Attenuation of oxidative stress and chromosomal aberrations in cultured macrophages and pulmonary cells following self-sustained high temperature synthesis of asbestos

Our plain-English summary of Attenuation of oxidative stress and chromosomal aberrations in cultured macrophages and pulmonary cells following self-sustained high temperature synthesis of asbestos, by S. La Maestra, R.T. Micale, M. Ferretti, et al (Scientific Reports, 2020).

The study

• Authors: S. La Maestra, R.T. Micale, M. Ferretti, A. Izzotti, L. Gaggero
• Journal: Scientific Reports
• Published: 2020;10(1):8581
• Cited by: 9 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Inhalation of asbestos fibres can cause lung and pleural diseases in humans and constitutes a severe public health threat worldwide. The aim of the present study was to assess the biological effects induced in both pulmonary cells (A549) and monocyte/macrophage (RAW 264.7) cell lines by combustion slags obtained from asbestos through a self-sustained high-temperature synthesis (SHS) reaction. The SHS reaction involves rapid thermal treatment and displays great ability to neutralise asbestos. Cytotoxicity, redox status imbalance, lipid peroxide production, DNA strand breaks (comet assay) and chromosomal aberrations (cytokinesis block micronucleus test) were evaluated in cells exposed either to untreated asbestos fibres or to grinded SHS-generated slags of different granulometry, tested in cultured cells at varying doses and for varying exposure times. Our results show that asbestos fibres cause redox status imbalance, especially in monocyte/macrophage cell lines. Moreover, they promote lipid peroxidation and trigger genomic alterations. When the cells were exposed to slag powders, which are the products of SHS asbestos treatment, generation of lipid peroxides and induction of DNA strand breaks still persisted, due to the high content in iron and other metals detected in these samples. However, there was an attenuation of redox status imbalance and an absence of chromosomal aberrations, which probably reflects the loss of the asbestos fibrous structure following SHS reaction, as demonstrated by electron microscopy analyses. In conclusions, SHS-treated asbestos wastes can potentially have deleterious health effects due to the oxidative stress induced by inhaled powders but they loose the asbestos ability to induce chromosomal alterations.

In plain English

This laboratory study tested whether a fast high-temperature treatment called self-sustained high-temperature synthesis (SHS) changes how asbestos waste affects cells grown in culture. No people or animals were studied. The authors ground the treated slag into powders of three grain sizes (under 10, under 3 and under 2 micrometres). They compared these powders with untreated chrysotile asbestos in two cell lines: A549, a human cell line derived from lung carcinoma, and RAW 264.7, a mouse macrophage line. Electron microscopy showed that the asbestos fibrous structure completely disappeared after treatment. Untreated chrysotile reduced cell survival at the highest doses and longest exposure times. It also significantly increased micronuclei, a sign of chromosome damage, in both cell lines. The slag powders still significantly raised lipid peroxidation, a marker of oxidative damage, and caused DNA damage, which was greater with smaller particles. The smallest powders raised micronuclei about 1.8-fold and 1.9-fold, but this was not statistically significant. The authors concluded that the slag powders can cause some harmful effects through oxidative stress but did not significantly increase micronuclei.

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) cell culture experiment comparing powders from SHS-treated asbestos waste with untreated chrysotile, which served as the positive control
• Who was studied: Two cultured cell lines: A549, a human alveolar basal epithelial cell line derived from lung carcinoma, and RAW 264.7, a mouse monocyte/macrophage cell line
• Exposure: SHS-treated asbestos-containing waste (loose fibres and asbestos cement), hand-ground and sieved into fractions under 10, under 3 and under 2 micrometres (samples A, B and C), compared with pure chrysotile (sample D). Doses ranged from 0.33 to 15.62 micrograms per square centimetre of culture surface.
• Main results:
  • After SHS treatment, scanning electron microscopy showed that the asbestos fibrous structure completely disappeared; the chrysotile broke down into newly formed olivine.
  • The main components of the 5 analysed slag samples were iron oxide, aluminium oxide, silica and magnesium oxide.
  • Untreated asbestos reduced viability of both cell lines at the highest concentrations and longest exposure times. For example, viability fell to 45.5% of controls in RAW 264.7 cells at 7.58 micrograms per square centimetre for 72 h, and to 54.9% in A549 cells at 15.62 for 72 h.
  • In A549 cells, toxicity of the under 3 and under 2 micrometre slag powders increased as particle size decreased and as contact time increased.
  • RAW 264.7 macrophage cells were more susceptible than A549 cells to redox (oxidative balance) changes caused by both slag powders and untreated asbestos.
  • Slag powders significantly increased lipid peroxidation products (TBARS) in A549 cells (P less than 0.01) and, to a greater extent, in RAW 264.7 cells (P less than 0.001).
  • In A549 cells, lipid peroxidation caused by asbestos was slightly but significantly higher than that caused by slag powders of any size (P less than 0.05).
  • In the comet assay (DNA strand breaks), DNA damage was strongly and inversely correlated with particle diameter.
  • At lower doses, untreated asbestos caused considerably more DNA damage than slag powders. At the highest doses, asbestos-related DNA damage was of the same order as that caused by the smallest slag particles.
  • Asbestos significantly increased micronuclei (a marker of chromosome damage). The rate was 9.59 per 1000 cells versus 1.81 in untreated A549 cells, and 7.60 versus 0.82 in untreated RAW 264.7 cells (P less than 0.05).
  • The smallest slag particles (under 2 micrometres) increased micronuclei 1.8-fold in A549 cells and 1.9-fold in RAW 264.7 cells, but these differences were not statistically significant.
• The authors' conclusion: The authors concluded that SHS-treated slag powders can cause some deleterious effects due to oxidative stress, but did not significantly increase the number of micronuclei. They attributed this probably to the loss of the asbestos fibrous structure.

Topics

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

Medical terms in this study, explained in our Lexicon: Oxidative Stress, Macrophage, Comet Assay.

Related studies

• The Self-sustained High temperature Synthesis (SHS) technology as novel approach in the management of asbestos waste — L. Gaggero, M. Ferretti (2018)
• Internalization of Libby amphibole asbestos and induction of oxidative stress in murine macrophages — D.J. Blake, C.M. Bolin, et al. (2007)
• Specificity of asbestos-induced chromosomal aberrations in short-term cultured human mesothelial cells — K. Olofsson, J. Mark (1989)
• Raw single-wall carbon nanotubes induce oxidative stress and activate MAPKs, AP-1, NF-kappaB, and Akt in normal and malignant human mesothelial cells — M. Pacurari, X.J. Yin, et al. (2008)
• Patterns of 8-hydroxydeoxyguanosine formation in DNA and indications of oxidative stress in rat and human pleural mesothelial cells after exposure to crocidolite asbestos — H. Fung, Y.W. Kow, et al. (1997)
• Activation of p38 MAP kinase by asbestos in rat mesothelial cells is mediated by oxidative stress — W.A. Swain, K.J. O'Byrne, et al. (2004)

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