S-Acetylglutathione (SALG) – (3054-47-5)

S-Acetylglutathione (SAG) is a stable derivative of glutathione (GSH), a crucial endogenous antioxidant. SAG is designed to enhance the bioavailability of glutathione by overcoming its limitations, such as poor absorption and instability in the bloodstream. This acetylated form of glutathione is stable in blood plasma and can be efficiently absorbed by cells, where it is converted back to glutathione by intracellular thioesterases.

In the context of liver health, SAG has demonstrated significant protective effects. Studies have shown that SAG can counteract the cytotoxicity induced by carbon tetrachloride (CCl4), a potent hepatotoxin. In vitro experiments on primary hepatic cells revealed that SAG pretreatment significantly protected against CCl4-induced cell death and reduced the release of liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST), indicating a protective effect on cell membranes.

SAG also showed efficacy in reducing liver fibrosis, as evidenced by decreased collagen deposition and hydroxyproline content, and by modulating the expression of fibrosis-related proteins like α-SMA and TGF-β. Furthermore, SAG improved liver function, as indicated by lower ALT and AST levels, and reduced histological damage.

The above information is displayed for information purpose only, and has not been reviewed by EON nor does EON attests or validates the accuracy nor does it constitutes a recommendation or validation.

S-Acetylglutathione (SAG) is a stable derivative of glutathione (GSH), a crucial endogenous antioxidant. SAG is designed to enhance the bioavailability of glutathione by overcoming its limitations, such as poor absorption and instability in the bloodstream. This acetylated form of glutathione is stable in blood plasma and can be efficiently absorbed by cells, where it is converted back to glutathione by intracellular thioesterases.

In the context of liver health, SAG has demonstrated significant protective effects. Studies have shown that SAG can counteract the cytotoxicity induced by carbon tetrachloride (CCl4), a potent hepatotoxin. In vitro experiments on primary hepatic cells revealed that SAG pretreatment significantly protected against CCl4-induced cell death and reduced the release of liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST), indicating a protective effect on cell membranes.

SAG also showed efficacy in reducing liver fibrosis, as evidenced by decreased collagen deposition and hydroxyproline content, and by modulating the expression of fibrosis-related proteins like α-SMA and TGF-β. Furthermore, SAG improved liver function, as indicated by lower ALT and AST levels, and reduced histological damage.

The above information is displayed for information purpose only, and has not been reviewed by EON nor does EON attests or validates the accuracy nor does it constitutes a recommendation or validation.
Sources:
https://pubchem.ncbi.nlm.nih.gov/compound/102929
https://www.medchemexpress.com/s-acetylglutathione.html
https://pmc.ncbi.nlm.nih.gov/articles/PMC9024626/
https://www.researchgate.net/publication/331475848_Oral_Administration_of_S-acetyl-glutathione_Impact_on_the_Levels_of_Glutathione_in_Plasma_and_in_Erythrocytes_of_Healthy_Volunteers
Other Names

S-acetyl-L-glutathione

IUPAC Name

5-[[3-acetylsulfanyl-1-(carboxymethylamino)-1-oxopropan-2-yl]amino]-2-amino-5-oxopentanoic acid

CAS

3054-47-5

Molecular Weight

349.36

Molecular Formula

C12H19N3O7S

SMILES

CC(=O)SCC(C(=O)NCC(=O)O)NC(=O)CCC(C(=O)O)N

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