Simultaneously demonstration of UV-type and ionizing radiatio-type DNA repair by the nucleotide sedimentation technique

Aldenhoff, P; Sperling, Karl

doi:10.1016/0167-8817(84)90053-1

Cited by 10 publications

(2 citation statements)

References 12 publications

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“…The nucleoid sedimentation assay developed by Cook and Braze11 (1976a) has been used as a sensitive assay for the study of DNA damage and its repair from exposure to irradiation (Cook and Brazell, 1976b;Yew and Johnson, 1979;Charles and Cleaver, 1982;Aldenhoff and Sperling, 1984), metals (Robison et al. 1984), and alkylating agents (Mattern et al, 1982;Romagna ef al., 1985).…”

Section: Discussionmentioning

confidence: 99%

Assessment of the role of DNA damage and repair in the survival of primary cultures of rat cutaneous keratinocytes exposed to bis(2-chloroethyl)sulfide

Ribeiro

Mitra

Bernstein

1991

Toxicology and Applied Pharmacology

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Toxicity manifests itself as vesication in human skin exposed topically to bis(2-chloroethyl)sulfide (BCES). The destruction of the proliferating population of epidermal cells is a major component of the pathogenic process. Available data strongly suggest that damage to cellular DNA is a critical factor in the loss of these cells. However, the influence of DNA repair on this toxic response has not been adequately studied. Therefore, a study was undertaken to ascertain the influence of DNA repair on the survival of primary monolayer cultures of rat cutaneous keratinocytes exposed to BCES. The sensitive nucleoid sedimentation assay was employed for the determination of DNA damage in cultures exposed to very low levels of BCES. Initial experiments demonstrated that within 1 hr of exposure to as little as 0.1 microM BCES the structural integrity of cellular DNA was compromised, presumably resulting from the appearance of single-strand breaks in the nucleic acid. This same effect was demonstrated in basal cells derived from a stratified, cornified culture grown at the air-liquid interface and exposed topically to the vesicant. Further studies with the monolayer culture demonstrated that the gross structural integrity of the DNA in cells exposed to as much as 5 microM BCES was completely restored within the first 22 hr following the exposure. However, this repair process appeared to be inefficient since a depression of thymidine incorporation into DNA and a significant loss of DNA were exhibited in exposed cultures as long as 72 hr after the initial exposure.

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Section: Discussionmentioning

confidence: 99%

Assessment of the role of DNA damage and repair in the survival of primary cultures of rat cutaneous keratinocytes exposed to bis(2-chloroethyl)sulfide

Ribeiro

Mitra

Bernstein

1991

Toxicology and Applied Pharmacology

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“…It has been observed that DNA strand breaks rapidly accumulate in cells incubated with HU and ara C in which a repair process is taking place that involves the incorporation of a relatively large number of nucleotides into the repaired region. However, few, if any, strand breaks are formed in cells performing repair in which only a small number of nucleotides are inserted into the site of repair (Aldenhoff and Sperling, 1984). The basis of this distinction may stem from the involvement of DNA polymerase a, which is inhibited by ara C, in long-patch repair.…”

Section: Introductionmentioning

confidence: 99%

Use of Metabolic Inhibitors to Investigate the Excision Repair of Pyrimidine Dimers and Non‐dimer Dna Damages Induced in Human and Icr 2a Frog Cells by Solar Ultraviolet Radiation

Chao

Rosenstein

1986

Photochem & Photobiology

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Abstract— ICR 2A frog and normal human skin fibroblasts were exposed to either 5 J/m2 of 254 nm UV or 50 kJ/m2 of the Mylar‐filtered solar UV wavelengths produced by a fluorescent sunlamp. Following these approximately equitoxic treatments, cells were incubated in medium containing the DNA synthesis inhibitors hydroxyurea (HU) and 1–β‐D‐arabinofuranosyl cytosine (ara C) for 0–20 min (human fibroblasts) or 0–4 h (frog cells) to accumulate DNA breaks resulting from enzymatic incision during excision repair. It was found that breaks were formed in human cells at about a 200‐f‐old higher rate compared with the ICR 2A cells indicating a relatively low capacity for excision repair in the frog cells. In addition, the rate of DNA break formation in solar UV‐irradiated cells was only one‐third of the level detected in 254 nm‐irradiated cells. This result is consistent with the conclusion that the pathway(s) involved in the repair of solar UV‐induced DNA damages differs from the repair of lesions produced in cells exposed to 254 nm UV.

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The use of metabolic inhibitors to compare the excision repair of pyrimidine dimers and nondimer dna damages in human skin fibroblasts exposed to 254‐NM and sunlamp‐produced >310‐NM ultraviolet radiation

1986

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Normal human skin fibroblasts were exposed to either 0-5 J/m2 of 254-nm ultraviolet (UV) radiation or 0-50 kJ/m2 of the Mylar-filtered UV (greater than 310 nm) produced by a fluorescent sunlamp. These cells were then incubated for 0-20 min in medium containing 10 mM hydroxyurea (HU) and 0.1 mM 1-beta-D-arabinofuranosyl cytosine (ara C), and the yield of DNA strand breaks was measured by means of the alkaline elution technique. For cells irradiated with 254-nm UV, which results primarily in the formation of cyclobutane pyrimidine dimers, a rapid increase in DNA strand breaks was detected following incubation with these metabolic inhibitors. In contrast, only a low level of strand breaks formed in cells incubated with HU and ara C after irradiation with approximately equitoxic fluences of sunlamp UV greater than 310 nm, which mainly causes the induction of nondimer DNA lesions. Hence, these results are consistent with the conclusion that the pathways involved in the repair of nondimer DNA damages induced by UV wavelengths greater than 310 nm differ from the repair of pyrimidine dimers.

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Simultaneously demonstration of UV-type and ionizing radiatio-type DNA repair by the nucleotide sedimentation technique

Cited by 10 publications

References 12 publications

Assessment of the role of DNA damage and repair in the survival of primary cultures of rat cutaneous keratinocytes exposed to bis(2-chloroethyl)sulfide

Assessment of the role of DNA damage and repair in the survival of primary cultures of rat cutaneous keratinocytes exposed to bis(2-chloroethyl)sulfide

Use of Metabolic Inhibitors to Investigate the Excision Repair of Pyrimidine Dimers and Non‐dimer Dna Damages Induced in Human and Icr 2a Frog Cells by Solar Ultraviolet Radiation

The use of metabolic inhibitors to compare the excision repair of pyrimidine dimers and nondimer dna damages in human skin fibroblasts exposed to 254‐NM and sunlamp‐produced >310‐NM ultraviolet radiation

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