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. Author manuscript; available in PMC: 2014 Oct 1.

Published in final edited form as: Free Radic Biol Med. 2013 May 10;63:175–186. doi: 10.1016/j.freeradbiomed.2013.05.009

Fig. 7 — (A) The level of TBARS in E47 or C34 cells treated with 100 mM ethanol alone or 30 μM AA alone or 300 μM BSO alone or AA plus ethanol or BSO plus ethanol in the absence or presence of the HIF-1α inhibitor 45 μM 2-ME. * p<0.05 compared to E47 cells treated with AA alone or ethanol alone or AA plus ethanol in the absence of 2-ME. # p<0.05 compared to E47 cells treated with BSO alone or BSO plus ethanol in the absence of 2-ME. & p<0.05 compared to C34 cells control without treatment. (B) The positive staining of 5 μM Mitosox in E47/C34 cells treated with AA or ethanol or BSO or AA plus ethanol or BSO plus ethanol in the absence or presence of 2ME was observed under the fluorescence microscope. (Red color, ×100)

Fig. 7 — (A) The level of TBARS in E47 or C34 cells treated with 100 mM ethanol alone or 30 μM AA alone or 300 μM BSO alone or AA plus ethanol or BSO plus ethanol in the absence or presence of the HIF-1α inhibitor 45 μM 2-ME. * p<0.05 compared to E47 cells treated with AA alone or ethanol alone or AA plus ethanol in the absence of 2-ME. # p<0.05 compared to E47 cells treated with BSO alone or BSO plus ethanol in the absence of 2-ME. & p<0.05 compared to C34 cells control without treatment. (B) The positive staining of 5 μM Mitosox in E47/C34 cells treated with AA or ethanol or BSO or AA plus ethanol or BSO plus ethanol in the absence or presence of 2ME was observed under the fluorescence microscope. (Red color, ×100)