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. 2018 Feb 9;8:2771. doi: 10.1038/s41598-018-20995-w

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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NTP compound plate screen. (A) Prescreen data from all compounds (A1–G2), showing all points and spread of data. Error bars represent mean +/− 95% CI. Also refer to Tables 1 and 2. Statistical analysis was conducted via a one-sided students t-test. (B) Representative graphs from four compounds. Compound B9 (Thiram) was one of the most genotoxic compounds tested. Cells exposed to compound F8 (another dithiocarbamate compound) also had high levels of DNA damage at low concentrations. Compounds F6 and B11 showed differential response based on p53 status of the cells. Symbols: squares = TK6 and circles = Jurkat (JK). Red symbols are etoposide internal controls for each of the cell lines. (C) Dose-response analysis of compound B11 shows that the JK cells (red) are slightly less sensitive to etoposide (+) control than the TK6 cells (green). Despite this, the JK cells show higher levels of DNA damage than the TK6 cells following treatment with compound B11 (****p < 0.0001). Statistical analysis was conducted via a two-sided Student’s t-test.