Enhanced lipid peroxidation and lysosomal enzyme activity in the lungs of rats with prolonged pulmonary deposition of crocidolite asbestos

Our plain-English summary of Enhanced lipid peroxidation and lysosomal enzyme activity in the lungs of rats with prolonged pulmonary deposition of crocidolite asbestos, by J. Jajte, I. Lao, J.M. Wiśniewska-Knypl (British Journal of Industrial Medicine, 1987).

The study

• Authors: J. Jajte, I. Lao, J.M. Wiśniewska-Knypl
• Journal: British Journal of Industrial Medicine
• Published: 1987;44(3):180-6
• Cited by: 22 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

The interaction of UICC crocidolite asbestos with biological membranes in vivo was studied in rats after a single intratracheal dose of a suspension of 20 mg of fibres per rat. Development of lung fibrosis (increased level of hydroxyproline, a collagen index together with corresponding pathomorphological alteration) confirmed the penetration of crocidolite fibres into the lungs in the course of seven months exposure. The pulmonary deposition of crocidolite affected the lysosomal membranes of lung cells as manifested by (1) enhanced lipid peroxidation with (2) stimulation (release) of activity of beta-glucuronidase and cathepsin D. Enhanced lipid peroxidation and activity of beta-glucuronidase may contribute to the delayed, carcinogenic effects of crocidolite asbestos.

In plain English

This was an animal experiment by researchers in Lodz, Poland. Male Wistar rats each received a single dose of 20 mg of UICC crocidolite asbestos fibres in saline, placed directly into the windpipe. Control rats received saline only. Rats were killed one, three and seven months later and their lungs were examined. Lung collagen, a marker of fibrosis, was higher in exposed rats (for example 75.87 versus 30.81 mg at three months), and microscopy showed granulomas containing fibres. The fibrotic reaction tended to diminish by seven months. Activity of two lysosomal enzymes, beta-glucuronidase and cathepsin D, rose most between one and three months and then tended to diminish. At seven months the beta-glucuronidase differences were not marked as statistically significant. Lipid peroxidation, a chemical process that can damage cell membranes, increased over time. At seven months it was more than twofold higher in lysosomes of exposed rats than in controls. The authors concluded that enhanced lipid peroxidation and beta-glucuronidase activity may contribute to the delayed, carcinogenic effects of crocidolite.

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 (rats given a single intratracheal dose of asbestos, compared with saline-treated controls)
• Who was studied: Male Wistar rats (200-250 g), studied at the Nofer Institute of Occupational Medicine, Lodz, Poland. Exposed and control rats were killed at one, three and seven months after dosing. Table 1 gives results for 16 rats, table 2 for groups of 10 rats and table 3 for groups of eight rats.
• Exposure: A single intratracheal instillation of 20 mg of UICC reference crocidolite asbestos fibres in 0.2 ml of physiological saline per rat. Controls received saline only.
• Main results:
  • Lung collagen (mg per lungs dry weight) was higher in crocidolite-exposed rats than in controls at every time point: 62.29 vs 28.87 at one month, 75.87 vs 30.81 at three months, and 52.22 vs 38.64 at seven months (all p = 0.001).
  • The fibrotic reaction tended to diminish between three and seven months after instillation.
  • Microscopy of exposed rats' lungs showed asbestos fibres inside phagocytes and giant cells, granulomas and strands of connective tissue.
  • Beta-glucuronidase and cathepsin D activity rose in exposed rats' lungs, most between one and three months. In lung homogenates at one month, beta-glucuronidase was 180 vs 52 nmoles per mg protein per 15 minutes in controls (p = 0.001). The increase tended to diminish by seven months but stayed above control values. At seven months, beta-glucuronidase in exposed rats (91 in homogenates, 90 in lysosomes) was not marked as significantly different from controls (66 and 70).
  • The authors interpreted the near-parallel rise of enzyme activity in lysosomes and whole homogenates as suggesting that crocidolite caused release of the enzymes from the lysosomal membrane.
  • Lipid peroxidation increased with time. At seven months, lysosomes of exposed rats had 7.53 vs 3.06 nmoles of malondialdehyde per mg protein in controls (p = 0.001), more than twofold. In lung homogenates the values were 1.17 vs 0.63 (p = 0.001). At one month, the lysosomal values (3.73 vs 3.44) were not marked as significantly different.
• The authors' conclusion: The authors concluded that crocidolite in the lungs damaged lysosomal membranes, and that enhanced lipid peroxidation and beta-glucuronidase activity may contribute to the delayed, carcinogenic effects of crocidolite asbestos.

Topics

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

Medical terms in this study, explained in our Lexicon: Deposition, Crocidolite, UICC, Fibrosis, Collagen, Carcinogenic.

Related studies

• Enhanced lipid peroxidation in lung lavage of rats after inhalation of asbestos — J.M. Petruska, K.O. Leslie, et al. (1991)
• Effects of chrysotile on a lysosomal enzyme preparation and on the hydrolytic enzyme activity of cultured alveolar macrophages — R. Desai, R.J. Richards (1983)
• Asbestos induces selective release of lysosomal enzymes from mononuclear phagocytes — P. Davies, A.C. Allison, et al. (1974)
• Lipid peroxidation in microsomes induced by crocidolite fibres — M. Gulumian, F. Sardianos, et al. (1983)
• Asbestos-catalysed lipid peroxidation and its inhibition by desferroxamine — S.A. Weitzman, A.B. Weitberg (1985)
• Crocidolite-induced lipid peroxidation in rat lung microsomes. I. Role of different ions — M. Gulumian, T.A. Kilroe-Smith (1987)

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