Table 4.
Summary of in vivo data on genotoxicity and gene expression endpoints in lung tissue.*
| Endpoint | MWCNT study and tube length | SWCNT study and tube length |
|---|---|---|
| DNA oxidation products | − Cao et al. (2014): 0.7–3, 0.4–4 μm | − Vesterdal et al. (2014b): 1 μm |
| − Pothmann et al. (2015): 1.1 μm | + Folkmann et al. (2009): 1 μm (oral exposure) | |
| DNA breaks (SB) | + (2% Fe) Kim et al. (2012): 20 μm | + Jacobsen et al. (2009): 1 μm (BALF cells) |
| + Poulsen et al. (2015): 4.1 μm | − Vesterdal et al. (2014b): 1 μm | |
| + Kato et al. (2013): 2 μm | − Naya et al. (2012): 4.4 μm | |
| + Cao et al. (2014): 0.7–3, 0.7.4 μm | ||
| + Poulsen et al. (2015): 0.85 μm | ||
| + (2% Fe) Kim et al. (2014): 0.33 μm | ||
| − Ema et al. (2013b): 2.7 μm | ||
| − Pothmann et al. (2015): 1.1 μm | ||
| Micronuclei | + Muller et al. (2008b): 0.7 μm | + Shvedova et al. (2014): 1–3 μm (inhalation) |
| Mutations | + Kato et al. (2013): 2 μm (gpt locus) | + Shvedova et al. (2008): 1 μm (inhalation) |
| − Shvedova et al. (2008): 1 μm (aspiration) | ||
| Gene expression | + Snyder-Talkington et al. (2013a) Egfr (downregul), Junb (upregul) | + Park et al. (2011a) p53 protein upregulation |
| + Guo et al. (2012) Bcl3 (slightly upregul), Egfr (downregul) | + Park et al. (2011b) p53 protein upregulation, purified sample | |
| + Huang et al. (2014) Cdkn1 (upregul) | + Park et al. (2013) p53 protein upregulation | |
| + Poulsen et al. (2013) Bcl3 (upregul), Aurka (upregul), Myb (downregul) |
Source: Adapted from Tables 4.4.2 and 4.4.3 of IARC monograph 111 (IARC, in press), which was originally developed by authors on this paper. This current table has been restructured and includes only the results in lung issue (e.g., excludes information from IP or GI routes of exposure).
Bcl3: B-cell cll/lymphoma 3; Cdkn1a: cyclin-dependent kinase inhibitor 1a (P21, Cip1); Egfr: epidermal growth factor receptor; Junb: Jun-B proto-oncogene; Myb: V-Myb avian myeloblastosis viral oncogene homolog.
Levels of DNA damage, mutations, chromosome damage and cellular transformation are increased (+) or unaltered (−) in exposed cells compared to unexposed controls. Gene expressions include oncogenes, tumor suppressor genes, and genes involved in DNA repair and cell cycle regulation. (+) means a differential expression between control (untreated) and treated cells.