4.5 Article

Inhibition of autophagy enhances Hydroquinone-induced TK6 cell death

Journal

TOXICOLOGY IN VITRO
Volume 41, Issue -, Pages 123-132

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.tiv.2017.02.024

Keywords

Autophagy; Hydroquinone; Apoptosis; 3-MA; CQ; PARP-1

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Hydroquinone (HQ), one of the metabolic products of benzene, is a carcinogen. It can induce apoptosis in lymphoma cells. However, whether HQcan induce autophagy and what roles autophagy plays in TK6 cells exposured to HQ remains unclear. In this study, we found that HQ could induce autophagy through techniques of qRT-PCR, Western blot, immunofluorescent assay of LC3 and transmission electron microscope. Furthermore, inhibiting autophagy using 3-methyladenine (3-MA) or chloroquine (CQ) significantly enhanced HQ-induced cell apoptosis, suggesting that autophagy may be a survival mechanism. Our study also showed that HQ activated PARP-1. Moreover, knockdown of PARP-1 strongly exhibited decreased autophagy related genes expression. In contrast, the absence of SIRT1 increased that. Altogether, our data provided evidence that HQ induced autophagy in TK6 cells and autophagy protected TK6 from HQ attack-induced injury in vitro, and the autophagy was partially mediated via activation of the PARP-1-SIRT1 signaling pathway. (C) 2017 Elsevier Ltd. All rights reserved.

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