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. Author manuscript; available in PMC: 2012 Aug 1.
Published in final edited form as: Toxicol Appl Pharmacol. 2011 May 12;254(3):299–310. doi: 10.1016/j.taap.2011.05.004

Figure 7.

Figure 7

Equal amounts of whole cell lysate from Hepa1c1c7 and Hepa C12 cell lines were examined for AHR expression levels by western blotting (A) Flow cytometric analysis of mitochondrial membrane potential were performed on Hepa1c1c7 (AHR+/+) and Hepa C12 (AHR deficient) cell lines exposed to DMSO (0.01% vehicle control) or TCDD (30 nM) for 6h. TMRM intensity showed a TCDD-induced shift to the right when compared to vehicle control in the Hepa1c1c7 cell line. This shift was not observed in the HepaC12 (AHR deficient) cell line (B). The TMRM signal represented in B was normalized to the MitoTraker Green (MTG) signal to confirm that the increased TMRM signal was not dependent upon increased mitochondrial number and further show it was AHR dependent. The values were normalized to DMSO treated Hepa1c1c7 signal (C).