Kinetics of Asbestos-Induced Haemolysis of Human Red Blood Cells

  • Robert Englman
Conference paper
Part of the NATO ASI Series book series (volume 85)


Encounters between chrysotile fibres and red blood cells (RBC) lead to the haemolysis of the latter and to the loss of capacity of the former to further damage the cells. Jaurand et al.’s in vitro experiments (1979) yield the evolution of concentrations of healthy RBC and of active chrysotile fibres. When it is assumed that once-reacted RBC are completely deactivated, the rate equations are solvable and show the observed concentrations. Moreover, they show precisely the experimentally observed linear relation beween the inverses of maximal haemolysis and of the ratios of fibre/RBC surtaxes. When the assumption of complete RBC deactivation is rescinded, systematic deviations from the data are found. Observation of the collision fingerprints on the fibres, e.g. by atomic force microscopes, is suggested.


Membrane Attack Complex Haemolytic Activity Chrysotile Asbestos Mineral Fibre Chrysotile Fibre 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. Beck EG, Holt PF, Manojlovic N (1972) Comparison of effects of macrophage cultures of glass fibre, glass powder and chrysotile asbestos. British J Ind Med 29: 280–6Google Scholar
  2. Benedek EG, Brody AR (1990) Changes in lipid ordering of phospholipid mem-. branes treated with chrysotile and crocidolite fibres, tnv Kes 53: 152–67Google Scholar
  3. Berke G (1989) in Fundamental Immunology. Raven Press New York: 753–64Google Scholar
  4. Bignon J, Peto J, Saracci R (eds) (1989) Non-occupational exposure to mineral fibres. IARC Sci Publ LvonGoogle Scholar
  5. Borenstein N, Brash JL (1986) Red blood cells deposit membrane components on contacting surfaces. J Biomed Mat Res 20: /23–30.Google Scholar
  6. Burt HM, Jackson JK, Kim KJ (1990) Role of membrane proteins in monosodium urate cystal-membrane interaction. J Rheumatology 17: 1353–8.Google Scholar
  7. Chapman RN (1931) Animal Ecology. McGraw-Hill NewYork Gingell D (1986) Cell contact with solid surfaces, in Biophysics of the cell surface ( Glaser R, Gingell D, eds) Springer Berlin: 264–85.Google Scholar
  8. Harington JS, Miller K, Mcnab G (1971) Haemolysis by asbestos. Environ Res 4: 95–117.PubMedCrossRefGoogle Scholar
  9. Iguchi H, Shoshuka K (1989) Possible generation of H2O2 and lipid peroxidation of erythrocyte membrane by asbestos. Boichem Inf 28:981–90.Google Scholar
  10. Jaurand MC (1989) Particulate-state carcinogenesis in non-occupational exposure to mineral fibres. In Bignon et al. (eds) ibidGoogle Scholar
  11. Jaurand MC,Magne L, Bignon J (1979) Inhibition by phospholipids of haemolytic action of asbestos. British J Ind Med 36: 113–6Google Scholar
  12. Light WG, Wei ET (1977) Surface charges and haemolytic activity of asbestos. Environ Res 13: 135–45PubMedCrossRefGoogle Scholar
  13. Macnab G, Harington JS (1967) Haemolytic activity of asbests and other mineral dusts. Nature 214: 522–3.PubMedCrossRefGoogle Scholar
  14. Malinski JA, Nelsestuen GL (1989) Membrane permeability to macromolecules mediated by the membrane attack complex, biochem 28: 61–70.Google Scholar
  15. Oscarson DW, van Scoyoc GE, Ahlrichs JC (1986) Lysis of erithrocytes by silicate minerals, clay and clay minerals. 34: 74–80Google Scholar
  16. Parsegian NA, Gingell D (1980) Red blood celll adhesion J Cell Sci 41: 151–7Google Scholar
  17. Schnitzer RJ, Pundsack FL (1970) Asbestos haemolysis. Environ Res 3: 1–13.PubMedCrossRefGoogle Scholar
  18. Trosic I, Horvat D, Racis J (1986) The effect of asbestos. Per Biol 88: 269–76Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1994

Authors and Affiliations

  • Robert Englman
    • 1
  1. 1.Soreq N.R.C.YavneIsrael

Personalised recommendations