Mutagenesis of Escherichia coli (CSH50) by asbestos

Our plain-English summary of Mutagenesis of Escherichia coli (CSH50) by asbestos, by M.G. Cleveland (Proceedings of the Society for Experimental Biology and Medicine, 1984).

The study

• Author: M.G. Cleveland
• Journal: Proceedings of the Society for Experimental Biology and Medicine
• Published: 1984;177(2):343-6
• Cited by: 5 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

The mutagenic character of richterite asbestos was detected in Escherichia coli strain CSH50, using a modified Ames test. Two sets of experimental plates which contained naturally occurring asbestos were used, to one set of which S-9 rat liver homogenate was added. Control plates contained no asbestos. Mutant colonies appeared in significantly greater frequency in both experimental sets as compared with controls, and experimental plates with rat liver homogenate contained the greatest number of mutant colonies. It is postulated that enzymes contained in rat liver metabolize some unknown mutagen introduced with the natural asbestos sample other than the inert richterite fibers themselves. This finding, together with the unlikelihood that bacterial cell walls could be easily penetrated by asbestos fibers, tends to negate fiber penetration as the mechanism of mutagenesis. The mutagenic mechanism operative in E. coli (CSH50) may be applicable to animal cell systems.

In plain English

This laboratory study tested whether asbestos causes mutations in bacteria. It used a modified Ames test with the bacterium Escherichia coli strain CSH50, which the author chose because its intact cell wall should hinder fibers from physically piercing the cells. The asbestos was richterite, an amphibole described as an alkali-rich analogue of tremolite, taken from natural rock in the Allamore Talc District of west Texas and added at 0.01 g per plate. Some plates also received S-9 rat liver homogenate, which supplies enzymes. Four trials of 12 plates each were run. Average mutant colony counts were 14.3 on control plates without liver homogenate, 15.4 on controls with it, 36.1 on plates with asbestos alone, and 150.1 on plates with asbestos plus liver homogenate. All comparisons between asbestos and control sets gave P values below 0.001. The author concluded that the natural richterite sample was mutagenic for this bacterium under these conditions. The author also concluded that fiber penetration was likely not the main mechanism, with impurities in the sample or some other mechanism more likely, but stated that fiber penetration was not ruled out.

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 bacterial mutagenicity experiment (modified Ames test), not a study of people or animals
• Who was studied: The bacterium Escherichia coli strain CSH50, tested in four trials of 12 petri plates each: 4 control plates, 4 plates with asbestos, and 4 plates with asbestos plus rat liver homogenate per trial
• Exposure: Richterite asbestos, an amphibole described as an alkali-rich analogue of tremolite, from natural rock in the Allamore Talc District of west Texas. It was ground by hand, autoclaved, and added at 0.01 g per plate, with or without S-9 rat liver homogenate.
• Main results:
  • Mutant colonies appeared more often in both sets of plates containing asbestos than in the control plates, and most often in the asbestos plus rat liver homogenate set
  • Average mutant colonies per plate: 14.3 for controls without liver homogenate, 15.4 for controls with liver homogenate, 36.1 for asbestos alone (experimental set 1), and 150.1 for asbestos plus liver homogenate (experimental set 2)
  • Student t tests gave P values below 0.001 in all comparisons between the experimental (asbestos) sets and the control set
• The authors' conclusion: The author concluded that richterite asbestos in its natural state was mutagenic for E. coli CSH50 under these experimental conditions. The author also concluded that fiber penetration was likely not the primary mechanism in E. coli and that at least one other mechanism, possibly impurities in the sample, was operating.
• Limitations the authors state:
  • The author stated that the study does not eliminate the possibility that the mutations resulted from fiber penetration
  • The author stated that the study did not rule out heavy metals in the asbestos as responsible, and that hydrocarbons or other undetermined impurities in the natural sample could account for the mutagenic effect

Topics

Medical terms in this study, explained in our Lexicon: richterite, naturally occurring asbestos (NOA).

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