, 54, and 108 cGy were given in single doses or in five equal fractions delivered at 24-h intervals in the biological channel of the RSV-TAPIRO reactor at CRE-Casaccia. Both cell inactivation and neoplastic transformation were more effectively induced by fission neutrons than by 250-kVp X rays. No significant effect on cell survival or neoplastic transformation was observed with split doses compared to single doses of fission-spectrum neutrons. Neutron RBE values relative to X rays determined from data for survival and neoplastic transformation were comparable.

Animals↗
PubMed1989

Radiation damage and chromatin structure.

The recent advances made in the knowledge of chromatin structure have important implications in molecular and cellular radiobiology. There are now many lines of evidence that the chromatin organization can affect the production, the distribution and the repair of radiation-induced damage in DNA. Experiments with polynucleosomes show that DNA double strand breaks (dsb) are not randomly distributed along the DNA molecule. Rather, they are preferentially localized in linker regions, while core regions are more resistant. Isolated DNA is about 4-fold more susceptible to dsb than DNA irradiated as a part of polynucleosomes. This differential radiosensitivity is apparently due to the close association of DNA with proteins. The analysis of DNA single strand breaks production and repair in a human erythroleukemic cell line that can be induced to differentiate in vitro, showed that the repair kinetics in differentiated cells appears significantly slower than in undifferentiated ones. This can be interpreted as a decrease in the genome accessibility to repair enzymes due to the presence of more structured regions in chromatin after differentiation. It appears that a high degree of genome compactness could imply, on one hand, a high DNA radioresistance and, on the other hand, a slow DNA repair so that the identification of chromatin domains which are critical, from the structural point of view, in determining cellular effects such as cell killing and mutation, should take into account a sort of balance between the amount of damage and the extent of repair.

Animals↗