Studies on the role of oxygen radicals in asbestos-induced cytopathology of cultured human lung mesothelial cells

Our plain-English summary of Studies on the role of oxygen radicals in asbestos-induced cytopathology of cultured human lung mesothelial cells, by E.W. Gabrielson, G.M. Rosen, R.C. Grafstrom, et al (Carcinogenesis, 1986).

The study

• Authors: E.W. Gabrielson, G.M. Rosen, R.C. Grafstrom, K.E. Strauss, C.C. Harris
• Journal: Carcinogenesis
• Published: 1986;7(7):1161-4
• Cited by: 43 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The possible role of oxygen radicals in mediating the cytopathologic effects of asbestos was studied using human mesothelial cells in culture. Electron paramagnetic resonance measurements of intact cells using the spin trap 5,5-dimethyl-1-pyrroline-1-oxide failed to detect any increase in oxygen radicals in mesothelial cells after exposure to amosite asbestos, although oxygen radicals were readily detected in cells exposed to menadione, an uncoupler of oxidation-reduction reactions. Cellular thiol levels were reduced after exposure to menadione, but were not affected by exposure to asbestos. Addition to the culture media of the free radical scavengers superoxide dismutase, reduced glutathione, N-acetylcysteine, or D-alpha-tocopherol had no affect on the dose-dependent cytotoxicity of amosite fibers. Furthermore, exposure of the mesothelial cells to amosite fibers resulted in no significant increase in the level of DNA single-strand breaks. These results all suggest that for cultured human mesothelial cells, oxygen free radicals are not important mediators of the cytopathic effect of asbestos.

In plain English

This laboratory study tested whether oxygen free radicals (highly reactive forms of oxygen) explain how asbestos injures human mesothelial cells, a cell type the authors describe as a selective target of asbestos's cancer-causing action. The authors grew normal human mesothelial cells from the pleural fluid of donors with no known cancers and exposed them to UICC amosite asbestos. They used menadione, a chemical that generates radicals, for comparison. A detection method called spin-trapping found oxygen radicals in menadione-treated cells, but no oxygen radicals were detected in amosite-exposed cells. Menadione significantly lowered the cells' thiol content at 5 and 24 hours. Amosite did not. Four radical scavengers (superoxide dismutase, reduced glutathione, N-acetylcysteine and D-alpha-tocopherol) did not change amosite's toxicity to the cells, and the differences were not statistically significant. Amosite at 10 or 100 micrograms per milliliter for 24 hours slightly increased a measure of DNA single-strand breaks. The authors regarded that level as insignificant. The authors concluded that free radicals do not appear to be important in this asbestos-induced cell injury and that other mechanisms should be sought.

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) study of cultured human cells
• Who was studied: Cultured normal human mesothelial cells grown from pleural fluid of donors with no known malignancies; the number of donors is not stated
• Exposure: UICC amosite asbestos: 10 micrograms per milliliter for radical detection and thiol measurements, up to 10 micrograms per milliliter in the toxicity tests, and 1, 10 or 100 micrograms per milliliter in the DNA-damage tests. Menadione (0.1 mM) was the radical-generating comparison.
• Main results:
  • Spin-trapping detected oxygen radicals in mesothelial cells exposed to menadione
  • No oxygen radicals were detected in mesothelial cells exposed to amosite
  • Menadione decreased cellular thiol content at 5 and 24 hours; amosite did not decrease thiol levels
  • The menadione-related thiol decreases at 5 and 24 hours were statistically significant (P less than 0.05)
  • None of the four free radical scavengers altered amosite's toxicity to the mesothelial cells
  • The differences in amosite toxicity among the scavenger treatment groups were not statistically significant
  • DNA elution increased slightly after 24 hours at 10 or 100 micrograms per milliliter of amosite
  • The authors regarded the amount of DNA single-strand break damage as insignificant
• The authors' conclusion: The authors concluded that free radicals do not appear to be important intermediates in asbestos-induced injury of cultured human mesothelial cells, and that other mechanisms should be sought.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Amosite.

Medical terms in this study, explained in our Lexicon: Cytopathology, Mesothelial Cells, Amosite, Superoxide, Glutathione (GSH).

Related studies

• Oxygen radical-mediated mutagenic effect of asbestos on human lymphocytes: suppression by oxygen radical scavengers — L.G. Korkina, A.D. Durnev, et al. (1992)
• Polyvinylpyridine-N-oxide and carboxymethyl cellulose inhibit mineral dust-induced production of reactive oxygen species by human macrophages — P. Nyberg (1991)
• Evidence supporting a role for active oxygen species in asbestos-induced toxicity and lung disease — B.T. Mossman, J.P. Marsh (1989)
• Microsomal lipid peroxidation and oxy-radicals formation are induced by insoluble iron-containing minerals — M. Fontecave, M. Jaouen, et al. (1990)
• Specificity of asbestos-induced chromosomal aberrations in short-term cultured human mesothelial cells — K. Olofsson, J. Mark (1989)
• Asbestos-induced injury to cultured human pulmonary epithelial-like cells: role of neutrophil elastase — D.W. Kamp, M. Dunne, et al. (1993)

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