Changes in pulmonary surfactant and phosphatidylcholine metabolism in rats exposed to chrysotile asbestos dust

Our plain-English summary of Changes in pulmonary surfactant and phosphatidylcholine metabolism in rats exposed to chrysotile asbestos dust, by T.D. Tetley, R.J. Richards, J.L. Harwood (The Biochemical Journal, 1977).

The study

• Authors: T.D. Tetley, R.J. Richards, J.L. Harwood
• Journal: The Biochemical Journal
• Published: 1977;166(3):323-9
• Cited by: 39 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

1. Pulmonary surfactant was isolated from rats that had been exposed to chrysotile asbestos dust for from 3 days to 15 weeks. 2. Asbestos-treated rats showed a progressive increase in amounts of surfactant. After 15 weeks, treated animals contained 4 times as much as non-treated. 3. No significant change was seen in the total protein or total fatty acid composition of surfactant with exposure. 4. The increase in surfactant phosphatidylcholine normally seen on maturation of rat lung was accelerated by exposure of animals to asbestos. 5. An increase in the activity of phosphorylcholine glyceride transferase in lung homogenates and free cell populations was found. 6. Lysosomal phospholipase A was relatively unaffected by dust exposure. 7. It is suggested that the increase in surfactant amounts could be due to an increase in its synthesis without a corresponding alteration in its degradation.

In plain English

In this animal experiment, young male Wistar rats were divided into two groups matched for age and weight. One group breathed Rhodesian chrysotile asbestos dust (12.5 mg/m3, 7 hours a day, 5 days a week) for 3 days to 15 weeks; the other did not. The authors washed out the lungs and measured pulmonary surfactant, the film that lines the air sacs. Exposed rats had twice as much surfactant as controls after 3 weeks (4.2 versus 2.0 mg per animal). The authors described a fourfold increase after 9 to 15 weeks; their table showed 7.7 versus 1.3 mg at 9 weeks and 6.5 versus 1.5 mg at 15 weeks. Its protein and fatty acid make-up changed little. At 3 days and 3 weeks its phosphorus content was higher, resembling that of older control rats. An enzyme that makes phosphatidylcholine, the main surfactant fat, became more active. In cells washed from the lungs it reached 7 times control levels at 15 weeks. A breakdown enzyme showed no consistent rise. The authors concluded that surfactant synthesis was likely increased without matching breakdown or clearance, so surfactant accumulated. They noted that very minor changes in the surfactant could not be excluded.

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 inhalation experiment comparing asbestos-exposed rats with unexposed control rats
• Who was studied: Male specific-pathogen-free Wistar rats, 7-9 weeks old at the start, split into a control group and a treated group matched for age and weight. Material was pooled from 3 or 4 animals per group at each time point. Inhalation facilities were at the M.R.C. Pneumoconiosis Unit, Llandough Hospital, Penarth, Wales.
• Exposure: Inhaled Rhodesian chrysotile asbestos (UICC standard reference sample) at 12.5 mg/m3 for 7 hours per day, 5 days per week, for periods of 3 days to 15 weeks
• Main results:
  • After 3 weeks of exposure, the treated rats had twice as much pulmonary surfactant as untreated controls (Table 1: 4.2 versus 2.0 mg dry weight per animal).
  • The authors described the difference as growing to a 4-fold increase after 9-15 weeks of exposure. Table 1 gives 7.7 mg (treated, pooled from 3 rats) versus 1.3 mg (untreated, pooled from 3 rats) per animal at 9 weeks, and 6.5 mg (treated, 3 rats) versus 1.5 mg (untreated, 4 rats) at 15 weeks. The table notes an average error of about 10% for surfactant weight estimates.
  • After 9 weeks of exposure, the treated rats showed a significant increase in the free cell population obtained by lavage.
  • No significant differences were found in the total protein content of surfactant, either between treated and control animals or with age.
  • Surfactant phosphorus content in treated rats was significantly different from controls after 3 days (2.99 versus 1.93%, P less than 0.01) and 3 weeks (3.53 versus 1.59%, P less than 0.005), but not at later times. The authors noted that these values were similar to those of older control rats.
  • At 3 weeks, the higher phosphorus in treated rats was accounted for by more phosphatidylcholine, which made up 59% of total surfactant, comparable with normal adult rats.
  • There were no extensive alterations in the fatty acid composition of total surfactant between treated and untreated rats.
  • Phosphorylcholine glyceride transferase, an enzyme in phosphatidylcholine synthesis, increased in both lung homogenates and lung free cells of exposed rats. The greatest difference was at 15 weeks, with a 7-fold increase over control values in the free cells.
  • Lysosomal phospholipase A activity showed no consistent increase in exposed rats and was frequently lower in treated than in untreated rats.
• The authors' conclusion: The authors concluded that chrysotile exposure caused a large quantitative rather than qualitative change in lung surfactant. They considered it highly likely that surfactant synthesis was promoted in asbestos-treated rats and that the material accumulated because its degradation or clearance from the alveolar space was not correspondingly stimulated.
• Limitations the authors state:
  • An exhaustive analysis of individual proteins, or of the fatty acid composition of all the acyl-lipids at each stage, was not done, so very minor changes in the surfactant cannot be excluded.

Topics

Medical terms in this study, explained in our Lexicon: Chrysotile.

Related studies

• Chrysotile-induced asbestosis: changes in the free cell population, pulmonary surfactant and whole lung tissue of rats — T.D. Tetley, P.M. Hext, et al. (1976)
• Studies on the fate of pulmonary surfactant in the lung — R. Desai, T.D. Tetley, et al. (1978)
• Changes in surfactant in bronchoalveolar lavage fluid after hemithorax irradiation in patients with mesothelioma — M. Hallman, P. Maasilta, et al. (1990)
• Effect of air pollutants on the pulmonary surfactant system — B. Müller, C. Seifart, et al. (1998)
• Experimental asbestosis. The development of lung cancer in rats with pulmonary deposits of chrysotile asbestos dust — P. Gross, R.T. DeTreville, et al. (1967)
• In vitro genotoxicity studies of chrysotile asbestos fibers dispersed in simulated pulmonary surfactant — J. Lu, M.J. Keane, et al. (1994)

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