Do Carbon Nanotubes and Asbestos Fibers Exhibit Common Toxicity Mechanisms?
Abstract
:1. Introduction
2. Do Asbestos and CNTs Have the Same Mechanism of Pathogenicity?
2.1. Oxidative Stress Theory
2.2. Chromosome Tangling
2.3. Adsorption Theory
2.4. Chronic Inflammation
3. Toxicogenomics Analysis of Altered Gene Expression Due to Asbestos and CNT Exposure
4. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Acknowledgments
Conflicts of Interest
References
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Fiber Type | Size | Test System | Key Findings | Refs. |
---|---|---|---|---|
Crocidolite asbestos | Length > 5 µm and diameter < 2 µm | 8-week-old transgenic F344 rats bearing multiple copies of λlacI shuttle vectors. Mutation frequencies after the administration of 2 and 5 mg of crocidolite were analyzed in DNA of omentum, a relevant target tissue for mesothelioma carcinogenesis. | Reactive oxygen or nitrogen species in crocidolite asbestos fibers induces mutagenesis. | [104] |
Crocidolite asbestos | Mean length 10 µm and mean diameter 0.21 µm | Human bronchial epithelial cancer (A549) cell line was exposed to asbestos, silica and TiO2 particles to analyze ROS, apoptosis and DNA double-strand breaks. | Crocidolite has a greater carcinogenic potential than silica and TiO2, judged by its ability to cause sustained genomic instability in normal lung cells. | [100] |
Crocidolite fibers | Length 3.2 ± 1.0 µm and diameter 0.22 ± 0.01 µm | Hamster hybrid (AL) cells, containinga standard set of CHO-K1 chromosomes and a single copy of humanchromosome 11 exposed to crocidolite fiber for various periods of time. | Extra-nuclear targets play an essential role in the initiation of oxidativedamage in fiber mutagenesis in mammalian cells. | [105] |
Crocidolite fibers | Length > 5 µm and diameter < 3 µm | Transgenic male LacI mice to study the mutagenesis potential of asbestos crocidolite. Mice were exposed to an aerosol containing 5.75 mg/m3 crocidolite dust for 6 hr/day and 5 consecutive days. | Significant increase of the mutant frequency of lung DNA after nose-only fiber inhalation. | [106] |
Chrysotile and Crocidolite asbestos | Length > 4 µm and diameter < 2 µm | Immortalized human SAE cells were treated with chrysotile or crocidolite at concentrations of 0.5, 1, 2 and/or 4 µg/cm2 for 12, 24 or 48 h. | Asbestos may initiate mitochondria-associated ROS, which mediate asbestos-induced nuclear mutagenic events and inflammatory signaling pathways in exposed cells. | [107] |
Fiber Type | Size | Test System | Key Findings | Refs. |
---|---|---|---|---|
SWCNT and MWCNT | SWCNT: (D) < 2 nm, (L) 4–15 μm MWCNT: (D) 10–30 nm, (L) 1–2 μm | Urinary mutagenicity study in male Fischer-344 rats by oral administration with a single dose of 50 mg/kg body weight of SWCNT or MWCNT. | No increase in urinary mutagenicity were observed in rat using Ames test. SWCNTs and MWCNTs were deposited in the lung and induced an acute lung and systemic effect, which was more pronounced in the MWCNT exposure. | [123] |
SWCNT and MWCNT | SWCNT: (D) 0.8–1.2 nm, (L) 0.1–1 μm MWCNT: (D) ~80 nm, (L) 10–20 μm | C57BL/6 mice were exposed by pharyngeal aspiration to vehicle, ultrafine carbon black, SWCNTs or MWCNTs at a dose of 40 μg per mouse and sacrificed 4 h postexposure. | Gene expression in lung and blood: Upregulation of genes involved in inflammation, oxidative stress, coagulation, tissue remodeling. Increased percentage of polymorphonuclear leucocytes (PMN) in blood and bronchoalveolar lavage (BAL). | [124] |
SWCNT | (D) 10–30 nm, (L) 2–3 μm | Male CD-ICR mice were exposed to SWCNTs using single tail vein injection at a dose of 40 μg/mouse, 200 μg/mouse and 1.0 mg/mouse. Accumulation determination and toxicological assays were carried out after 90 days post-exposure. | Inflammation: dose-dependent thickening of the alveolar lining. Particles deposition were observed even after 3 months. | [79] |
SWCNT | Mean diameter 1.8 nm, Medium length 4.4 μm | SWCNTs exposure to rat in single instillation (1.0 mg/kg body weight) or repeated intratracheal instillation (0.2 mg/kg body weight) once a week for five weeks. | Inflammatory response (hemorrhage in the alveolus, infiltration of alveolar macrophages and neutrophiles), but no DNA damage, in the lungs in rats. SWCNTs were not genotoxic in the comet assay following intratracheal instillation in rats. | [125] |
SWCNT and MWCNT | SWCNT: (D) 1.2–1.5 nm (L) 2–5 µm MWCNT: (D) 10–30 nm (L) 0.5–50 µm | The mouse macrophage cell line RAW 264.7 were treated with different concentrations of CNTs for 24, 48 or 72 h for cytotoxicity, genotoxicity analysis and detection of ROS. | CNTs exposure increase ROS production and are cyto- and genotoxic to mouse macrophage cell line. Due to CNTs exposure necrosis and chromosomal aberrations were detected, although no inflammatory responses were observed. | [126] |
MWCNT | (D) 10–15 nm, ~20 μm | Eight-week-old rats were subjected to whole-body exposure to low (0.01 mg/m3), middle (0.1 mg/m3), high-concentration (1 mg/m3) of MWCNT aerosol and clean air control for 6 h/day for 5 days. Lung cells were analyzed using comet assay for DNA damages on day 0 and 1 month after the exposure. | MWCNTs caused a statistically significant increase in lung DNA damage and genotoxicity at high concentration when compared with the negative control group on day 0 with the lung burden retained for 1 month post exposure. | [127] |
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Gupta, S.S.; Singh, K.P.; Gupta, S.; Dusinska, M.; Rahman, Q. Do Carbon Nanotubes and Asbestos Fibers Exhibit Common Toxicity Mechanisms? Nanomaterials 2022, 12, 1708. https://doi.org/10.3390/nano12101708
Gupta SS, Singh KP, Gupta S, Dusinska M, Rahman Q. Do Carbon Nanotubes and Asbestos Fibers Exhibit Common Toxicity Mechanisms? Nanomaterials. 2022; 12(10):1708. https://doi.org/10.3390/nano12101708
Chicago/Turabian StyleGupta, Suchi Smita, Krishna P. Singh, Shailendra Gupta, Maria Dusinska, and Qamar Rahman. 2022. "Do Carbon Nanotubes and Asbestos Fibers Exhibit Common Toxicity Mechanisms?" Nanomaterials 12, no. 10: 1708. https://doi.org/10.3390/nano12101708