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The millimolar GSH intracellular concentrations, the low plasma micromolar concentrations and the low GSH redox potential ( E 0 = 240 mV) make GSH an ideal and perfect cellular redox buffer (Figure 2) (42)

[66] presented evidence that the overexpression of Trx2 or TrxR2 attenuated NO-evoked HIF-1 accumulation and the transactivation of HIF-1 in HEK293 cells

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ATP-P2X7 binding appears to be integral to NLRP3 inflammasome-driven IL1- release, independently causing oligomerization of NLRP3 with ASC and pro-caspase-1 and subsequent induction of TNF [115]

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