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. Author manuscript; available in PMC: 2015 May 1.
Published in final edited form as: Toxicol Appl Pharmacol. 2014 Feb 25;276(3):165–170. doi: 10.1016/j.taap.2014.02.005

Fig. 1.

Fig. 1

Involvement of oxidative stress in As3+-induced kinase activation and EZH2 phosphorylation in BEAS-2B cells. (A) BEAS-2B cells were treated with 20 µM As3+ for 0, 1, 2, or 4 h with or without NAC pretreatment for 2 h. S21 phosphorylation of the EZH2 (pEZH2S21) protein was determined by Western blotting. The most right lanes (0 h As3+) are NAC only treatment. (B–D) The activation of Akt (B), STAT3 and JNK (C), and Erk and p38 (D) were determined in the BEAS-2B cells treated with 20 or 80 µM As3+ for 2 h in the presence or absence of NAC pretreatment for 2 h. In each panel, the most right lanes (without As3+, —) are NAC only groups. (E) H2O2 induces pEZH2S21 and Akt activation in a time-dependent manner. (F) Dose-dependent activation of Akt kinase in the BEAS-2B cells treated with the indicated concentrations of H2O2 for 5 min.