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Chemical Compound Review:

GSH-MEE (2S)-2-amino-4-[[(1S)-1...

Synonyms: CHEMBL511330, AG-D-40735, AC1L3URZ, CTK0H5371, LS-191673, ...

Salama, S.A. et al., Abe, Y. et al., Dick, C.A. et al., Rosenson-Schloss, R.S. et al., Sudo, H. et al., et al.

Dick, Brown, Donaldson, Stone,

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Disease relevance of Glutathione ethyl ester

The GEE/DEVD-sensitive death was sensitive to pertussis toxin and was due to G(o)-interacting His(657)-Lys(676) domain [1].
Glutathione-ethyl-ester inhibited neuronal death by anti-APP antibody, but not death by Abeta1-42, whereas serum attenuated toxicity by Abeta1-42, but not by anti-APP antibody [2].

High impact information on Glutathione ethyl ester

Therefore, GSHME is protective against NNK-induced CA with more dominant effect in cells with the GSTM1 positive genotype [3].
Treatment of the cells with 1 mM glutathione monoethyl ester (GSHME) significantly reduced NNK-induced CA in all cells regardless of their genotypes [3].
The GEE/DEVD-sensitive cytotoxicity by M239V-PS2 was likely through NADPH oxidase and the GEE-sensitive/DEVD-resistant cytotoxicity through xanthine oxidase (XO) [4].
M239V-PS2 exerted three forms of cytotoxicity: one was sensitive to both an antioxidant glutathione-ethyl-ester (GEE) and a caspase inhibitor Ac-DEVD-CHO (DEVD); the second was sensitive to GEE but resistant to DEVD; and the third was resistant to both [4].
A role for free radicals and reactive oxygen species (ROS) in mediating ultrafine inflammation is further strengthened by the ability of the antioxidants N-acetylcysteine (NAC) and glutathione monoethyl ester (GSHme) to block the particle induced release of tumour necrosis factor-alpha (TNF-alpha) from alveolar macrophages in vitro [5].

Biological context of Glutathione ethyl ester

To identify a multifocal strategy against LDL-induced apoptosis, we evaluated the role of cellular preconditioning by glutathione-ethyl ester (GSH-Et), a native redox regulator, in the prevention of the uptake and apoptotic effects of an oxidizable scavenger receptor-specific ligand, acetylated low-density lipoprotein (Ac-LDL) [6].

References

Multiple mechanisms underlie neurotoxicity by different types of Alzheimer's disease mutations of amyloid precursor protein. Hashimoto, Y., Niikura, T., Ito, Y., Nishimoto, I. J. Biol. Chem. (2000) [Pubmed]
Secreted Abeta does not mediate neurotoxicity by antibody-stimulated amyloid precursor protein. Sudo, H., Hashimoto, Y., Niikura, T., Shao, Z., Yasukawa, T., Ito, Y., Yamada, M., Hata, M., Hiraki, T., Kawasumi, M., Kouyama, K., Nishimoto, I. Biochem. Biophys. Res. Commun. (2001) [Pubmed]
Role of polymorphic GSTM1 and GSTT1 genotypes on NNK-induced genotoxicity. Salama, S.A., Abdel-Rahman, S.Z., Sierra-Torres, C.H., Hamada, F.A., Au, W.W. Pharmacogenetics (1999) [Pubmed]
Cytotoxic mechanisms by M239V presenilin 2, a little-analyzed Alzheimer's disease-causative mutant. Abe, Y., Hashimoto, Y., Tomita, Y., Terashita, K., Aiso, S., Tajima, H., Niikura, T., Matsuoka, M., Nishimoto, I. J. Neurosci. Res. (2004) [Pubmed]
The role of free radicals in the toxic and inflammatory effects of four different ultrafine particle types. Dick, C.A., Brown, D.M., Donaldson, K., Stone, V. Inhalation toxicology. (2003) [Pubmed]
Glutathione preconditioning attenuates Ac-LDL-induced macrophage apoptosis via protein kinase C-dependent Ac-LDL trafficking. Rosenson-Schloss, R.S., Chnari, E., Brieva, T.A., Dang, A., Moghe, P.V. Exp. Biol. Med. (Maywood) (2005) [Pubmed]

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