Asbestos effects on superoxide production. An in vitro study of hamster alveolar macrophages

Our plain-English summary of Asbestos effects on superoxide production. An in vitro study of hamster alveolar macrophages, by B.W. Case, M.P. Ip, M. Padilla, et al (Environmental Research, 1986).

The study

• Authors: B.W. Case, M.P. Ip, M. Padilla, J. Kleinerman
• Journal: Environmental Research
• Published: 1986;39(2):299-306
• Cited by: 42 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Inhaled asbestos induces accumulation of alveolar macrophages (AM) and polymorphonuclear leukocytes (PMN) in lung. Asbestos-enhanced production of superoxide anion (O2-) by AM and/or PMN may be involved in the pathogenesis of asbestos-induced fibrosis, either through direct effects on collagen synthesis or via mediation of tissue injury and repair. In in vivo experiments, bronchoalveolar lavage (BAL) 3 to 8 weeks following intratracheal asbestos injections showed increases in both PMN and AM, with AM representing 78 to 82% of cells recovered. Inhalation models, generally regarded as more analagous to human exposures, have confirmed AM as the predominant component of the cellular response to inhaled asbestos. In this study, the in vitro effects of asbestos fiber on O2- production by AM have been determined in cell populations derived from the Syrian golden hamster. AM for in vitro study were obtained by BAL. O2- production was monitored as superoxide dismutase (SOD) - inhibitable cytochrome c reduction. Significant rises in O2- release by AM were noted in the presence of 0.4 mg/ml crocidolite (2.53 +/- 0.33 nmole cytochrome c reduced/10(6) cells/30 min, 37 degrees C; controls 1.13 +/- 0.18 nmole; P less than 0.02). Chrysotile induced levels of O2- release in AM which were similar to those evoked by crocidolite.

In plain English

This was a laboratory study in animals. The authors washed out hamster lungs (bronchoalveolar lavage) to collect immune cells called alveolar macrophages. They then measured how much superoxide, a reactive form of oxygen, the cells released with and without asbestos. There were four experiments with crocidolite at 0.4 mg per ml, using cells from 31 hamsters in total. Superoxide release was measured as the part of cytochrome c reduction that the enzyme superoxide dismutase could block, per million cells per 30 minutes. The average rose from 1.13 nmole (standard error 0.18) in control cells to 2.53 nmole (standard error 0.33) in crocidolite-exposed cells, with P less than 0.02. A single experiment with short-fiber chrysotile gave a nearly identical result. In separate experiments, hamsters were injected in the windpipe with 1 mg chrysotile. Their lung washings held more inflammatory cells than those of controls; macrophages were about 80% of cells recovered. The authors concluded that asbestos fiber induces superoxide production by these cells. They said future work should test the effect in living animals after controlled inhalation exposure.

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: Animal experiment: laboratory (in vitro) tests on lung macrophages from hamsters, plus small intratracheal injection experiments in live hamsters
• Who was studied: Male Syrian golden hamsters weighing 100-140 g. For the cell tests, macrophages were collected by lung lavage from six to nine hamsters per experiment. In the injection experiments, groups had 4 hamsters each in experiment 1 and 2 each in experiment 2 (per Table 1). Dates and location of the experiments are not stated beyond the authors' institutions in New York and Montreal.
• Exposure: In the cell tests: crocidolite and short-fiber chrysotile, each at a final concentration of 0.4 mg per ml. In live animals: 1 mg Coalinga chrysotile injected into the trachea (once, or twice 6 weeks apart), compared with salt solution alone.
• Main results:
  • Superoxide release by hamster alveolar macrophages, measured as superoxide dismutase-inhibitable cytochrome c reduction per million cells per 30 minutes, averaged 1.13 nmole (standard error 0.18) in control cells and 2.53 nmole (standard error 0.33) in crocidolite-exposed cells.
  • In the crocidolite results, the figures are means, and the plus-or-minus values are standard errors.
  • The crocidolite results came from four experiments at 0.4 mg crocidolite per ml, and the difference from controls had P less than 0.02 (paired t test).
  • Cells for the crocidolite experiments came from 31 hamsters in total.
  • In one experiment, short-fiber chrysotile gave a nearly identical result to crocidolite.
  • Three weeks after a single chrysotile injection, asbestos-treated hamsters showed a ninefold increase in polymorphonuclear leukocytes (PMN) and a small increase in macrophages compared with controls.
  • After two injections 6 weeks apart, PMN increased 17-fold and macrophages threefold in asbestos-treated hamsters.
  • In both injection experiments, macrophages were about 80% of the cells recovered from asbestos-treated hamsters.
• The authors' conclusion: The authors concluded that their study establishes that asbestos fiber induces superoxide production by alveolar macrophages, as indicated by superoxide dismutase-inhibitable cytochrome c reduction.
• Limitations the authors state:
  • The effect was seen in cells in the laboratory. The authors said future work should try to replicate it in living animals after controlled inhalation exposure.
  • The authors noted that intratracheal injection models like theirs produce a large influx of PMN. They contrasted this with inhalation models, which generally show macrophages as the chief cell response.

Topics

Medical terms in this study, explained in our Lexicon: Superoxide, Alveolar Macrophage, Fibrosis, Collagen, Bronchoalveolar Lavage (BAL), Crocidolite, Chrysotile.

Related studies

• Dehydroepiandrosterone inhibits the spontaneous release of superoxide radical by alveolar macrophages in vitro in asbestosis — W.N. Rom, T. Harkin (1991)
• IgG specifically enhances chrysotile asbestos-stimulated superoxide anion production by the alveolar macrophage — R.K. Scheule, A. Holian (1989)
• Brief inhalation of asbestos compromises superoxide production in cells from bronchoalveolar lavage — J.M. Petruska, J. Marsh, et al. (1990)
• Differences between particulate and peptide stimuli on activation of oxidant production in alveolar macrophages — G.E. Hatch, A. Spock, et al. (1980)
• Stimulation of oxidant production in alveolar macrophages by pollutant and latex particles — G.E. Hatch, D.E. Gardner, et al. (1980)
• Leaching of chrysotile asbestos in human lungs. Correlation with in vitro studies using rabbit alveolar macrophages — M.C. Jaurand, J. Bignon, et al. (1977)

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