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. 2012;7(9):e46397.
doi: 10.1371/journal.pone.0046397. Epub 2012 Sep 27.

Terahertz electromagnetic fields (0.106 THz) do not induce manifest genomic damage in vitro

Henning Hintzsche  1 , Christian Jastrow, Thomas Kleine-Ostmann, Uwe Kärst, Thorsten Schrader, Helga Stopper
Affiliations

Terahertz electromagnetic fields (0.106 THz) do not induce manifest genomic damage in vitro

Henning Hintzsche et al. PLoS One. 2012.

Abstract

Terahertz electromagnetic fields are non-ionizing electromagnetic fields in the frequency range from 0.1 to 10 THz. Potential applications of these electromagnetic fields include the whole body scanners, which currently apply millimeter waves just below the terahertz range, but future scanners will use higher frequencies in the terahertz range. These and other applications will bring along human exposure to these fields. Up to now, only a limited number of investigations on biological effects of terahertz electromagnetic fields have been performed. Therefore, research is strongly needed to enable reliable risk assessment.Cells were exposed for 2 h, 8 h, and 24 h with different power intensities ranging from 0.04 mW/cm(2) to 2 mW/cm(2), representing levels below, at, and above current safety limits. Genomic damage on the chromosomal level was measured as micronucleus formation. DNA strand breaks and alkali-labile sites were quantified with the comet assay. No DNA strand breaks or alkali-labile sites were observed as a consequence of exposure to terahertz electromagnetic fields in the comet assay. The fields did not cause chromosomal damage in the form of micronucleus induction.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Scheme of the exposure set-up showing the exposure incubator and the source of the THz electromagnetic fields.
Figure 2
Figure 2. DNA migration (Tail DNA %) at different exposure conditions.
Columns represent means and error bars represent standard deviations of at least three independent experiments (2×50 cells per replicate). Untreated controls (C) and positive controls (MMS) are presented as historical controls performed at different time points during the experiment series (12 independent replicates). Results are shown for HaCaT (2a, 2c) and HDF (2b, 2d) cells. MMS-treated cells showed significantly higher DNA migration compared to untreated cells (*, p<0.05).
Figure 3
Figure 3. Micronucleus frequency after different exposure conditions.
Columns represent means and error bars represent standard deviations of at least three independent experiments (2×1,000 cells per replicate). Untreated controls (C) and positive controls (MMC and VIN) are presented as historical controls performed at different time points during the experiment series (12 independent replicates). Results are shown as number of micronucleated cells per 1,000 binucleated cells for HaCaT (3a) and as number of micronucleated cells per 1,000 mononucleated cells for HDF (3b) cells. MMC-treated HaCaT cells showed a micronucleus frequency of 495±369 MN/1,000 BNC (Fig. 3a). MMC- and VIN-treated cells showed significantly higher micronucleus frequencies compared to untreated cells (*, p<0.05).
Figure 4
Figure 4. Proliferation rate after different exposure conditions.
Columns represent means and error bars represent standard deviations of at least three independent experiments (2×1,000 cells per replicate). Untreated controls (C) and positive controls (MMC and VIN) are presented as historical controls performed at different time points during the experiment series (12 independent replicates). Results are shown as cytochalasin B proliferation index for HaCaT cells (4a) and as number of EdU-positive cells per 1,000 cells for HDF cells (4b). MMC- and VIN-treated HaCaT cells showed significantly lower proliferation indices compared to untreated cells (*, p<0.05).
Figure 5
Figure 5. Micronucleus frequency after different exposure conditions.
Columns represent means and error bars represent standard deviations of at least three independent experiments (at least 5×2,000 cells per replicate for exposed and sham-exposed samples; at least 3×2,000 cells per replicate for control samples). Results are shown as number of micronucleated cells per 1,000 binucleated cells for HaCaT (5a) and AL (5c) cells and as number of micronucleated cells per 1,000 mononucleated cells for HDF (5b) cells. MMC-treated cells showed significantly higher micronucleus frequencies compared to untreated cells (*, p<0.05).
Figure 6
Figure 6. Proliferation rate after different exposure conditions.
Columns represent means and error bars represent standard deviations of at least three independent experiments (at least 5×1,000 cells per replicate for exposed and sham-exposed samples; at least 3×1,000 cells per replicate for control samples). Results are shown as cytochalasin B proliferation index for HaCaT (6a) and AL (6c) cells and as number of EdU-positive cells per 1,000 cells for HDF (6b) cells. MMC-treated HaCaT and AL cells showed significantly lower proliferation indices compared to untreated cells (*, p<0.05).
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Grants and funding

This study was funded by the German Federal Office for Radiation Protection (Bundesamt für Strahlenschutz). The publication was funded by the German Research Foundation (DFG) and the University of Wuerzburg in the funding program Open Access Publishing. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

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