Cytotoxic and genotoxic effects of calcium silicates on human lymphocytes in vitro

Our plain-English summary of Cytotoxic and genotoxic effects of calcium silicates on human lymphocytes in vitro, by M. Aslam, N. Fatima, Q. Rahman (Mutation Research, 1993).

The study

• Authors: M. Aslam, N. Fatima, Q. Rahman
• Journal: Mutation Research
• Published: 1993;300(1):45-8
• Cited by: 1 article, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Calcium silicate has been considered as a possible replacement for asbestos due to its heat and fire resistance. We describe the cytotoxic and genotoxic potential of calcium silicate using peripheral human blood lymphocytes. Calcium silicates at concentrations of 10 and 100 micrograms/ml significantly increased the frequencies of chromosomal aberrations (CAs) and sister-chromatid exchanges (SCEs). The increases in CAs and SCEs were dose-dependent, though not linearly. A significant decrease in the proliferation rate index was observed with increased dose of calcium silicates. The induction of chromatid-type aberrations indicates that the clastogenic activity of calcium silicate is S-phase-dependent.

In plain English

This laboratory study tested whether three calcium silicate products, Kemolit ASB-3, Kemolit-N and Kemolit A-60, damage human white blood cells. Calcium silicate had been considered a possible substitute for asbestos because of its heat resistance. Lymphocytes from the blood of one 30-year-old male non-smoking volunteer were grown in culture with the dusts at 0.1 to 100 micrograms per millilitre. At 10 and 100 micrograms per millilitre, all three samples significantly increased the share of cells with chromosome damage. For the chromosome-damage test, 100 dividing cells (metaphases) were scored. Counting gaps, Table 1 lists 4% of these with damage in control cultures and 11%, 13% and 15% at the highest dose. Sister-chromatid exchanges, another sign of genetic damage, also rose significantly at those doses. For Kemolit A-60, for example, they rose from 7.9 to 15.7 per cell. Cell division slowed as the dose rose. The increases followed the dose, but not in a straight line. Most damage was of the chromatid type. The authors concluded that calcium silicates induced cell cycle delay and genotoxicity. The experiments were done on cultured cells, not on 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 cultured human peripheral blood lymphocytes, measuring chromosomal aberrations, sister-chromatid exchanges and proliferation rate index
• Who was studied: Lymphocytes from the blood of a single donor, a 30-year-old male non-smoking volunteer who was not on any medication, at the Industrial Toxicology Research Centre, Lucknow, India
• Exposure: Three calcium silicate samples (Kemolit ASB-3, Kemolit-N and Kemolit A-60) from Wolkem Pvt. Ltd., Udaipur, India. They were about 97% pure, had particle size less than 30 micrometres, and were added to cultures at 0.1 to 100 micrograms per millilitre. Control cultures received medium only.
• Main results:
  • All three calcium silicates significantly increased the frequency of aberrant metaphases at 10 and 100 micrograms per millilitre compared with controls (p less than 0.005, chi-square test). These are percentages of the 100 metaphases scored for the chromosome-aberration test, with gaps included. Table 1 lists 4% aberrant metaphases in controls. At 10 micrograms per millilitre it lists 9% (ASB-3), 10% (Kemolit-N) and 12% (A-60). At 100 micrograms per millilitre it lists 11%, 13% and 15%.
  • The response followed the dose, though not linearly. Gap-type aberrations were the most common type. Chromatid-type aberrations, rather than chromosome-type, were generally observed.
  • Sister-chromatid exchanges per metaphase, analysed in 50 second-division cells, rose significantly at the higher concentrations (p less than 0.05, Student's t-test, at 10 and 100 micrograms per millilitre). The rise from control to 100 micrograms per millilitre was 8.2 to 14.0 for Kemolit ASB-3, 7.8 to 14.8 for Kemolit-N, and 7.9 to 15.7 for Kemolit A-60.
  • The proliferation rate index, determined from 200 metaphases, fell as concentration rose. From control to 100 micrograms per millilitre it fell from 2.39 to 1.88 for Kemolit ASB-3, from 2.41 to 1.89 for Kemolit-N, and from 2.39 to 1.83 for Kemolit A-60. No marked effect on proliferation was seen at lower concentrations.
• The authors' conclusion: The authors concluded that calcium silicates significantly induced cell cycle delay and genotoxicity in these cells. They also concluded that the predominance of chromatid-type aberrations indicates the chromosome-damaging effect most likely occurs by an S-phase-dependent mechanism.
• Limitations the authors state:
  • The authors state that their data do not allow them to assess the specific stage of the cell cycle at which the delay occurred.

Topics

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

Related studies

• Biological reactivity of calcium silicate composites--in vitro studies — J. Hunt, F.D. Pooley, et al. (1981)
• The biological reactivity of calcium silicate composites: in vivo studies — R.J. Richards, T.D. Tetley, et al. (1981)
• Chromosomal aberrations induced by chrysotile and crocidolite in human lymphocytes in vitro — F. Valerio, M. de Ferrari, et al. (1983)
• Cell toxicity, hemolytic action and clastogenic activity of asbestos and its substitutes — K. Koshi, N. Kohyama, et al. (1991)
• Reduction of chrysotile asbestos-induced genotoxicity in human peripheral blood lymphocytes by garlic extract — K. Bhattacharya, S. Yadava, et al. (2004)
• Genotoxic effects of asbestos in humans — M. Dusinská, A. Collins, et al. (2004)

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