Asbestos-catalysed lipid peroxidation and its inhibition by desferroxamine

Our plain-English summary of Asbestos-catalysed lipid peroxidation and its inhibition by desferroxamine, by S.A. Weitzman, A.B. Weitberg (The Biochemical Journal, 1985).

The study

• Authors: S.A. Weitzman, A.B. Weitberg
• Journal: The Biochemical Journal
• Published: 1985;225(1):259-62
• Cited by: 106 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

In an effort to understand the properties of asbestos fibres that might contribute to their being toxic, we incubated three different varieties of asbestos with phospholipid emulsions and looked for evidence of lipid peroxidation. Although all three types of asbestos were able to catalyse lipid peroxidation in the native state, this catalytic activity was inhibited by pre-washing of the asbestos with the iron chelator desferroxamine. This suggests that: lipid peroxidation may be one of the mechanisms by which asbestos produces tissue injury, and treatment with iron chelators might diminish the potential to produce this injury.

In plain English

This was a laboratory experiment done in test tubes, not a study of people or animals. The authors mixed three types of asbestos (crocidolite, amosite and Canadian chrysotile, all standard reference samples) with an emulsion of soya-bean fats. They then measured lipid peroxidation, a chemical breakdown of fats. All three types caused significant lipid peroxidation by 15 minutes, while fat samples without asbestos changed little. Chrysotile caused the most, crocidolite an intermediate amount and amosite the least. Washing the asbestos beforehand with desferroxamine, a substance that binds iron, reduced the peroxidation for all three types. Amosite was the most affected and chrysotile the least. For chrysotile, the average measured level fell from 1.00 micromolar without washing to 0.510 micromolar after washing with 10 mM desferroxamine. Adding ADP, another iron-binding substance, increased peroxidation with chrysotile and amosite but reduced it with crocidolite. The authors concluded that lipid peroxidation might be one mechanism by which asbestos damages tissue. They also concluded that treating asbestos with chelating agents in the desferroxamine family might inhibit this process.

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: Laboratory (in vitro, test-tube) biochemical experiment; no human or animal subjects
• Who was studied: No people or animals. Emulsions of asolectin, a mixture of soya-bean phospholipids (5 mg/ml), were incubated with asbestos at 37°C in room air. The work was done at Massachusetts General Hospital and Harvard Medical School, Boston, and published in 1985.
• Exposure: UICC reference standard samples of crocidolite, amosite and Canadian chrysotile, at a final concentration of 500 micrograms per ml, incubated for up to 15 minutes. In some tests the asbestos was pre-washed with desferroxamine (1, 5 or 10 mM), or ADP (1 mM) was added.
• Main results:
  • All three asbestos types caused significant lipid peroxidation by 15 minutes. Control incubations of asolectin without asbestos showed little change.
  • The three types differed significantly from one another. Canadian chrysotile caused the most peroxidation, crocidolite an intermediate amount, and amosite the least. In Table 1 (15 minutes, mean of thiobarbituric acid-reactive material), the levels were 0.360 micromolar for the control, 1.00 for chrysotile, 0.690 for crocidolite and 0.535 for amosite.
  • Pre-washing the asbestos with desferroxamine reduced peroxidation for all three types. Amosite was the most sensitive, crocidolite intermediate and chrysotile the least sensitive. Table 1 values:
• Chrysotile: 1.00 fell to 0.750 (1 mM), 0.575 (5 mM) and 0.510 (10 mM).
• Crocidolite: 0.690 fell to 0.485 (1 mM) and 0.355 (5 mM).
• Amosite: 0.535 fell to 0.325 (1 mM).
  • Desferroxamine also inhibited peroxidation when it was added to the incubations at the same time as the asbestos and asolectin.
  • Adding 1 mM ADP markedly increased peroxidation with chrysotile (2.01 micromolar) and amosite (0.850 micromolar). It decreased peroxidation with crocidolite (0.352 micromolar).
• The authors' conclusion: The authors concluded that lipid peroxidation might be an important mechanism by which asbestos produces tissue damage. They also concluded that it might be possible to inhibit this process by treating asbestos with chelating agents in the desferroxamine family. They stated that the iron content of the asbestos appears to be responsible for much of the activity.

Related studies

• 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)
• The role of catalytic iron in asbestos induced lipid peroxidation and DNA-strand breakage in C3H10T1/2 cells — C.J. Turver, R.C. Brown (1987)
• Iron enhances uptake of mineral particles and increases lipid peroxidation in tracheal epithelial cells — B. Keeling, K.Y. Li, et al. (1994)
• Fibre-induced lipid peroxidation leads to DNA adduct formation in Salmonella typhimurium TA104 and rat lung fibroblasts — P.J. Howden, S.P. Faux (1996)
• Microsomal lipid peroxidation and oxy-radicals formation are induced by insoluble iron-containing minerals — M. Fontecave, M. Jaouen, et al. (1990)
• Lipid peroxidation in microsomes induced by crocidolite fibres — M. Gulumian, F. Sardianos, et al. (1983)

Browse more research in The Biochemical Journal, or return to medical research.