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Strand Breaks in Plasmid DNA after Positional Changes of Auger Electron-Emitting Iodine-125: Direct Compared to Indirect Effects

Amin I. Kassis, Ravi S. Harapanhalli and S. James Adelstein
Radiation Research
Vol. 152, No. 5 (Nov., 1999), pp. 530-538
DOI: 10.2307/3580150
Stable URL: http://www.jstor.org/stable/3580150
Page Count: 9
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Strand Breaks in Plasmid DNA after Positional Changes of Auger Electron-Emitting Iodine-125: Direct Compared to Indirect Effects
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Abstract

To elucidate the nature and kinetics of DNA strand breaks caused by low-energy Auger electron emitters, we compared the yields of DNA breaks in supercoiled pUC19 DNA in the presence of the ${}^{\bullet}{\rm OH}$ scavenger dimethyl sulfoxide (DMSO) after the decay of 125 I (1) in proximity to DNA after minorgroove binding (${}^{125}{\rm I}\text{-iodoHoechst}$ 33342, ${}^{125}{\rm IH}$) and (2) at a distance from DNA (${}^{125}{\rm I}\text{-iodoantipyrine}$, ${}^{125}{\rm IAP}$). DMSO is efficient at protecting supercoiled plasmid DNA from the decay of 125 I free in solution (dose modification factor, DMF = 59 ± 4) and less effective when the 125 I decays occur close to DNA (DMF = 3.8 ± 0.3). This difference is due mainly to the inability of DMSO to protect DNA from the double-strand breaks produced by groove-bound 125 I (DMF = 1.0 ± 0.2). Additionally, the fragmentation of plasmid DNA beyond the production of single-strand and double-strand breaks that is seen after the decay of ${}^{125}{\rm IH}$ and not ${}^{125}{\rm IAP}$ (Kassis et al., Radiat. Res. 151, 167-176, 1999) cannot be modified by DMSO. These results demonstrate that the mechanisms underlying double-strand breaks caused by the decay of ${}^{125}{\rm IH}$ differ in nature from those caused by the decay of ${}^{125}{\rm IAP}$.

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