Red blood cell damage by wollastonite: in vitro study

Our plain-English summary of Red blood cell damage by wollastonite: in vitro study, by M. Aslam, M.J. Arif, O. Rahman (Journal of Applied Toxicology, 1995).

The study

• Authors: M. Aslam, M.J. Arif, O. Rahman
• Journal: Journal of Applied Toxicology
• Published: 1995;15(1):27-31
• Cited by: 10 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Asbestos is known to cause lung diseases in occupationally exposed workers. These properties have restricted its use. Industries have been exploring the possibility of other mineral fibres to replace the asbestos. In this direction, wollastonite has gained great attention owing to its high thermal resistance. In the present paper, the toxicity of three samples of Indian wollastonite was compared to that of chrysotile. Dust suspensions were added to the red blood cell suspensions to obtain a final dust concentration of 1.0-5.0 mg ml-1 in the system. The wollastonite varieties were found to have smaller haemolytic potential in human red blood cells than that of chrysotile in vitro. Chrysotile also was more effective in inducting peroxidative damage of polyunsaturated fatty acid (PUFA) than wollastonites in the present system. The peroxidative damage of PUFA and the haemolysis were both time and dose dependent. A higher value of malonaldehyde (a lipid peroxidation product) formation in low-speed supernatant of haemolysate was observed than in the intact cells. As the free-radical scavengers vitamin E and reduced glutathione prevent haemolysis and lipid peroxidation, these data are consistent with the involvement of lipid peroxidation in the haemolytic process.

In plain English

This was a laboratory (in vitro) study from the Industrial Toxicology Research Centre in Lucknow, India. The authors exposed human red blood cells from four healthy blood-bank donors to three commercial Indian wollastonite samples (Kemolit ASB-3, Kemolit-N and Kemolit A-60) and compared them with chrysotile asbestos. They measured haemolysis (bursting of the cells) and lipid peroxidation (oxidative damage to membrane fats, measured as malonaldehyde). Chrysotile caused haemolysis that levelled off by 10 minutes. The wollastonites caused less haemolysis, which was still rising at 120 minutes. Among the wollastonites, Kemolit A-60 caused the most haemolysis and Kemolit ASB-3 the least. All four dusts increased lipid peroxidation, but the wollastonites less than chrysotile. Damage was lower in intact cells than in the low-speed supernatant of broken cells. Bovine serum albumin was the agent that best reduced haemolysis. Vitamin E best reduced lipid peroxidation. The authors concluded that the protection by vitamin E and reduced glutathione is consistent with lipid peroxidation being involved in haemolysis. The study tested cells, not exposed people.

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 experiment on human red blood cells
• Who was studied: Red blood cells from blood collected from four healthy donors at a local blood bank in Lucknow, India
• Exposure: Three commercial Indian wollastonite samples (Kemolit ASB-3, Kemolit-N, Kemolit A-60) from Wolkem Pvt. Ltd, compared with chrysotile from Andhra Pradesh Mining Corporation Ltd. Particle size was below 30 micrometres (printed as "30 pm"). Lipid peroxidation tests used 1.0 to 5.0 mg per ml of dust. Haemolysis tests went up to 15 mg per ml.
• Main results:
  • Chrysotile-induced haemolysis reached a plateau by 10 minutes.
  • Wollastonite-induced haemolysis had not plateaued by 120 minutes and was lower than that caused by chrysotile.
  • The wollastonites caused maximum lysis at 10 mg per ml after 2 hours. Chrysotile caused maximum lysis at 2.85 mg per ml after 10 minutes.
  • Among the wollastonites, Kemolit A-60 produced the greatest haemolysis and Kemolit ASB-3 the least.
  • Lipid peroxidation caused by the wollastonite samples was lower than that caused by chrysotile, in both intact cells and the low-speed supernatant of haemolysate. In intact cells at 5.0 mg per ml, malonaldehyde (nmol per mg protein over 2 hours) was 0.5391 for chrysotile, 0.4537 for Kemolit A-60, 0.4093 for Kemolit-N and 0.3575 for Kemolit ASB-3.
  • Oxidative damage was lower in intact cells than in the low-speed supernatant. For example, at 5.0 mg per ml of chrysotile, malonaldehyde was 0.5391 in intact cells and 1.068 in the supernatant (nmol per mg protein over 2 hours).
  • Haemolysis and lipid peroxidation were both time dependent. At 5 mg per ml and 120 minutes, haemolysis was 75.19% for Kemolit A-60, 68.09% for Kemolit-N and 64.92% for Kemolit ASB-3.
  • Five agents inhibited haemolysis caused by chrysotile and the wollastonites. In order of effectiveness: bovine serum albumin, then polyvinyl pyrrolidone, vitamin E, reduced glutathione and dipalmitoyl lecithin.
  • Vitamin E was the most effective agent against lipid peroxidation, followed by reduced glutathione and bovine serum albumin. Polyvinyl pyrrolidone and dipalmitoyl lecithin did not suppress it.
• The authors' conclusion: The authors concluded that the inhibition of haemolysis by vitamin E and reduced glutathione is consistent with lipid peroxidation being involved in the haemolytic process.

Topics

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

Medical terms in this study, explained in our Lexicon: Wollastonite, Chrysotile, Glutathione (GSH).

Related studies

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• Pulmonary toxicity of wollastonite in vivo and in vitro — E. Tátrai, Z. Kováciková, et al. (2004)
• Wollastonite exposure and lung fibrosis — M.S. Huuskonen, A. Tossavainen, et al. (1983)
• Fibrogenic effect of wollastonite compared with asbestos dust and dusts containing quartz — E.E. McConnell (1995)
• Cytotoxicity of respirable dusts from industrial minerals: comparison of two naturally occurring and two man-made silicates — D. Nadeau, L. Fouquette-Couture, et al. (1987)
• Biological reactivity of calcium silicate composites--in vitro studies — J. Hunt, F.D. Pooley, et al. (1981)

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