Aryl hydrocarbon hydroxylase induction in mitogen-stimulated lymphocytes by benzanthracene or cigarette tars adsorbed to asbestos fibers

Our plain-English summary of Aryl hydrocarbon hydroxylase induction in mitogen-stimulated lymphocytes by benzanthracene or cigarette tars adsorbed to asbestos fibers, by T.L. McLemore, W.T. Jenkins, M.S. Arnott, et al (Cancer Letters, 1979).

The study

• Authors: T.L. McLemore, W.T. Jenkins, M.S. Arnott, N.P. Wray
• Journal: Cancer Letters
• Published: 1979;7(2-3):171-7
• Cited by: 10 articles, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

Human mitogen-stimulated lymphocytes, cultured in the presence of amosite asbestos (AS), demonstrated a slight increase in aryl hydrocarbon hydroxylase (AHH) activity compared with non-induced (control) cultures (P = 0.005). A much greater increase in enzyme activity occurred following addition of the inducers benzanthracene (BA) or cigarette tars (CT) to cell cultures (P less than 0.001 in both instances). Significant enzyme induction also occurred when AS fibers were first preincubated with CT or BA, washed with acetone, then added to lymphocyte cultures (P less than 0.003 in all instances). This increase in AHH activity was not as great, however, as the induction observed when BA or CT was added to cell cultures. No further increase in enzyme activity was noted when AS and CT or AS and BA were simultaneously added to culture lymphocytes (P greater than 0.070 in all instances). The results demonstrate that polycyclic aromatic hydrocarbons (PAH), such as BA and other components of CT, are adsorbed and transported by amosite AS particles. These AS-PAH complexes are capable of inducing AHH in cultured human lymphocytes.

In plain English

This was a laboratory experiment on cells, not a study of people's health. The authors grew white blood cells (lymphocytes) from healthy volunteers and measured aryl hydrocarbon hydroxylase (AHH). They describe AHH as an enzyme that converts components of cigarette smoke into products with greater mutagenic and carcinogenic potential. Cells were exposed to amosite asbestos, to the chemical benzanthracene, to cigarette tars, or to amosite fibers first soaked in benzanthracene or tars and then washed with acetone. Amosite alone raised enzyme activity slightly (mean 100 versus 83 milliunits per million cells in untreated cultures, 17 donors). Benzanthracene and tars raised it much more. Fibers pre-soaked in either chemical also raised activity, though less than the chemicals added directly. Adding asbestos together with either chemical gave no further increase. The authors concluded that such chemicals can stick to amosite particles, which then carry them into cells. They suggested asbestos might act similarly in the lung, but said this was a hypothesis they had begun testing in animal studies.

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 (in vitro) experiment measuring AHH, an enzyme the authors describe as converting components of cigarette smoke into intermediate products with enhanced mutagenic and carcinogenic potential, in cultured human blood lymphocytes
• Who was studied: Mitogen-stimulated lymphocytes from the blood of normal healthy volunteers; each comparison used cells from 7, 8 or 17 donors
• Exposure: Amosite asbestos at 50 micrograms per ml; benzanthracene at 20 micromolar; cigarette tars at 6 micrograms per ml. Also amosite pre-incubated with benzanthracene or cigarette tars, then washed with acetone, added at 50 micrograms per ml, and amosite added together with either chemical. Fiber length is given as 5 to 100 micrometres in the methods and approximately 5 to 70 micrometres in the table footnote.
• Main results:
  • Amosite alone slightly increased AHH activity compared with untreated control cultures: mean 100 plus or minus 9 versus 83 plus or minus 6 milliunits per million lymphoblasts, P = 0.005, 17 donors. The authors suggested this was probably due to trace amounts of inducing chemicals remaining on the fibers after washing.
  • Benzanthracene and cigarette tars each produced a much greater increase. For benzanthracene the mean was 981 plus or minus 92, compared with 100 plus or minus 9 for asbestos alone (P less than 0.001, 17 donors). Tar-induced activity (966 plus or minus 77) did not differ significantly from benzanthracene-induced activity (1178 plus or minus 122) in 8 donors (P = 0.061).
  • Amosite fibers pre-incubated with benzanthracene or tars and washed with acetone still increased AHH activity over asbestos alone. Benzanthracene-treated fibers gave 447 plus or minus 83 versus 96 plus or minus 16 (P = 0.003, 7 donors). Tar-treated fibers gave 284 plus or minus 29 versus 123 plus or minus 12 (P less than 0.001, 8 donors).
  • Activity with pre-treated fibers was lower than with the chemicals added directly. Benzanthracene-treated fibers gave 447 plus or minus 83 versus 887 plus or minus 157 with benzanthracene alone (7 donors). Tar-treated fibers gave 284 plus or minus 29 versus 966 plus or minus 77 with tars alone (P less than 0.001, 8 donors).
  • Adding amosite at the same time as either chemical gave no further increase. Benzanthracene alone gave 887 plus or minus 157 versus 833 plus or minus 170 with asbestos added (P = 0.213, 7 donors). Tars alone gave 966 plus or minus 77 versus 896 plus or minus 85 with asbestos added (P = 0.073, 8 donors).
  • Fluorometric measurement showed the benzanthracene bound to the asbestos particles was equivalent to a final concentration of approximately 2.5 micromolar. The authors said this was close to the 50% effective dose and consistent with the induction seen with pre-treated fibers.
• The authors' conclusion: The authors concluded that polycyclic aromatic hydrocarbons such as benzanthracene and components of cigarette tars can be adsorbed to amosite particles, which then act as carriers transporting these compounds into cells. They also concluded that induction by the coated particles reflected the amount of chemical bound to them, not a synergistic interaction between asbestos and the chemicals. They suggested asbestos might play a similar role in the airways of the lung.
• Limitations the authors state:
  • The authors said further investigation would be needed before the exact mechanisms of asbestos's harmful effects could be defined.
  • The proposed role in the lung was a hypothesis the authors had not yet tested; they reported that animal studies had recently been started to test it.

Topics

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

Related studies

• Aryl hydrocarbon hydroxylase in asbestos workers — S.M. Naseem, P.V. Tishler, et al. (1978)
• Effect of asbestos fibers on aryl hydrocarbon hydroxylase and aminopyrine N-demethylase activities of rat liver microsomes — C. Kandaswami, M. Rahimtula, et al. (1986)
• In vitro depression of human lymphocyte mitogen response (phytohaemagglutinin) by asbestos fibres — R.G. Barbers, W.W. Shih, et al. (1982)
• Investigations on the effects of chronic cigarette-smoke inhalation in Syrian golden hamsters — W. Dontenwill, H.J. Chevalier, et al. (1973)
• A study of the synergistic interaction of asbestos fibers with cigarette tar extracts for the generation of hydroxyl radicals in aqueous buffer solution — A. Valavanidis, H. Balomenou, et al. (1996)
• Biological effects of asbestos fibers on human cells in vitro--especially on lymphocytes and neutrophils — A. Ueki (2001)

Browse more research in Cancer Letters, or return to medical research.