Fig. 6.

Zn deficiency inhibits the expression of antiapoptotic proteins. IMR-32 cells and rat cortical neurons (RCN) were incubated in control non-chelated media (C) or chelated media containing 1.5 or 15 μM Zn (for IMR-32 cells) or chelated media containing 1.5 μM Zn (1.5 Zn) (for rat cortical neurons) for 36 and 24 h, respectively. a EMSA for NF-κB in nuclear fractions. To determine the specificity of the NF-κB-DNA complex, the control nuclear fraction (C) was incubated in the presence of 100-fold molar excess of unlabeled oligonucleotide containing the consensus sequence for either NF-κB (C + NF-κB) or OCT-1 (C + OCT-1) before the binding assay. After the EMSA assays, bands were quantitated and values referred to controls. Results are shown as means ± SEM of three independent experiments. * Significantly different compared to the C and 15 μM Zn groups (P < 0.05, one-way ANOVA test). b The content of different antiapoptotic proteins was evaluated by Western blot in total cell fractions isolated from IMR-32 cells (left panel) or rat cortical neurons (right panel) as described in “Materials and methods” section. Representative images out of two to three independent experiments are shown. Numbers under the figures are means from two to three independent experiments. * Significantly different (P < 0.05) compared to controls