Interrelationship between hemolysis and lipid peroxidation of human erythrocytes induced by silicic acid and silicate dusts

Our plain-English summary of Interrelationship between hemolysis and lipid peroxidation of human erythrocytes induced by silicic acid and silicate dusts, by S.V. Singh, Q. Rahman (Journal of Applied Toxicology, 1987).

The study

• Authors: S.V. Singh, Q. Rahman
• Journal: Journal of Applied Toxicology
• Published: 1987;7(2):91-6
• Cited by: 13 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Silicic acid and silicate dusts (slate dust and chrysotile asbestos) cause hemolysis of erythrocytes in vitro. The peroxidation of polyunsaturated fatty acids (PUFA) of erythrocyte membrane lipids is also enhanced by incubating the erythrocytes with silicic acid and silicate dusts in in vitro. Hemolysis of erythrocytes elicited by silicic acid and silicate dusts is inhibited significantly by polyvinyl-pyrrolidone and dipalmitoyl lecithin (DPL). These agents, however, have no effect on silicic acid and silicate dust induced peroxidation of erythrocyte membrane lipids. On the other hand, peroxidation of erythrocyte membrane lipids, induced by silicic acid and silicate dusts, is inhibited almost completely by adding superoxide dismutase and catalase to the incubation system, whilst the hemolysis of erythrocytes induced by silicic acid and silicate dusts is unaffected by these agents. Similarly the lysis of erythrocytes, induced by silicic acid and silicate dusts, proceeds at a much faster rate than silicic acid and silicate dust induced lipid peroxidation. These results indicate that silicic acid and silicate dust induced hemolysis and lipid peroxidation represent two independent processes.

In plain English

This was a laboratory study at the Industrial Toxicology Research Center in Lucknow, India, using red blood cells from human volunteers. The authors exposed the cells to UICC chrysotile asbestos, slate dust and silicic acid. They measured two effects: bursting of the cells (hemolysis), and damage to fats in the cell membranes (lipid peroxidation, measured as malonaldehyde). Chrysotile at 3 mg/ml burst up to 95% of cells, and this was complete within 10 minutes. Slate dust at 10 mg/ml reached 80% over 2 hours. With 5 mg of chrysotile, malonaldehyde rose 94% above control in intact cells and 120% in a broken-cell preparation. Slate dust gave smaller rises (29% and 38%). After 10 minutes, by which time chrysotile and silicic acid had burst up to 90% of cells, malonaldehyde was only 2% above the basal level. Dipalmitoyl lecithin and polyvinyl pyrrolidone reduced hemolysis, but superoxide dismutase and catalase did not. Superoxide dismutase was the most effective agent against lipid peroxidation. The authors concluded that hemolysis and lipid peroxidation caused by these dusts are two independent processes.

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 (erythrocytes) from human volunteers, collected at the Blood Bank of K.G. Medical College, Lucknow, India. The number of donors is not stated.
• Exposure: UICC chrysotile asbestos (particle size below 30 micrometres), slate dust from Mandasaur, India (reduced to below 5 micrometres), and silicic acid solution
• Main results:
  • Maximum hemolysis was 95% with chrysotile at 3 mg/ml and 80% with slate dust at 10 mg/ml
  • Chrysotile hemolysis was complete within 10 minutes. Slate dust hemolysis increased over 2 hours.
  • Silicic acid (90 micromolar) caused up to 90% lysis of red blood cells within 10 minutes
  • At 25 micromolar silicic acid, malonaldehyde rose 50% (intact cells) and 22% (low-speed supernatant of hemolysate) over the basal level. Higher concentrations inhibited malonaldehyde formation.
  • 5 mg of chrysotile increased malonaldehyde by 94% in intact cells and by 120% in the low-speed supernatant of the hemolysate, compared with control
  • With slate dust, malonaldehyde increased 29% in intact cells and 38% in the low-speed supernatant over basal level. Chrysotile was more effective than slate dust at stimulating lipid peroxidation.
  • With chrysotile and silicic acid, malonaldehyde production was only 2% over basal level after 10 minutes, when lysis had already reached up to 90%
  • Dipalmitoyl lecithin and polyvinyl pyrrolidone inhibited hemolysis caused by silicic acid, chrysotile and slate dust
  • Superoxide dismutase and catalase did not inhibit hemolysis
  • Superoxide dismutase was the most effective agent in inhibiting dust-induced lipid peroxidation
• The authors' conclusion: The authors concluded that hemolysis and lipid peroxidation induced by silicic acid and silicate dusts are two independent processes. In the discussion they also wrote that a possible relationship between the two may exist, and that the sites of the two effects appear to differ.
• Limitations the authors state:
  • The authors could not establish whether lipid peroxidation is the definitive factor in dust-induced hemolysis
  • The authors could not determine the reason for the biphasic response to silicic acid
  • The suggestion that differences in chemical composition and lattice structure explain the different behaviour of chrysotile and slate dust was not supported by data from this study
  • The authors could not rule out that dust interaction with membrane constituents initiates lipid peroxidation, and said further studies are needed

Topics

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

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

Related studies

• Plasma lipid peroxides among workers exposed to silica or asbestos dusts — A.A. Kamal, A. Gomaa, et al. (1989)
• Haemolytic activity of asbestos and other mineral dusts — G. Macnab, J.S. Harington (1967)
• 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)
• A comparative study on the hemolytic action of short asbestos fibers on human, rat, and sheep erythrocytes — J.P. Pelé, R. Calvert (1983)
• Dusts causing pneumoconiosis generate .OH and produce hemolysis by acting as Fenton catalysts — T.P. Kennedy, R. Dodson, et al. (1989)
• The prevention of asbestos-induced hemolysis — R. Desai, P. Hext, et al. (1975)

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