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. 2014 Mar 6;99(8):E1556–E1563. doi: 10.1210/jc.2013-3844

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Copyright © 2014 by the Endocrine Society

This article has been published under the terms of the Creative Commons Attribution License (CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Copyright for this article is retained by the author(s). Author(s) grant(s) the Endocrine Society the exclusive right to publish the article and identify itself as the original publisher.

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Figure 3. — Knockdown of TXNRD2 impairs mitochondrial redox homeostasis in a human adrenocortical cell line. A, TXNRD2 is widely expressed in human tissues with highest the TXNRD2 mRNA levels in the adrenal cortex. B, Stable TXNRD2 knockdown (TXNRD2-KD) in H295R cells, confirmed by Western blot analysis with 95% knockdown of protein levels (n = 4). C, Increased pressure on the glutathione system is observed with a significant decrease in the reduced:oxidized glutathione (GSH:GSSG) ratio. Oxidative stress induced by 25 μM menadione in the control cells reduced this ratio to 0.4 ± 0.1 (n = 4). D, TXNRD2-KD leads to a decrease in the reduced to oxidized PRDX3 ratio [Western blot with densitometric analysis (n = 3)]. E, Quantitative analysis of superoxide production by MitoSOX, after fluorescence-activated cell sorting (FACS) shows a significant increase in superoxide production in KD cells relative to controls (n = 3). Error bars represent SD. *, P < .05.