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editorial
. 2014 Dec 4;5:267. doi: 10.3389/fphar.2014.00267

Figure 1.

Figure 1

Slow vs. fast GSH depletion produce opposite effects on cell survival. Top: BSO induce slow GSH depletion (hours); the disulfides formed after reaching a threshold level of redox imbalance possess a cell-survival activity (e.g., the p50 subunit of NF-kappaB). Bottom: the very rapid GSH extrusion occurring in apoptosis promote the formation of pro-apoptotic disulfides (e.g., Bax). The arrows indicate a hypothetical threshold level of GSH depletion after which sulfhydryls (SH, HS) are oxidized to disulfides (S-S) in each condition.