DNA repair in human bronchial epithelial cells

Our plain-English summary of DNA repair in human bronchial epithelial cells, by A.J. Fornace, J.F. Lechner, R.C. Grafstrom, et al (Carcinogenesis, 1982).

The study

• Authors: A.J. Fornace, J.F. Lechner, R.C. Grafstrom, C.C. Harris
• Journal: Carcinogenesis
• Published: 1982;3(12):1373-7
• Cited by: 47 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The purpose of this investigation was to compare the response of human cell types (bronchial epithelial cells and fibroblasts and skin fibroblasts) to various DNA damaging agents. Repair of DNA single strand breaks (SSB) induced by 5 krads of X-ray was similar for all cell types; approximately 90% of the DNA SSB were rejoined within one hour. During excision repair of DNA damage from u.v.-radiation, the frequencies of DNA SSB as estimated by the alkaline elution technique, were similar in all cell types. Repair replication as measured by BND cellulose chromatography was also similar in epithelial and fibroblastic cells after u.v.-irradiation. Similar levels of SSB were also observed in epithelial and fibroblastic cells after exposure to chemical carcinogens: 7,12-dimethylbenz[a]anthracene; benzo[a]pyrene diol epoxide (BPDE); or N-methyl-N-nitro-N-nitrosoguanidine. Significant repair replication of BPDE-induced DNA damage was detected in both bronchial epithelial and fibroblastic cells, although the level in fibroblasts was approximately 40% of that in epithelial cells. The pulmonary carcinogen asbestos did not damage DNA. DNA-protein crosslinks induced by formaldehyde were rapidly removed in bronchial cells. Further, epithelial and fibroblastic cells, which were incubated with formaldehyde and the polymerase inhibitor combination of cytosine arabinoside and hydroxyurea, accumulated DNA SSB at approximately equal frequencies. These results should provide a useful background for further investigations of the response of human bronchial cells to various DNA damaging agents.

In plain English

This was a laboratory study of human cells grown in dishes, not of people. The authors compared how normal bronchial (airway) epithelial cells, bronchial fibroblasts and skin fibroblasts responded to X-rays, ultraviolet light and several chemical carcinogens, and also tested asbestos and formaldehyde on the bronchial cells. The bronchial cells came from tissue taken from donors at autopsy. After X-rays, about 90% of DNA single strand breaks were rejoined within the first hour. Repair after ultraviolet light was similar across the cell types. After the chemical benzo[a]pyrene diol epoxide, repair replication in bronchial fibroblasts was 39% of that in epithelial cells. The asbestos tested was amosite and crocidolite (spelled "crocodolite" in the article's table), applied at 100 micrograms per 4 ml for 14.5 hours. It produced no appreciable DNA single strand breaks, and no sign of excision repair was detected. DNA-protein crosslinks caused by formaldehyde were removed rapidly. The authors concluded that the cell types appeared to have a similar capability to repair DNA damage.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Laboratory (in vitro) experiment on cultured human cells comparing responses to DNA-damaging agents
• Who was studied: Cultured normal human bronchial epithelial cells and bronchial fibroblasts from bronchial tissue obtained at autopsy, plus normal human skin fibroblast strains AG 1522 and CRL 1220; National Cancer Institute, Bethesda, USA
• Exposure: X-rays, ultraviolet light, DMBA, BPDE, MNNG, formaldehyde, and UICC reference amosite or crocidolite asbestos (100 micrograms per 4 ml for 14.5 hours); the asbestos and formaldehyde experiments used bronchial cells
• Main results:
  • After 5 krad of X-rays, about 90% of single strand breaks were rejoined in the first hour, in both bronchial fibroblasts and epithelial cells
  • After BPDE, repair replication in bronchial fibroblasts was 39% of that in bronchial epithelial cells
  • After ultraviolet light, repair replication in fibroblasts was 84% of that in epithelial cells
  • Asbestos exposure produced no appreciable DNA single strand breaks in bronchial cells
  • With asbestos plus the polymerase inhibitors, no DNA single strand breaks accumulated, so no sign of low-level excision repair was found; unwashed amosite gave the same result (data not shown)
  • Formaldehyde induced DNA-protein crosslinks to an equivalent extent in both bronchial cell types, and these were rapidly removed
• The authors' conclusion: The authors concluded that human bronchial epithelial and fibroblastic cells and human skin fibroblasts appear to have a similar capability to repair DNA damage
• Limitations the authors state:
  • The authors stated that the cause of the single strand breaks produced by BPDE is not known
  • The authors stated that whether the lower repair replication in fibroblasts after BPDE reflects lower repair of a specific type of damage remains to be determined
  • The authors stated that the lesions detected by alkaline elution after MNNG are uncertain

Topics

Medical terms in this study, explained in our Lexicon: Fibroblast.

Related studies

• Cellular ingestion, toxic effects, and lesions observed in human bronchial epithelial tissue and cells cultured with asbestos and glass fibers — A. Haugen, P.W. Schafer, et al. (1982)
• Asbestos exposure increases human bronchial epithelial cell fibrinolytic activity — T.J. Gross, S.M. Cobb, et al. (1993)
• Asbestos induces tissue factor in Beas-2B human lung bronchial epithelial cells in vitro — A. Iakhiaev, U. Pendurthi, et al. (2004)
• Malignant transformation of immortalized human bronchial epithelial cells by asbestos fibers — T.K. Hei, L.J. Wu, et al. (1997)
• Changes in DNA 8-hydroxyguanine levels, 8-hydroxyguanine repair activity, and hOGG1 and hMTH1 mRNA expression in human lung alveolar epithelial cells induced by crocidolite asbestos — H.N. Kim, Y. Morimoto, et al. (2001)
• Uptake and cytotoxic effects of multi-walled carbon nanotubes in human bronchial epithelial cells — S. Hirano, Y. Fujitani, et al. (2010)

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