Asbestos, the mesothelial cell and malignancy: a matter of life or death

Our plain-English summary of Asbestos, the mesothelial cell and malignancy: a matter of life or death, by V.C. Broaddus (American Journal of Respiratory Cell and Molecular Biology, 1997).

The study

• Author: V.C. Broaddus
• Journal: American Journal of Respiratory Cell and Molecular Biology
• Published: 1997;17(6):657-9
• Type of article: Comment, Editorial
• Cited by: 25 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Summary of the article

In this Perspective, the author commented on a study by Levresse and colleagues, published in the same issue, of the effects of crocidolite and chrysotile asbestos on the cell cycle of rat pleural mesothelial cells. The author noted that asbestos was known to be a complete carcinogen for mesothelioma, but its mechanisms of action remained in question. Neither generation of reactive oxygen species nor mechanical effects alone could account for all known facts about asbestos toxicity. The author described how cells respond to DNA damage by either cell cycle arrest or apoptosis, both of which appear to depend on p53. Levresse and colleagues found evidence of arrest at G1/S and G2/M and an increase in p53 protein, mainly with chrysotile and to a lesser extent with crocidolite. They found little apoptosis (0.05% of cells exposed to crocidolite for 24 h), whereas earlier studies had reported 17 to 25%. The author suggested this difference might reflect experimental conditions, including shorter crocidolite fibers, cell growth phase and the presence of serum. The author cited her group's recent finding that incubating crocidolite with serum suppressed asbestos-induced apoptosis without decreasing DNA damage. Because mesothelioma appears to express wild-type p53, the author proposed that evasion of arrest or apoptosis may arise through other pathways. The author concluded that an important future question was how mesothelial cells evade these protective mechanisms so that asbestos-induced genetic abnormalities persist and accumulate.

PubMed has no abstract for this study, and the article doesn't print one. We wrote this summary from the full article with the help of AI. It is not the authors' wording.

In plain English

This article is a short commentary (a "Perspective"), not an original study, and it reports no new data of its own. The author discussed a laboratory study by Levresse and colleagues, published in the same journal issue. That study exposed rat pleural mesothelial cells grown in culture to crocidolite (an amphibole asbestos) and chrysotile (a serpentine asbestos). As described here, that study found that chrysotile, and to a lesser extent crocidolite, halted the cell division cycle at two checkpoints and raised levels of p53, a protein that responds to DNA damage. It found little apoptosis (a form of cell death): 0.05% of cells exposed to crocidolite for 24 hours, compared with 17 to 25% in earlier studies. The author suggested that differences in experimental conditions might explain this gap, including shorter crocidolite fibers, the cells' growth phase and the presence of serum. The author also noted that the author's own group had found serum suppressed asbestos-induced apoptosis without reducing DNA damage. The author concluded that asbestos can steer mesothelial cells toward either arrest or apoptosis. In the author's view, an important question for the future is how cells evade both protective responses, letting genetic abnormalities accumulate.

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: Commentary (Perspective) on a laboratory study by Levresse and colleagues in the same journal issue; no original data
• Who was studied: No study population of its own; the commented study used rat pleural mesothelial cells in culture
• Exposure: Crocidolite (amphibole) and chrysotile (serpentine) asbestos fibers, as used in the Levresse study
• Main results:
  • The commentary reports that Levresse and colleagues found, for chrysotile and to a lesser extent crocidolite, cell cycle arrest at the G1/S and G2/M checkpoints and an increase in p53 protein in rat pleural mesothelial cells
  • The commentary reports that Levresse and colleagues found little apoptosis (0.05% of cells exposed to crocidolite for 24 hours), compared with 17 to 25% of crocidolite-exposed cells in earlier studies
  • The author suggested the difference may reflect experimental conditions, noting that the crocidolite in the Levresse study was shorter than in the earlier studies and that cell growth phase and serum presence differed
  • The author reported separate recent work by the author's own group: incubating crocidolite with serum suppressed asbestos-induced apoptosis without decreasing asbestos-induced DNA damage
• The authors' conclusion: The author concluded that asbestos can direct mesothelial cells toward either cell cycle arrest or apoptosis. In the author's view, an important future question is how mesothelial cells evade these two protective mechanisms so that asbestos-induced genetic abnormalities persist and accumulate.

Topics

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

Medical terms in this study, explained in our Lexicon: Mesothelial Cells, Crocidolite, Chrysotile, Mesothelioma, Reactive Oxygen Species (ROS), Apoptosis.

Related studies

• Effect of simian virus large T antigen expression on cell cycle control and apoptosis in rat pleural mesothelial cells exposed to DNA damaging agents — V. Levresse, S. Moritz, et al. (1998)
• Effects of asbestos on initiation of DNA damage, induction of DNA-strand breaks, P53-expression and apoptosis in primary, SV40-transformed and malignant human mesothelial cells — B. Burmeister, T. Schwerdtle, et al. (2004)
• Crocidolite asbestos and SV40 are cocarcinogens in human mesothelial cells and in causing mesothelioma in hamsters — B. Kroczynska, R. Cutrone, et al. (2006)
• Patterns of 8-hydroxydeoxyguanosine formation in DNA and indications of oxidative stress in rat and human pleural mesothelial cells after exposure to crocidolite asbestos — H. Fung, Y.W. Kow, et al. (1997)
• Early mesothelial cell proliferation after asbestos exposure: in vivo and in vitro studies — I.Y. Adamson (1997)
• DNA breakage in asbestos-treated normal and transformed (TSV40) rat pleural mesothelial cells — V. Levresse, A. Renier, et al. (2000)

Browse more research in American Journal of Respiratory Cell and Molecular Biology, or return to medical research.