Asbestos affects the in vitro uptake and detoxification of aromatic compounds

Our plain-English summary of Asbestos affects the in vitro uptake and detoxification of aromatic compounds, by R.C. Brown, G.T. Fleming, A.I. Knight (Environmental Health Perspectives, 1983).

The study

• Authors: R.C. Brown, G.T. Fleming, A.I. Knight
• Journal: Environmental Health Perspectives
• Published: 1983;51:315-8
• Cited by: 9 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

A number of mineral dusts were tested for their ability to catalyze the transformation of benzo(a)pyrene from the microcrystalline state into lipid solution. The findings of Lakowicz and his co-workers, that fibrous dusts were more active than nonfibrous dusts, were confirmed. Macromolecular binding metabolites of BaP were formed in A549 cells to a similar extent whether the BaP was added in solution or adsorbed to fibers; however, the level of water-soluble metabolites was lower in cultures treated with adsorbed hydrocarbon. It was found that asbestos can also inhibit the accumulation of 1-naphthyl glucuronide in cultures treated with 1-naphthol. The significance of this in asbestos pathogenesis is briefly discussed.

In plain English

This laboratory study used cells and rat liver preparations, not people. The authors tested whether asbestos changes how cells take up and process the chemicals benzo(a)pyrene (BaP) and 1-naphthol. In rat liver microsomes, UICC amosite was far more efficient at moving BaP from crystals into lipid than milled, essentially nonfibrous amosite. Pulverized fuel ash did not speed the transfer. In human A549 lung tumor cells, BaP added stuck to crocidolite gave lower levels of water-soluble metabolites in the medium than BaP added in solution. For 15 micromolar BaP with 100 micrograms crocidolite per mL, the figures were 4.55 versus 10.15 nmole per mg protein. Adsorbed BaP did not lower the amount of bound hydrocarbon. UICC crocidolite significantly inhibited 1-naphthyl glucuronide formation in A549 cells, and milled crocidolite inhibited it much less. Neither had a significant effect at 50 micrograms per mL. Similar inhibition was seen in rat embryo fibroblasts. Macrophage-like P388D1 cells showed early stimulation that disappeared later. The authors suggested asbestos may increase uptake of such chemicals and inhibit glucuronide accumulation, possibly raising toxic metabolite levels in asbestos-damaged tissue. They noted wide variation between experiments.

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: In vitro laboratory experiments using cultured cells and rat liver microsomes
• Who was studied: Human alveolar epithelial type II tumor cells (A549), primary rat embryo fibroblasts, the macrophage-like P388D1 cell line, and rat liver microsomes
• Exposure: UICC asbestos samples (amosite, crocidolite, and chrysotile in P388D1 cells), milled amosite and milled crocidolite, and pulverized fuel ash, combined with benzo(a)pyrene or 1-naphthol
• Main results:
  • In rat liver microsomes, UICC amosite was far more efficient than milled (essentially nonfibrous) amosite at promoting transfer of BaP from the microcrystalline state into lipid. Pulverized fuel ash did not accelerate the transfer.
  • In A549 cells, BaP added adsorbed to crocidolite reduced water-soluble metabolites in the medium. For 15 micromolar BaP in solution the level was 10.15 plus or minus 1.05 nmole/mg protein; adsorbed to 100 micrograms crocidolite/mL it was 4.55 plus or minus 0.4. Covalently bound hydrocarbon was not lowered and increased in one series of cultures.
  • In A549 cells, UICC crocidolite significantly inhibited formation of 1-naphthyl glucuronide, and milled crocidolite inhibited it much less. Neither dust had a significant effect at 50 micrograms/mL.
  • In primary rat embryo fibroblasts given 25 micromolar 1-naphthol, glucuronide formed was 24.6, 69.3 and 55.7 nmole/mg protein at 8, 24 and 72 hours. With crocidolite at 100 micrograms/mL the figures were 24.7, 46.5 and 35.1.
  • In macrophage-like P388D1 cells, the picture was more complex: there was early stimulation of glucuronide formation that disappeared later.
• The authors' conclusion: The authors suggested that asbestos can mediate increased uptake of xenobiotics and inhibition of glucuronide accumulation. They proposed these could increase toxic metabolite levels in asbestos-damaged tissue and the probability of malignant transformation.
• Limitations the authors state:
  • Wide variation in metabolite levels between experiments, and attempts to induce maximal, reproducible hydrocarbon metabolism in the cells failed

Topics

Medical terms in this study, explained in our Lexicon: A549 Cells.

Related studies

• Effects of particulate matter on rates of membrane uptake of polynuclear aromatic hydrocarbons — D.R. Bevan, S.C. Riemer, et al. (1981)
• Elemental modifications and polycyclic aromatic hydrocarbon metabolism in human fibroblasts — R.W. Hart, F.B. Daniel, et al. (1980)
• Mass transfer rates of polycyclic aromatic hydrocarbons between micron-size particles and their environment--theoretical estimates — P. Gerde, P. Scholander (1989)
• Benzo[a]pyrene uptake into rat liver microsomes: effects of adsorption of benzo[a]pyrene to asbestos and non-fibrous mineral particulates — J.R. Lakowicz, D.R. Bevan (1980)
• In vitro reactivity of alveolar macrophages and red blood cells with asbestos fibres treated with oxalic acid, sulfur dioxide and benzo-3,4-pyrene — M.C. Jaurand, L. Magne, et al. (1981)
• The effect of asbestos-associated metal ions on the binding of benzo(a)pyrene to macromolecules in vitro — R. Thomson, T.A. Kilroe-Smith, et al. (1978)

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