Glutathione ethyl ester

Glutathione (GSH) ethyl ester is a cell-permeable derivative of GSH (Item No. 10007461), a nucleophilic co-substrate to glutathione transferases.¹ It increases mitochondrial GSH levels in C38 and IB3-1 epithelial lung cystic fibrosis cells when used at a concentration of 10 mM.² GSH ethyl ester (10 mM) decreases reactive oxygen species (ROS) levels and TNF-α-induced IL-8 secretion in IB3-1 cells. GSH ethyl increases mitochondrial complex I, also known as NADH dehydrogenase, function and reduces depolarization of the mitochondrial membrane potential in IB3-1 when used at concentrations of 10 mM and 1mM, respectively. It decreases lipid oxidation and ferroptosis in cystine-deficient PANC-1, AsPC-1, BxPC-3, and S2-013 pancreatic cancer cells.³ GSH ethyl ester increases the viability of irradiated human lymphoid cells when used at a concentration of 5 mM.¹

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1. Wellner, V.P., Anderson, M.E., Puri, R.N., et al. Radioprotection by glutathione ester: Transport of glutathione ester into human lymphoid cells and fibroblasts. Proc. Natl. Acad. Sci. USA 81(15), 4732-4735 (1984).

2. Kelly-Aubert, M., Trudel, S., Fritsch, J., et al. GSH monoethyl ester rescues mitochondrial defects in cystic fibrosis models. Hum. Mol. Genet. 20(14), 2745-2759 (2011).

3. Badgley, M.A., Kremer, D.M., Maurer, H.C., et al. Cysteine depletion induces pancreatic tumor ferroptosis in mice. Science 368(6486), 85-89 (2020).

Kremer, D.M., Nelson, B.S., Lin, L., et al. GOT1 inhibition primes pancreatic cancer for ferroptosis through the autophagic release of labile iron. bioRxiv (2020).

Bailey, C.P., Figueroa, M., Gangadharan, A., et al. Scaffolding LSD1 inhibitors impair NK cell metabolism and cytotoxic function through depletion of glutathione. Front. Immunol. 11, 2196 (2020).