The involvement of ionic interactions during asbestos-induced enzyme release from polymorphonuclear leukocytes

Our plain-English summary of The involvement of ionic interactions during asbestos-induced enzyme release from polymorphonuclear leukocytes, by J.G. Elferink, M. Deierkauf, J.A. Kramps, et al (Chemico-biological Interactions, 1989).

The study

• Authors: J.G. Elferink, M. Deierkauf, J.A. Kramps, H.K. Koerten
• Journal: Chemico-biological Interactions
• Published: 1989;72(1-2):215-27
• Cited by: 2 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Chrysotile asbestos permeabilizes the plasma membrane of rabbit polymorphonuclear leukocytes (PMNs) which is evident from the release of the cytoplasmic enzyme lactate dehydrogenase (LDH) from the cell. When Ca2+ is present in the medium exocytosis is observed, evident from the release of the granule associated enzyme lysozyme which is not liberated in the absence of Ca2+. Asbestos-induced enzyme release is inhibited by polyanions or by removal of positive charges on asbestos, and resembles enzyme release induced by synthetic polycations. Pretreatment of PMNs with neuraminidase does not affect the ability of asbestos to induce enzyme release from these cells. Asbestos induces release of glucose from glucose-loaded liposomes, and this effect can be inhibited by the polyanion poly-D-glutamic acid. The results are compatible with the view that positive charges play a decisive role in the interaction between PMNs and asbestos, and that the primary target of asbestos could be the lipid bilayer of the membrane. The interaction results in a permeabilized plasma membrane. When Ca2+ is present in the medium it moves into the cell and causes exocytosis of the granule enzyme lysozyme. Inhibition of cytotoxicity by polyanion may cause a diminished Ca2+-influx and hence inhibition of lysozyme release.

In plain English

This was a laboratory study of white blood cells called polymorphonuclear leukocytes (PMNs), taken from rabbits and exposed to chrysotile asbestos. The authors measured the release of two enzymes. One was LDH, which normally stays inside the cell, so its leakage signals membrane damage. The other was lysozyme, which is stored in small sacs called granules. Without calcium, asbestos (100 µg) caused 54% LDH release but only 8% lysozyme release. With calcium, LDH release was 23% and lysozyme release was 62%. Negatively charged substances (poly-D-glutamic acid, heparin, dextran sulfate) strongly blocked enzyme release. Asbestos that had been pretreated with poly-D-glutamic acid lost its effect, but pretreated cells still released enzymes. Albumin, serum and catalase also reduced release. Acid-leached chrysotile had a much smaller effect. Oxygen-radical scavengers did not change release, and removing sialic acid from the cells had little effect. Asbestos also released glucose from both positively and negatively charged artificial fat bubbles (liposomes), and poly-D-glutamic acid inhibited this. The authors concluded that positive charges play a decisive role in the interaction between asbestos and these cells.

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) experiments on isolated rabbit cells and on artificial lipid vesicles (liposomes)
• Who was studied: Polymorphonuclear leukocytes (PMNs) collected from the abdominal cavity of rabbits injected with glycogen; 3 million cells per 1 ml were used in experiments. Egg-lecithin liposomes with positive or negative charge were also tested.
• Exposure: Sonicated chrysotile asbestos, mostly at 200 µg per ml for 30 minutes. Some experiments used chrysotile leached with hydrochloric acid, which removes magnesium and the fiber's positive charge.
• Main results:
  • Calcium changed which enzymes were released. With 100 µg asbestos and no calcium (EDTA), LDH release was 54 ± 3% and lysozyme release 8 ± 3%. With 1 mM calcium, LDH release was 23 ± 2% and lysozyme release 62 ± 5%.
  • Poly-D-glutamic acid strongly inhibited asbestos-induced enzyme release, and other polyanions (heparin, dextran sulfate) did so equally.
  • Asbestos pretreated with poly-D-glutamic acid and then washed lost its enzyme-releasing effect. Cells pretreated the same way released enzymes as before (LDH 54 ± 1% without calcium; lysozyme 58 ± 3% with calcium).
  • With calcium and 200 µg/ml asbestos, enzyme release without any additive was 61 ± 4% LDH and 69 ± 4% lysozyme. 100 µg albumin reduced this to 9 ± 3% LDH and 15 ± 3% lysozyme. Serum and catalase gave similar reductions.
  • Superoxide dismutase, thiourea and desferal did not affect asbestos-induced enzyme release.
  • The hydrogen acceptor PVPNO inhibited enzyme release only moderately, and only at very high concentrations.
  • Acid-leached chrysotile had a much smaller enzyme-releasing effect than untreated chrysotile.
  • Neuraminidase treatment, which removes sialic acid from the cells, had little effect on asbestos-induced enzyme release.
  • Asbestos released glucose from both positively and negatively charged liposomes. With calcium and 1000 µg asbestos, release was 33 ± 3% for positive liposomes and 25 ± 2% for negative liposomes. Poly-D-glutamic acid inhibited this effect.
  • The pattern of enzyme release from asbestos resembled that from synthetic polycations: much LDH release and little lysozyme release without calcium.
• The authors' conclusion: The authors concluded that positive charges play a decisive role in the interaction between asbestos and the PMN.
• Limitations the authors state:
  • The authors state that how asbestos interacts with the lipid structure of liposomes remains to be determined.
  • The authors note that destroying liposomes required relatively high asbestos concentrations.

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, Lactate Dehydrogenase (LDH).

Related studies

• Production of reactive oxygen species by man-made vitreous fibres in human polymorphonuclear leukocytes — M. Ruotsalainen, M.R. Hirvonen, et al. (1999)
• Asbestos-induced chemiluminescence response of human polymorphonuclear leukocytes — M. Rola-Pleszczynski, D. Rivest, et al. (1984)
• Cellular mechanisms of reactive oxygen metabolite generation from human polymorphonuclear leukocytes induced by crocidolite asbestos — T. Ishizaki, E. Yano, et al. (1997)
• Crocidolite-induced reactive oxygen metabolites generation from human polymorphonuclear leukocytes — T. Ishizaki, E. Yano, et al. (1994)
• Mineral fiber-induced leukocyte activation: the role of intra- and extracellular calcium — M. Ruotsalainen, J. Naarala, et al. (1995)
• Asbestos induces selective release of lysosomal enzymes from mononuclear phagocytes — P. Davies, A.C. Allison, et al. (1974)

Browse more research in Chemico-biological Interactions, or return to medical research.