Skip to main content
. Author manuscript; available in PMC: 2014 Sep 20.
Published in final edited form as: Biometals. 2011 Mar 22;24(5):875–890. doi: 10.1007/s10534-011-9441-6

Fig. 2.

Fig. 2

DTPA-antagonism of ZnPT-induced impairment of genomic integrity, PARP activation, and energy crisis in human skin keratinocytes. a NHEKs were exposed to ZnSO4 (1 μM) or ZnPT (1 μM; 1 h) in the presence or absence of DTPA (60 μM) or PJ34 (2 μM), and DNA damage was detected using the alkaline comet assay. As a positive control, cells were exposed to H2O2 (100 μM, 30 min). Representative comets as visualized by fluorescence microscopy are displayed. b Formation of poly(ADP-ribose) polymer (PAR)-modified cellular proteins as detected by immunoblotting of cellular extracts obtained from NHEKs exposed to ZnPT (5 μM; 15 min) in the absence or presence of DTPA (60 μM) or PJ-34 (2 μM). In addition, cells exposed to ZnSO4 (50 μM, 15 min) or left untreated were analyzed. c Cellular ATP depletion in NHEKs exposed to ZnPT (1 μM, 6 h) in the absence or presence of zinc chelators (DTPA, 60 μM; TPEN, 10 μM) or PJ-34 (2 μM). In addition, cells exposed to ZnSO4 (50 μM, 6 h) or left untreated were analyzed; (mean + SD, n = 3)