Interactions of chrysotile asbestos with erythrocyte membranes

Our plain-English summary of Interactions of chrysotile asbestos with erythrocyte membranes, by A.R. Brody, L.H. Hill (Environmental Health Perspectives, 1983).

The study

• Authors: A.R. Brody, L.H. Hill
• Journal: Environmental Health Perspectives
• Published: 1983;51:85-9
• Cited by: 9 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Chrysotile asbestos causes lysis of red blood cells. It has been proposed that the mechanism of hemolysis is mediated through interactions between asbestos and cell membrane glycoproteins. Our studies support this concept and the following results are reported. Electron microscopy shows that asbestos fibers distort red blood cells and bind to cell membranes which may become wrapped around the fibers. This reaction is prevented by pretreatment of the cells with neuraminidase. The distribution of lectins which bind to membrane glycoproteins is altered by treating the cells with asbestos. Cell distortion and membrane deformation consequent to asbestos treatment correlate with a clear increase in the ratio of intracellular Na+:K+ ions.

In plain English

This laboratory study exposed red blood cells taken from white rats to short chrysotile asbestos fibers. No living animals or people were exposed. The authors tested whether chrysotile harms cells by binding to sialic acid-containing molecules (glycoproteins) on the cell surface. Over 80% of untreated cells kept their normal shape after 4 hours. Chrysotile distorted 75-80% of cells within 15 minutes, and membranes appeared drawn around the fibers. Removing sialic acid beforehand with the enzyme neuraminidase protected over 75% of cells from this distortion. On distorted, asbestos-treated cells, sites labeled per unit area of surface by a gold-tagged marker (wheat germ agglutinin) fell to less than 30% of the control level. Silica-treated cells stayed evenly labeled. The mean sodium-to-potassium ratio inside cells was 0.56 in untreated cells and 1.28 in cells 5 to 15 minutes after asbestos treatment. The authors concluded that their results support asbestos-induced red cell injury through membrane glycoproteins. They noted that how cell distortion relates to cell bursting is not known. Whether this applies to lung cells was left for ongoing studies.

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) experiment on isolated red blood cells, using scanning electron microscopy, gold-labeled lectin markers and X-ray energy spectrometry
• Who was studied: red blood cells from white rats; over 120 cells were analyzed for sodium and potassium in three separate experiments
• Exposure: chrysotile asbestos fibers at 0.1 mg/mL, of which 95% had diameters less than 0.2 micrometers and lengths less than 6 micrometers; crystalline silica was used as a comparison
• Main results:
  • Chrysotile distorted 75-80% of red cells within 15 minutes, while over 80% of untreated cells kept normal biconcave shape after 4 hours
  • Pretreating cells with neuraminidase protected over 75% of them from asbestos-induced deformation
  • On distorted, asbestos-treated cells, the number of gold-labeled wheat germ agglutinin sites per unit area of cell surface fell to less than 30% of the control level
  • Silica-treated cells were labeled evenly before and after treatment
  • Mean intracellular sodium-to-potassium ratio was 0.56 (range 0.30-0.85) in untreated cells
  • Mean intracellular sodium-to-potassium ratio was 1.28 (range 0.82-2.57) in cells analyzed 5 to 15 minutes after asbestos treatment
  • In preliminary work with Limulus lectin, cell regions next to bound fibers were essentially devoid of the label
• The authors' conclusion: The authors concluded that their studies lend supporting evidence to the concept of asbestos-induced red cell injury mediated through interactions with membrane glycoproteins. They also concluded that neuraminidase protection suggests a role for negatively charged sialic acid in binding to chrysotile.
• Limitations the authors state:
  • The relevance of the observed cell deformation to the events that produce hemolysis is not known
  • The Limulus lectin experiments were preliminary and not adequately controlled, so no firm conclusions could be drawn from them
  • Whether these mechanisms operate in lung cells was not studied here

Topics

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

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

Related studies

• Interaction of erythrocyte membranes with particulates — A.C. Ottolenghi, L.B. Joseph, et al. (1983)
• A spin label study of the effect of chrysotile asbestos on erythrocyte membranes — E. Gendek, G. Bartosz, et al. (1984)
• Influence of the sialic acid content of the membrane on its susceptibility to chrysotile — J. Depasse (1982)
• Changes in lipid ordering of model phospholipid membranes treated with chrysotile and crocidolite asbestos — E.G. Gendek, A.R. Brody (1990)
• A spin label study of the effects of asbestos, quartz, and titanium dioxide dusts on the bovine erythrocyte membrane — W. Leyko, E. Gendek (1985)
• Hemolysis by chrysotile asbestos fibers. I. Influence of the sialic acid content in human, rat, and sheep red blood cell membranes — J.P. Pelé, R. Calvert (1983)

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