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. 2016 Sep 23;12(5):3723–3730. doi: 10.3892/ol.2016.5181

Figure 3.

Figure 3.

(A) Cisplatin could trigger an ER stress response in Mahlavu cells by activating the pro-apoptotic ATF4-ATF3-CHOP pathway. (B) The cisplatin-induced ER stress response concomitantly caused cellular GSH depletion in a concentration-dependent manner. (C) The cisplatin-induced cellular GSH depletion was demonstrated to be due to a strong inhibition of γ-GCSh, an enzyme involved in the regulation of GSH biosynthesis. ER, endoplasmic reticulum; ATF, activating transcription factor; CHOP, C/emopamil binding protein homologous protein; CMF, 5-chloromethylfluorescein; GSH, glutathione; γ-GCSh, γ-glutamylcysteine synthetase heavy chain.