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. 2018 Apr 18;9:388. doi: 10.3389/fphar.2018.00388

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Copyright © 2018 Zhang, den Braver-Sewradj, den Braver, Hiemstra, Vermeulen, van de Water, Commandeur and Vos.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Proposed model for the toxicity of AQ-QI and DEAQ-QI and GSTP1-mediated protection in HepG2 cells. Reactive moieties in the QIs are indicated in red. For AQ-QI, R = -CH₂CH₃; for DEAQ-QI, R = -H. AQ-QI and DEAQ-QI deplete cellular GSH and are conjugated into AQ-SG and DEAQ-SG, respectively. The ER stress response (CHOP) is activated by QI-mediated protein modification and apoptosis is subsequently induced. GSTP1-mediated protection against reactive QIs of AQ is due to enhanced GSH-conjugation and inhibition of apoptosis.