Fig. 1.

Genetic and pharmacological IKKβ pathway inactivation causes GSH deficiency. A, wild-type, knockout and Ikkβ(−/−) cells infected with Ad β-gal [β(−/−)-β-gal] or Ad IKKβ [β(−/−)-IKKβ]. B, wild-type fibroblasts treated for 24 h with 0.1% DMSO, 10 μM JSH23, 1 μM BMS-345541, and 0.5 μM TPCA-1, as indicated, were collected, and cell lysates were used for measurement of GSH and GSSG contents and calculation of GSH/GSSH redox potentials. All results are presented as the mean values ± S.E. from at least three independent experiments. Statistical analyses were done compared with the mean values in control wild-type cells and **, p < 0.01; ***, p < 0.001 were considered significant.