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. Author manuscript; available in PMC: 2014 May 1.
Published in final edited form as: Autoimmun Rev. 2012 Dec 29;12(7):741–751. doi: 10.1016/j.autrev.2012.12.007

Figure 5.

Figure 5

Overview on the mechanisms of glutathione induced cell death. Apoptosis includes cellular shrinking, chromatin condensation and margination at the nuclear periphery with the eventual formation of membrane-bound apoptotic bodies that contain organelles, cytosol and nuclear fragments and are phagocytosed without triggering inflammatory processes. Depletion of GSH might be a prerequisite for the generation of ROS. GSH depletion and the concomitant decrease in GSH/GSSG ratio might increase the availability of GSSG to exert its redox signaling and modulate both intrinsic as well as extrinsic pathway of apoptosis. GSH depletion triggers the permeability transition pore of the mitochondria, the pro-apoptotic function of released Cyt C, the formation of the apoptosome, and the activation of executioner caspases and lead to intrinsic apoptosis pathway. Furthermore, GSH depletion might trigger aggregation of death receptors, activation of Fas/FasL and caspase-3.