Enhanced lipid peroxidation in lung lavage of rats after inhalation of asbestos

Our plain-English summary of Enhanced lipid peroxidation in lung lavage of rats after inhalation of asbestos, by J.M. Petruska, K.O. Leslie, B.T. Mossman (Free Radical Biology & Medicine, 1991).

The study

• Authors: J.M. Petruska, K.O. Leslie, B.T. Mossman
• Journal: Free Radical Biology & Medicine
• Published: 1991;11(4):425-32
• Cited by: 41 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Exposure of phagocytic cells to asbestos in vitro results in an augmented production of reactive oxygen metabolites and increased peroxidation of lipids. The aim of this investigation was to assess the extent of lipid peroxidation both in cells and fluid obtained from bronchoalveolar lavage (BAL), and in lungs of rats exposed to crocidolite asbestos or titanium dioxide (TiO2), a nonfibrous particulate control. In comparison to sham and TiO2-exposed rats, the BAL fluid and cells of crocidolite-exposed animals contained significantly elevated levels of malondialdehyde (MDA), a breakdown product of lipid peroxidation detected using high-pressure liquid chromatography (HPLC). In contrast, no significant differences in MDA were detected in lavaged lung tissue from these animals. Inhalation of crocidolite caused an early inflammatory response characterized by elevated numbers of polymorphonuclear leukocytes and lymphocytes, as well as enhanced total protein in BAL. Pulmonary fibrosis and increased lung hydroxyproline also were observed after 20 days of exposure. Exposure to TiO2 did not cause inflammation, pulmonary fibrosis, or elevated amounts of hydroxyproline in the lung. Our results show that exposure to the fibrogenic and inflammatory mineral, crocidolite, results in an enhanced lipid peroxidation in BAL cells and fluid not observed after inhalation of the particulate TiO2. These novel observations suggest that MDA in BAL may be useful as a biomarker of exposure to inhaled asbestos or other oxidants.

In plain English

In this animal experiment at the University of Vermont, male Fischer 344 rats breathed clean air (sham), crocidolite asbestos, or titanium dioxide, a non-fibrous dust. Dust levels were about 10 mg per cubic meter, 6 hours daily, 5 days a week. In each experiment, three rats per group were examined at 1, 5, 10 and 20 days, and 15 weeks after a 20-day exposure; experiments were repeated, with extra rats for microscopy. The researchers measured malondialdehyde (MDA), a breakdown product of oxidative fat damage (lipid peroxidation), in lung washings (lavage cells and fluid) and lung tissue. Crocidolite rats had significantly more MDA in lavage cells and fluid than sham or titanium dioxide rats (p less than 0.0001). MDA in washed lung tissue did not change significantly. Crocidolite rats also showed a higher share of PMN white blood cells, more lavage protein, more lung hydroxyproline (a collagen measure) and, after 20 days, focal interstitial fibrosis. Titanium dioxide did not cause these changes. The authors concluded that detecting lipid peroxidation in lavage should be pursued as a tool for indicating exposure to asbestos and other toxic agents.

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 in rats comparing crocidolite asbestos, titanium dioxide and clean air
• Who was studied: Male Fischer 344 rats aged eight to nine weeks, at the University of Vermont. In each experiment, three rats per group were killed at 1, 5, 10 and 20 days of exposure, and at 15 weeks after a 20-day exposure. Additional rats were used for histopathology. Inhalation experiments were repeated in duplicate or triplicate.
• Exposure: Inhaled NIEHS crocidolite asbestos or the anatase form of titanium dioxide (a nonfibrous particulate), each at about 10 mg per cubic meter of air, 6 hours a day, 5 days a week. Sham rats were held in dust-free chambers.
• Main results:
  • In lavage (BAL) cells and fluid, crocidolite-exposed rats had significantly more MDA than sham rats (p less than 0.0001) and titanium dioxide-exposed rats (p less than 0.0001).
  • MDA in lavage cells and fluid did not differ significantly between sham and titanium dioxide-exposed rats.
  • In lavaged (washed) lung tissue, crocidolite exposure produced no significant change in MDA.
  • In unlavaged lung tissue from additional rats examined at 20 days and at 15 weeks after a 20-day exposure, crocidolite caused a significant increase in MDA compared with sham controls (p less than 0.05). The data were not shown.
  • Overall, the percentages of PMN (polymorphonuclear leukocytes) and of alveolar macrophages in lavage differed significantly in crocidolite-exposed rats compared with sham and titanium dioxide groups (p less than 0.05). For example, after 1 day PMN made up 9.86 plus or minus 1.54 percent of lavage cells in crocidolite rats, versus 0.16 plus or minus 0.12 percent in sham rats.
  • Total numbers of cells recovered in lavage did not differ significantly among groups (p = 0.93).
  • Total protein in lavage fluid was significantly higher overall in crocidolite-exposed rats than in the other groups (p less than 0.05).
  • Crocidolite significantly raised total lung hydroxyproline (a measure of collagen) after 5, 10 and 20 days of exposure and 15 weeks after exposure ended. Titanium dioxide caused no significant change compared with sham.
  • After 20 days, focal pulmonary interstitial fibrosis was seen in asbestos-exposed rats. Clean air or titanium dioxide did not produce appreciable fibrosis.
• The authors' conclusion: The authors concluded that crocidolite inhalation led to inflammation, fibrosis and increased lipid peroxidation in lavage cells and fluid, which titanium dioxide did not. They suggested that early detection of lipid peroxidation in lavage should be pursued as a tool for indicating exposure to asbestos and other toxic agents.

Topics

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

Medical terms in this study, explained in our Lexicon: Bronchoalveolar Lavage (BAL), Crocidolite, BAL Fluid, Pulmonary Fibrosis, Inflammation, Fibrogenic, Biomarker.

Related studies

• Detection of lipid peroxidation in lung and in bronchoalveolar lavage cells and fluid — J.M. Petruska, S.H. Wong, et al. (1990)
• Enhanced lipid peroxidation and lysosomal enzyme activity in the lungs of rats with prolonged pulmonary deposition of crocidolite asbestos — J. Jajte, I. Lao, et al. (1987)
• Fibre-induced lipid peroxidation leads to DNA adduct formation in Salmonella typhimurium TA104 and rat lung fibroblasts — P.J. Howden, S.P. Faux (1996)
• Brief inhalation of asbestos compromises superoxide production in cells from bronchoalveolar lavage — J.M. Petruska, J. Marsh, et al. (1990)
• Chrysotile inhibits glutathione-dependent protection against the onset of lipid peroxidation in rat lung microsomes — J.M. Arif, I. Ahmad, et al. (1996)
• Microsomal lipid peroxidation and oxy-radicals formation are induced by insoluble iron-containing minerals — M. Fontecave, M. Jaouen, et al. (1990)

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