Fig. 1.

Copper exposure induces apoptosis in dopaminergic cells. In A–B, cell survival after CuCl₂ treatment (48h) was determined in cells co-stained with PI and mBCl. Two-dimensional 5% probability contour plots in A display cell death (PI uptake) vs GSH content (mBCl). Healthy cells were identified as PI- and high mBCl fluorescence (broken line regions in A) and quantified in the corresponding bar graphs in B. Numbers in quadrants (A) reflect number of cells in %. In C, well death was evaluated via Calcein retention assay and data was normalized vs control (DMSO). When indicated, cells were pre-treated with 50 μM pan-caspase (Z-VAD-FMK) or caspase 3 inhibitor (DMQD-CHO) for 1 h and inhibitors remained present throughout the experiment. In D, WB analysis of CuCl₂-induced caspase 3 cleavage/activation. Numbers (italics) represent the densitometry analysis of cleaved caspase 3 normalized to β-actin signal with respect to control. The WB is cropped for simplification, but the unmodified version is found in Supplementary Fig. 1. Data in graphs represent means ± SE of at least n = 3. Two-way ANOVA, Holm-Sidak post hoc test, ^ap < 0.05 vs DMSO only; ^bp < 0.05 zVAD or Ac-DMQD vs DMSO within the corresponding [CuCl₂] category.