Scavengers of active oxygen species prevent cigarette smoke-induced asbestos fiber penetration in rat tracheal explants

Our plain-English summary of Scavengers of active oxygen species prevent cigarette smoke-induced asbestos fiber penetration in rat tracheal explants, by A. Churg, J. Hobson, K. Berean, et al (The American Journal of Pathology, 1989).

The study

• Authors: A. Churg, J. Hobson, K. Berean, J. Wright
• Journal: The American Journal of Pathology
• Published: 1989;135(4):599-603
• Cited by: 33 articles, as counted by NIH iCite
• Read it: PubMed · Free full text

Abstract

It was previously shown that rat tracheal explants first exposed to cigarette smoke and then to amosite asbestos take up more asbestos fibers than explants exposed to air and asbestos. To examine the mechanism of this process, the same experimental design was followed but test groups were added in which the asbestos was mixed with catalase or superoxide dismutase, scavengers of active oxygen species, or deferoxamine, an iron chelator that prevents formation of hydroxyl radical. All three agents protected against the cigarette smoke effect. Heat inactivated catalase or superoxide dismutase was not protective. These observations indicate that active oxygen species, probably derived from the cigarette smoke, play a role in smoke-mediated fiber transport into tracheobronchial epithelia.

In plain English

This was an organ-culture experiment using tracheal explants from 200-g male Sprague-Dawley rats. Explants were exposed for 10 minutes to cigarette smoke or air (sham smoke), then covered for 1 hour with 5 mg/ml UICC amosite asbestos. In each of three experiments the sham-smoke group received asbestos alone; smoke-exposed groups received asbestos alone, asbestos plus catalase (1300 U/ml), superoxide dismutase (600 U/ml), or heat-inactivated enzyme, or asbestos preincubated for 24 hours with 10 mM deferoxamine and then washed. After 1, 3, or 7 days, six to eight segments per group were sectioned; fibers longer than 4 micrometers in or under the epithelium were counted per mm of epithelium, excluding hyperplastic lesions, whose extent was measured separately because of the huge numbers of fibers in them. Smoke followed by asbestos increased both measures compared with sham smoke followed by asbestos; all three agents variably, but usually completely, abolished the increase, while heat-inactivated enzymes did not. The authors concluded that active oxygen species, probably derived from the smoke, play a role in smoke-mediated fiber transport into tracheobronchial epithelia.

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: Experimental laboratory study using rat tracheal explants (organ culture), with three separate experiments and treatment groups
• Who was studied: Tracheal explants from 200-g male Sprague-Dawley rats; six to eight segments removed from each test group at each time point (1, 3 and 7 days); laboratory in Vancouver, British Columbia, Canada
• Exposure: Cigarette smoke (or sham air) for 10 minutes, followed by 5 mg/ml UICC amosite asbestos for 1 hour; in the smoke-exposed test groups the asbestos was given with catalase (1300 U/ml), superoxide dismutase (600 U/ml), heat-inactivated enzyme, or after preincubation with 10 mM deferoxamine
• Main results:
  • In the group given cigarette smoke followed by amosite asbestos, the number of fibers penetrating the tracheal epithelium and the extent of hyperplastic lesions were increased, repeating the authors' earlier observations
  • Catalase, superoxide dismutase, or deferoxamine preincubation variably but usually completely abolished the smoke-mediated increase in fiber penetration, and the same applied to hyperplastic lesions
  • Heat-inactivated catalase and heat-inactivated superoxide dismutase gave no protection to the epithelium
• The authors' conclusion: The authors concluded that active oxygen species, probably derived from the cigarette smoke, play a role in smoke-mediated fiber transport into tracheobronchial epithelia, with hydroxyl radical suggested as a major factor
• Limitations the authors state:
  • The authors noted considerably more variation in the extent of hyperplastic lesions than in fiber counts per mm at any given time
  • The authors offered the lipid-peroxidation mechanism only as a suggestion, not as something the study established

Topics

Medical terms in this study, explained in our Lexicon: Amosite, Superoxide, Hydroxyl Radical.

Related studies

• Active oxygen species mediate asbestos fiber uptake by tracheal epithelial cells — J. Hobson, J.L. Wright, et al. (1990)
• Relationship of fiber surface iron and active oxygen species to expression of procollagen, PDGF-A, and TGF-beta(1) in tracheal explants exposed to amosite asbestos — J. Dai, A. Churg (2001)
• Effects of cigarette smoke dose and time after smoke exposure on uptake of asbestos fibers by rat tracheal epithelial cells — A. Churg, J. Hobson, et al. (1990)
• Prevention of asbestos-induced cell death in rat lung fibroblasts and alveolar macrophages by scavengers of active oxygen species — M.A. Shatos, J.M. Doherty, et al. (1987)
• Cigarette smoke increases amosite asbestos fiber binding to the surface of tracheal epithelial cells — A. Churg, J. Sun, et al. (1998)
• Effects of cigarette smoke on epithelial uptake of non-asbestos mineral particles in tracheal organ culture — B. Keeling, J. Hobson, et al. (1993)

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