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High concentration of GSH in many tumors together with its high reactivity leads towards utilization of GSH as an activator of prodrugs, possibly leading to GSH depletion as well as release of toxic chemotherapeutic agents

By lowering the expression of genes involved in de novo lipogenesis, such as SREBP-1c, FAS, and ACC1, and by guarding against oxidative stress, inflammation, and steatosisall of which are critical elements in the development of the diseasesililymarin improves lipid metabolism in NAFLD (169, 170)

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Tumor necrosis alpha induces coordinated activation of rat GSH synthetic enzymes via NFB and AP-1

Endoplasmic reticulum stress-activated transcription factor ATF6 requires the disulfide isomerase PDIA5 to modulate chemoresistance

10.1093/MOLEHR/GAAB042 39 TatenoH.KrapfD.HinoT.Snchez-CrdenasC.DarszonA.YanagimachiR.et al (2013)