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. 2019 Dec 11;48(3):e13. doi: 10.1093/nar/gkz1077

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© The Author(s) 2019. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 4. — Role of metabolic activation in induction of SSBs by AFB₁ and B[a]P. Cells were treated with AFB₁ or B[a]P for 24 h in the presence of 1 mM HU and 10 μM AraC and analyzed with the alkaline CometChip. To inhibit AFB₁ metabolic activation, 5 μM KET was added to AFB₁ treatment (blue lines in (A), (B) and (C)). To inhibit B[a]P bioactivation, 25 μM ANF was added to B[a]P treatment (teal lines in (D), (E) and (F)). Gray lines represent treatment conditions without KET and ANF. (A) and (D) TK6 cells. (B) HepaRG™ cells (same-day treatment). (E) HepaRG™ (day-7 treatment). (C) and (F) HepG2 cells. n 3. Error bars are standard error of the mean. * P < 0.05, two-way ANOVA with post hoc analysis by Bonferroni test.

Inline graphic — Role of metabolic activation in induction of SSBs by AFB₁ and B[a]P. Cells were treated with AFB₁ or B[a]P for 24 h in the presence of 1 mM HU and 10 μM AraC and analyzed with the alkaline CometChip. To inhibit AFB₁ metabolic activation, 5 μM KET was added to AFB₁ treatment (blue lines in (A), (B) and (C)). To inhibit B[a]P bioactivation, 25 μM ANF was added to B[a]P treatment (teal lines in (D), (E) and (F)). Gray lines represent treatment conditions without KET and ANF. (A) and (D) TK6 cells. (B) HepaRG™ cells (same-day treatment). (E) HepaRG™ (day-7 treatment). (C) and (F) HepG2 cells. n 3. Error bars are standard error of the mean. * P < 0.05, two-way ANOVA with post hoc analysis by Bonferroni test.