The Dampening of DNA Replication Cycles after X-Irradiation or Ultraviolet Light Irradiation

Billen, Daniel; Bruns, Laura

doi:10.1016/s0006-3495(70)86316-0

Cited by 9 publications

(1 citation statement)

References 8 publications

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“…The dose was determined with X8 thermoluminescent dosimeter chips (Landauer, Glenwood, IL). Cells were starved before irradiation to halt any initiated rounds of replication (30); this procedure enhances the reproducibility of the x-ray survival curves. When cells were incubated postirradiation, they were incubated in the same buffer without nutrients to continue to suppress initiation of new rounds of DNA replication.…”

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confidence: 99%

Abortive base-excision repair of radiation-induced clustered DNA lesions in Escherichia coli

Blaisdell

Wallace

2001

Proc. Natl. Acad. Sci. U.S.A.

204

112

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It has been postulated that ionizing radiation produces a unique form of cellular DNA damage called ''clustered damages'' or ''multiply damaged sites''. Here, we show that clustered DNA damages are indeed formed in Escherichia coli by ionizing radiation and are converted to lethal double-strand breaks during attempted baseexcision repair. In wild-type cells possessing the oxidative DNA glycosylases that cleave DNA at repairable single damages, doublestrand breaks are formed at radiation-induced clusters during postirradiation incubation and also in a dose-dependent fashion. E. coli mutants lacking these enzymes do not form double-strand breaks postirradiation and are substantially more radioresistant than wild-type cells. Furthermore, overproduction of one of the oxidative DNA glycosylases in mutant cells confers a radiosensitive phenotype and an increase in the number of double-strand breaks. Thus, the effect of the oxidative DNA glycosylases in potentiating DNA damage must be considered when estimating radiation risk.A pproximately 70% of radiation-induced DNA damages are formed by reactive-free radicals produced by the radiolysis of water in the vicinity of DNA (1). These radiation-induced DNA damages are repaired by base-excision repair (2) and overlap substantially with those formed during normal oxidative metabolism (3), which are produced at significant rates in unirradiated cells (4). This overlap of damages has led to a controversy with respect to determining radiation risk. Proponents of a ''threshold effect'' claim that because endogenous oxidative damages are effectively repaired and adaptive responses have been demonstrated for certain radiation endpoints, then a threshold must exist for the carcinogenic and lethal consequences of ionizing radiation (5, 6). This issue is an important one because much of the projected radiation exposures associated with human activity over the next hundred years will come from low doses associated with medical tests, waste cleanup, and materials associated with nuclear weapons and nuclear power. Whether a threshold exists for the consequences of radiation damage will significantly influence risk estimates for low-dose exposures. Currently, risk estimates for individuals or groups exposed to low radiation doses are determined from epidemiological data obtained from populations exposed to high doses, and a ''linear-no-threshold'' estimation is used for assessment. Proponents of the linear-no-threshold model hold that the biologically important radiation damages in DNA, such as double-strand breaks, are substantially different from single, repairable oxidative lesions. It also has been predicted that ionizing radiation produces a unique form of DNA damage called ''clustered damages '' (1, 7, 8). If, indeed, clustered damages can be demonstrated in living cells and if, unlike the single lesions from which they are formed, they are poorly repaired, these facts would provide additional support for the linear-nothreshold model.Modeling of radiation track structures (9, 10) ...

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confidence: 99%

Abortive base-excision repair of radiation-induced clustered DNA lesions in Escherichia coli

Blaisdell

Wallace

2001

Proc. Natl. Acad. Sci. U.S.A.

204

112

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Physiological Responses of Escherichia coli to Far-Ultraviolet Radiation

Swenson

1976

Photochemical and Photobiological Reviews

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DNA synthesis inEscherichia coli B/r after UV-irradiation

Kučerová

Věchet

1982

Folia Microbiol

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When studying the kinetics of DNA synthesis, growth and cell division in Escherichia coli B/r after irradiation with different doses of UV-radiation (254 nm) we could demonstrate, by means of pulse incorporation of 3H-thymidine, a lag in DNA synthesis after the irradiation. The relative rate of the restored DNA synthesis (related to the number of viable cells) was higher than in the non-irradiated culture. After 3 h the rate of DNA synthesis settled at a constant value, which was identical with the control rate up to the "critical dose" of 20 J/m2. The irradiated cell population is heterogenous and contains basically two categories of cells--surviving and non-surviving. Cells of both types contribute to DNA synthesis restored after the lag period to a different extent. During the first hour after the irradiation even the nonviable portion of the population, i.e. cells that do not form colonies but are still penicillin-sensitive, is involved in the DNA synthesis.

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The Dampening of DNA Replication Cycles after X-Irradiation or Ultraviolet Light Irradiation

Cited by 9 publications

References 8 publications

Abortive base-excision repair of radiation-induced clustered DNA lesions in Escherichia coli

Abortive base-excision repair of radiation-induced clustered DNA lesions in Escherichia coli

Physiological Responses of Escherichia coli to Far-Ultraviolet Radiation

DNA synthesis inEscherichia coli B/r after UV-irradiation

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