Oxygen radicals and asbestos-mediated disease

Our plain-English summary of Oxygen radicals and asbestos-mediated disease, by T.R. Quinlan, J.P. Marsh, Y.M. Janssen, et al (Environmental Health Perspectives, 1994).

The study

• Authors: T.R. Quinlan, J.P. Marsh, Y.M. Janssen, P.A. Borm, B.T. Mossman
• Journal: Environmental Health Perspectives
• Published: 1994;102 Suppl 10(Suppl 10):107-10
• Type of article: Review
• Cited by: 50 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Asbestos fibers are potent elaborators of active oxygen species whether by reactions involving iron on the surface of the fiber, or by attempted phagocytosis of fibers by cell types resident in the lung. The link between production of active oxygen species and the pathogenesis of asbestos-mediated disease has been highlighted by studies outlined here exploring the use of antioxidant scavengers which inhibit the cytotoxic effects of asbestos both in vitro and in vivo. The use of antioxidant enzymes ameliorates the induction of certain genes necessary for cell proliferation, such as ornithine decarboxylase, implicating oxidants as causative factors in some abnormal cell replicative events. Based on these observations, antioxidant enzymes likely represent an important lung defense mechanism in response to oxidative stress. In addition, their gene expression in lung or in cells from bronchoalveolar lavage might be a valuable biomarker of chronic inflammation and pulmonary disease after inhalation of oxidants.

In plain English

This article, presented at a 1993 conference, reviewed research from the authors' own laboratory on how asbestos may harm lung cells through active oxygen species (oxygen radicals). It described earlier cell-culture and rat experiments, not studies of people. In those studies, chrysotile and crocidolite asbestos caused less damage to hamster airway cells when oxygen-radical scavengers were added. This protection was seen with long asbestos fibers but not with short chrysotile or glass fibers. In rats that inhaled crocidolite for 20 days, a pump-delivered antioxidant enzyme (PEG-catalase) reduced signs of lung injury, while PEG-SOD did not. Asbestos raised levels of protective antioxidant enzymes in cultured cells and in rat lungs. In rats inhaling crocidolite, Mn-SOD gene activity rose to approximately 5-fold above sham controls. Asbestos also raised the activity of genes linked to cell division, such as ornithine decarboxylase and c-jun. The authors concluded that antioxidant enzymes likely represent an important lung defense. They also concluded that the enzymes' gene expression in lung or in lung-lavage cells might be a valuable marker of chronic inflammation and lung disease after inhalation of oxidants.

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: Review of the authors' own laboratory's earlier cell-culture and rat inhalation studies, presented at the Conference on Oxygen Radicals and Lung Injury (1993); no new data
• Who was studied: Cultured cells (hamster tracheal epithelial cells, rat lung fibroblasts, rat alveolar macrophages, human pleural mesothelial cells, human adult lung fibroblasts, rat mesothelial cells) and rats in inhalation experiments; numbers of animals not given
• Exposure: Chrysotile and crocidolite asbestos in cell cultures. Crocidolite (7-10 mg/m3 air) and cristobalite silica inhaled by rats. Glass fibers, riebeckite (a nonfibrous analog of crocidolite) and polystyrene beads used for comparison.
• Main results:
  • In hamster tracheal epithelial cell cultures, oxygen-radical scavengers reduced cell damage from long asbestos fibers (over 10 in length; the unit is garbled by scanning) but not from short chrysotile or glass fibers
  • In rats inhaling crocidolite for 20 days, indicators of lung injury were reduced in rats infused with PEG-catalase compared with control rats
  • In the same rat model, PEG-SOD did not inhibit the effects of asbestos
  • Human pleural mesothelial cells exposed to chrysotile or crocidolite showed dose-dependent increases in Mn-SOD and heme oxygenase mRNA; there was no induction with polystyrene beads or riebeckite
  • In rats inhaling crocidolite, Mn-SOD mRNA in lung rose from 1.4-fold above sham controls at 1 day to approximately 5-fold, peaking at 3 days
  • In rats inhaling cristobalite silica, Mn-SOD mRNA rose to higher levels than seen after similar concentrations of asbestos
  • In hamster tracheal epithelial cells, asbestos raised ornithine decarboxylase (ODC) mRNA and activity; antioxidant enzymes and scavengers reduced these increases
  • ODC mRNA rose in rat lungs after 9 and 20 days of crocidolite inhalation
  • c-jun and AP-1 binding to DNA were induced in a dose-responsive way in rat mesothelial and hamster tracheal epithelial cells exposed to crocidolite or chrysotile
• The authors' conclusion: The authors concluded that antioxidant enzymes likely represent an important lung defense against oxidative stress. They also concluded that the enzymes' gene expression in lung or in bronchoalveolar lavage cells might be a valuable biomarker of chronic inflammation and pulmonary disease after inhalation of oxidants.

Topics

Medical terms in this study, explained in our Lexicon: Phagocytosis, Oxidative Stress, Bronchoalveolar Lavage (BAL), Biomarker, Chronic Inflammation.

Related studies

• The role of oxygen free radicals in occupational and environmental lung diseases — V. Vallyathan, X. Shi (1997)
• Interactions of exogenous or evoked agents and particles: the role of reactive oxygen species — A. Churg (2003)
• Increased mineral dust-induced production of reactive oxygen species by blood monocytes from patients with malignant diseases — P.W. Nyberg, S.A. Nordman, et al. (1994)
• Tobacco smoke: involvement of reactive oxygen species and stable free radicals in mechanisms of oxidative damage, carcinogenesis and synergistic effects with other respirable particles — A. Valavanidis, T. Vlachogianni, et al. (2009)
• Involvement of protein kinase C, phospholipase C, and protein tyrosine kinase pathways in oxygen radical generation by asbestos-stimulated alveolar macrophage — Y. Lim, S.H. Kim, et al. (1997)
• Multiple roles of oxidants in the pathogenesis of asbestos-induced diseases — A. Shukla, M. Gulumian, et al. (2003)

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