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The functionalities of bioalerts are illustrated in a tutorial (Additional file 2) using three diverse bioactivity data sets, namely: (1) Ames mutagenicity data for 1752 compounds [27], (2) (hbox {pIC}_{50}) values for 2311 compounds on human cyclooxygenase (COX) 2 [16], and (3) blood brain barrier (BBB) data for 157 organic compounds [28].
Table 2 shows the mutagenicity data for the organic extracts from airborne particulate matter in rev/m.
Table 3 and Figure 2 show the mutagenicity data for two samples from the chlorinated pool and two from the brominated pool in strain TA100.
In pooling data sets on sucrose, invert sugar, honey, and HFCS from various studies and laboratories (Roemer et al., 2010; Coggins et al., 2011), mutagenicity data for these two testing conditions did not show any increase in activity with increasing single sugar application levels (TPM-based comparison, Figure 5A and B).
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Mutagenicity data from these experiments support the theory of formation of direct-acting mutagens, probably due to nitration.
Ames mutagenicity data from a study by Kazius et al. [57].
The COMPACT predictions have also been compared with published Ames mutagenicity data and with our own Hazardexpert predictions for carcinogenicity.
Consequently, without the ability to metabolize formaldehyde, in vitro mutagenicity data may not provide an adequate basis for determining what role, if any, mutations might have played in the development of formaldehyde-induced rat nasal tumors.
In addition, toxic compounds were filtered out using a categorical SVM model for prediction of mutagenicity trained on Ames-test mutagenicity data (5-fold ROC score: 0.8948).
Kazius et al. provided an analysis of mutagenicity data correlating chemical substructures to mutagenicity [21, 27, 28].
Table 1 Aryl-amine mutagenicity data sets considered in this study.
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