Skip to main content
. Author manuscript; available in PMC: 2013 Jan 13.
Published in final edited form as: Chem Res Toxicol. 2011 Nov 16;25(1):113–121. doi: 10.1021/tx200272v

Figure 2.

Figure 2

AKR1A1 overexpression protects lung cells from the toxic effects of PAH metabolites at the expense of increased oxidative stress. A) H358 cells were treated with various concentrations BPQ and anti-BPDE, grown for 24 hrs and cell viability determined using the trypan blue exclusion method. B) Cell viability of H358 and H358/AKR1A1 cells treated with various concentrations of B[a]P-7,8-trans-dihydrodiol for 24 hrs. C) H358/AKR1A1 cells were treated with B[a]P-7,8-trans-dihydrodiol and an AKR1A1 inhibitor (statil) for 24 hrs and cell viability determined. D) Western blot analysis showing overexpression of AKR1A1 in H358/AKR1A1 cells compared to H358 cells.