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. Author manuscript; available in PMC: 2018 Feb 6.
Published in final edited form as: Toxicol Lett. 2017 Jul 4;278:30–37. doi: 10.1016/j.toxlet.2017.07.007

Figure 1. TAT-Gap24 and TAT-Gap19 block extracellular release of ATP.

Figure 1

Primary rat hepatocytes were isolated and cultivated as specified in “Materials and Methods”. 24 hours after cell seeding, cultured hepatocytes were exposed during 30 minutes to 20 µM TAT-Gap24, 20 µM TAT-Gap19, 50 µM carbenoxolone (CBX) or solvent control. Thereafter, the cells were exposed to HBSS-Hepes, considered as the baseline condition, and divalent-free buffer. After 2.5 minutes incubation at room temperature, ATP assay mix was added and luminescence was measured spectrophotometrically. ATP release in the divalent-free buffer were plotted and expressed as percentage of ATP release triggered by divalent-free medium. At least 6 wells per experiment were examined, with a total of 5 experiments (i.e. hepatocytes isolated from 5 different rats). Data are expressed as means ± SEM, with **p < 0.01 and ****p < 0.0001 compared to ATP release triggered by divalent-free medium.