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. Author manuscript; available in PMC: 2014 Nov 6.
Published in final edited form as: Nat Commun. 2014 May 6;5:3739. doi: 10.1038/ncomms4739

Figure 4. Effects of ketoconazole and buthionine sulfoximine (BSO) on CYP3A4-expressing THLE-2 cells on the TeamChip.

Figure 4

(a) Toxicity of acetaminophen against THLE-2 cells expressing CYP3A4 on the chip: (top) scanned image of the chip containing THLE-2 cells (control, 15 MOI of Ad-Null) and THLE-2 cells expressing CYP3A4 (15 MOI of Ad-CYP3A4) exposed to 5 μM of ketoconazole as well as 50 μM of BSO in the presence of varying concentrations of acetaminophen for 48 h. (b) Dose response curves for acetaminophen under different conditions (n = 3). The corresponding IC50 values are summarized in Supplementary Table 4. (c) GSH content in THLE-2 cells on the TeamChip: scanned image of the chip after staining with a thiol green dye in the intracellular GSH assay kit. (d) Quantitative analysis of GSH levels in THLE-2 cells on the TeamChip (n = 3). (e) Western blot analysis of nuclear Nrf2 levels in THLE-2 cells exposed to vehicle (0.1 % dimethyl sulfoxide) or different concentrations of acetaminophen for 12 h after transduction with Ad-Null or Ad-CYP3A4 (left). Positive control (293 cells expressing Nrf2) and negative control (293 cells with no Nrf2 expression) were used to authenticate Nrf2 expression (bottom). Actin was probed as a loading control (top right). Abbreviation: C means control (no viral transduction); AAP indicates acetaminophen. (f) Bar graph represents densitometric analysis of nuclear Nrf2 content in AAP-treated THLE-2 cells.