Direct radiation damage to crystalline DNA : what is the source of unaltered base release?

Y. Razskazovskiy, M.G. Debije, W.A. Bernhard

Research output: Contribution to journalArticleAcademicpeer-review

38 Citations (Scopus)

Abstract

The radiation chemical yields of unaltered base release have been measured in three crystalline double-stranded DNA oligomers after X irradiation at 4 K. The yields of released bases are between 10 and 20% of the total free radical yields measured at 4 K. Using these numbers, we estimate that the yield of DNA strand breaks due to the direct effect is about 0.1 µmol J–1. The damage responsible for base release is independent of the base type (C, G, A or T) and is not scavenged by anthracycline drugs intercalated in the DNA. For these reasons, reactions initiated by the hydroxyl radical have been ruled out as the source of base release. Since the intercalated anthracycline scavenges electrons and holes completely but does not inhibit base release, the possibility for damage transfer from the bases to the sugars can also be ruled out. The results are consistent with a model in which primary radical cations formed directly on the sugar-phosphate backbone react by two competing pathways: deprotonation, which localizes the damage on the sugar, and hole tunneling, which transfers the damage to the base stack. Quantitative estimates indicate that these two processes are approximately equally efficient.
LanguageEnglish
Pages436-441
Number of pages6
JournalRadiation Research
Volume153
Issue number4
DOIs
StatePublished - 2000

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Anthracyclines
radiation damage
deoxyribonucleic acid
sugars
Radiation
Sugar Phosphates
damage
DNA Breaks
DNA
Hydroxyl Radical
Free Radicals
Cations
Electrons
hydroxyl radicals
estimates
oligomers
Pharmaceutical Preparations
strands
free radicals
phosphates

Cite this

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title = "Direct radiation damage to crystalline DNA : what is the source of unaltered base release?",
abstract = "The radiation chemical yields of unaltered base release have been measured in three crystalline double-stranded DNA oligomers after X irradiation at 4 K. The yields of released bases are between 10 and 20{\%} of the total free radical yields measured at 4 K. Using these numbers, we estimate that the yield of DNA strand breaks due to the direct effect is about 0.1 µmol J–1. The damage responsible for base release is independent of the base type (C, G, A or T) and is not scavenged by anthracycline drugs intercalated in the DNA. For these reasons, reactions initiated by the hydroxyl radical have been ruled out as the source of base release. Since the intercalated anthracycline scavenges electrons and holes completely but does not inhibit base release, the possibility for damage transfer from the bases to the sugars can also be ruled out. The results are consistent with a model in which primary radical cations formed directly on the sugar-phosphate backbone react by two competing pathways: deprotonation, which localizes the damage on the sugar, and hole tunneling, which transfers the damage to the base stack. Quantitative estimates indicate that these two processes are approximately equally efficient.",
author = "Y. Razskazovskiy and M.G. Debije and W.A. Bernhard",
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journal = "Radiation Research",
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Direct radiation damage to crystalline DNA : what is the source of unaltered base release? / Razskazovskiy, Y.; Debije, M.G.; Bernhard, W.A.

In: Radiation Research, Vol. 153, No. 4, 2000, p. 436-441.

Research output: Contribution to journalArticleAcademicpeer-review

TY - JOUR

T1 - Direct radiation damage to crystalline DNA : what is the source of unaltered base release?

AU - Razskazovskiy,Y.

AU - Debije,M.G.

AU - Bernhard,W.A.

PY - 2000

Y1 - 2000

N2 - The radiation chemical yields of unaltered base release have been measured in three crystalline double-stranded DNA oligomers after X irradiation at 4 K. The yields of released bases are between 10 and 20% of the total free radical yields measured at 4 K. Using these numbers, we estimate that the yield of DNA strand breaks due to the direct effect is about 0.1 µmol J–1. The damage responsible for base release is independent of the base type (C, G, A or T) and is not scavenged by anthracycline drugs intercalated in the DNA. For these reasons, reactions initiated by the hydroxyl radical have been ruled out as the source of base release. Since the intercalated anthracycline scavenges electrons and holes completely but does not inhibit base release, the possibility for damage transfer from the bases to the sugars can also be ruled out. The results are consistent with a model in which primary radical cations formed directly on the sugar-phosphate backbone react by two competing pathways: deprotonation, which localizes the damage on the sugar, and hole tunneling, which transfers the damage to the base stack. Quantitative estimates indicate that these two processes are approximately equally efficient.

AB - The radiation chemical yields of unaltered base release have been measured in three crystalline double-stranded DNA oligomers after X irradiation at 4 K. The yields of released bases are between 10 and 20% of the total free radical yields measured at 4 K. Using these numbers, we estimate that the yield of DNA strand breaks due to the direct effect is about 0.1 µmol J–1. The damage responsible for base release is independent of the base type (C, G, A or T) and is not scavenged by anthracycline drugs intercalated in the DNA. For these reasons, reactions initiated by the hydroxyl radical have been ruled out as the source of base release. Since the intercalated anthracycline scavenges electrons and holes completely but does not inhibit base release, the possibility for damage transfer from the bases to the sugars can also be ruled out. The results are consistent with a model in which primary radical cations formed directly on the sugar-phosphate backbone react by two competing pathways: deprotonation, which localizes the damage on the sugar, and hole tunneling, which transfers the damage to the base stack. Quantitative estimates indicate that these two processes are approximately equally efficient.

U2 - 10.1667/0033-7587(2000)153[0436:DRDTCD]2.0.CO;2

DO - 10.1667/0033-7587(2000)153[0436:DRDTCD]2.0.CO;2

M3 - Article

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EP - 441

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JF - Radiation Research

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