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. Author manuscript; available in PMC: 2009 Oct 15.
Published in final edited form as: Biochem Pharmacol. 2009 Jun 21;78(8):959–965. doi: 10.1016/j.bcp.2009.06.019

Fig. 5.

Fig. 5

Effect of CYP1A1 and PARP inhibition on the PCB 104-mediated increase in endothelial cell oxidative stress (A), CYP1A1 activity (B), PARP activity (C) and NADPH depletion (D). Inhibition of CYP1A1 with α-naphthoflavone (0.3 μM) prevents the increase in oxidative stress, CYP1A1 and PARP activity, plus the NADPH depletion observed following 4 h exposure to PCB 104 (10 μM). Inhibition of PARP either pharmacologically with PJ-34 (3 μM) or via gene knockout had no effect on PCB 104-mediated increase in oxidative stress or CYP1A1 activity but did inhibit the increase in PARP activity and NADPH depletion. Data is expressed as mean ± SEM from 4 separate experiments with 3–6 replicates per experiment; *p < 0.05, **p < 0.01 vs. untreated cells and †p < 0.01 vs. PCB 104 treated cells.