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Journal Articles

Modelling the effect of incorporated halogenated pyrimidine on radiation-induced DNA strand breaks

Watanabe, Ritsuko; Nikjoo, H.*

International Journal of Radiation Biology, 78(11), p.953 - 966, 2002/11

 Times Cited Count:39 Percentile:89.72(Biology)

Incorporation of halogenated pyrimidines, iodo- and bromo-deoxyuridines (HP), into DNA is known to sensitize cells to radiation. The aim of this study is to estimate the enhancement of DNA strand break induced by low LET radiation in the presence of HP and examine source, complexity and clustering properties of damage that could provide correlation between DNA damage and lethality. Monte Carlo track structure methods were used to model the induction of strand breakage by X-ray photons. As a result, the increase of strand breaks due to Br/IdU incorporation could be explained by the mechanism of uracilyl radical production originated from e-aq and direct hits on bases. The significant contribution of electron migration along DNA within limited distance is shown. It is also shown that the incorporation of Br/IdU causes a spectral shift towards greater complexity of clustered DNA damage. Further, it has been supported that DSB is responsible for radiation-induced cell killing.

Journal Articles

Reparability of lethal lesions produced by phosphorus photoabsorption in yeast cells

Usami, Noriko*; Yokoya, Akinari; Ishizaka, Shozo*; Kobayashi, Katsumi*

Journal of Radiation Research, 42(3), p.317 - 331, 2001/09

 Times Cited Count:8 Percentile:28.07(Biology)

The characteristics of DNA lesions produced by the phosphorus K-shell absorption in yeast cells were studied using monochromatized soft X-rays tuned to the phosphorus K-edge peak (2153 eV) and below the peak energy (2147 eV). The repaired fractions of DNA double-strand breaks (dsb) were measured relatively by using both a mutant, (${it rad 54-3}$), which shows the temperature-sensitive dsb repair-deficient, and a wild-type strain. The repaired fraction of lesion in ${it rad 54-3}$, which corresponds to the relative yield of dsb reparable by the ${it RAD 54}$ pathway, was not affected by the phosphorus photoabsorption. Repair of the produced lesions in the wild-type cells was also measured by comparing the surviving fraction of the immediately plated cells to that of those cells plated after holding in a non-nutrient medium for 80 hrs. The recovery of the surviving fraction after the holding treatment was dependent upon the soft X-ray energy. These results suggest that irrepairable lesions are produced by the inner-shell photoabsorption of phosphorus in DNA, although its yield is small.

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