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. Author manuscript; available in PMC: 2017 Mar 1.
Published in final edited form as: J Inorg Biochem. 2015 Dec 9;156:22–34. doi: 10.1016/j.jinorgbio.2015.12.002

Fig. 7.

Fig. 7

Compounds 2b, 2c, cisplatin and Titanocene Y impaired the viability of Caki-1 cells by inducing apoptosis. Following a 72 h incubation period, the compounds (5 μM) 2b or 2c or (30 μM) Cisplatin or Titanocene Y reduced Caki-1 viability by 61% (cisplatin), 48% (Titanocene Y), 56% (2b) and 84% (2c); induced necrosis in 9% (cisplatin), 5% (Titanocene Y), 17% (2b) and 6% (2c), and induced apoptosis in 38% (cisplatin), 33% (Titanocene Y), 38 % (2b) and 76 % (2c) of treated cells. The effect of cisplatin and Titanocene Y, 2b and 2c on viability, necrosis and apoptosis was assessed by measuring protease activity using the non-cell-permeable substrates, cell-permeable substrates and by measuring the total caspase-3 and -7 activities with the ApoTox-Glo Triplex Assay. The effect of each treatment was determined by comparing treated and untreated cells. From the Apotox assay a cell population that was neither necrotic nor apoptotic was detected and their mode of death could not be assigned. Those cells were not included in the graph.