Vegetarian S-Acetyl Glutathione – 60 caps (out of stock)

** Daily Value not established.

Reduced glutathione, commonly known as glutathione or GSH, is a tripeptide consisting of L-glutamine, L-cysteine, and glycine. It is ubiquitous in living systems. Glutathione biosynthesis can be affected by biochemical individuality and/or dietary factors. Chronic oxidative stress can also deplete cellular glutathione. Precursors to
glutathione, such as whey protein, vitamin C, and glutamine, are often
recommended to boost glutathione levels in the body; however, results
are inconsistent. Biological individuality is such that not every body
has equivalent ability to metabolize the precursor to raise glutathione.*
Why Not Give Pure Glutathione? Unfortunately, most oral forms of
glutathione are foul smelling, but more importantly, the majority of an
oral dose is oxidized before it can be absorbed and used by the cells.
This formulation delivers a unique preparation of glutathione that
overcomes these usual limitations. The stability of S-acetylglutathione
through the intestinal wall and the plasma is well documented in the
literature. Oral intake of S-acetylglutathione increases total glutathione
and percent-reduced glutathione. Percent-reduced glutathione is a
very significant biomarker of health status.*[1-5]
Mechanism of Absorption S-acetylglutathione, a lipid-like
compound, is taken up intact by chylomicrons in the gut. The acetyl
bond is placed on its thiol group or sulfur group, which prevents
oxidation and allows the molecule to pass diffusively into the cell
after absorption in the gut. The bond is then cleaved by non-specific
enzymes inside the cell. Acetylation prevents the breakdown of
glutathione, and S-acetylglutathione does not require energy
expenditure to be cleaved to reduced glutathione once it crosses the
cell wall.*[1-8]
Antioxidant Activity Glutathione functions extensively in tissues
and organs throughout the body. It plays critical roles in protecting
the body from oxidative stress, maintaining cellular functions, and
supporting healthy immune function.[1,4] Many factors can increase
cellular exposure to oxidative insult, and therefore increase cellular
consumption of nutrients—such as glutathione—that provide
antioxidant activity. This may result in a fierce cycle of oxidative stress
and challenges to detoxification. Complete biotransformation and
protection from oxidative stress are important to maintaining cellular
integrity and tissue health.*[2,5]
Other Benefits of Maintaining Healthy Glutathione Levels Much
information related to mitochondrial health has surfaced in the
literature. Mitochondria, the energy-producing powerhouses of cells,
are also the primary intracellular site of oxygen consumption and the
major source of reactive oxygen species (ROS). S-acetylglutathione
has been shown to cross the membrane of the mitochondria,
increasing the organelle’s activity and minimizing ROS.[8,9] Reduction
of ROS is associated with maintaining mitochondrial integrity and
function, and improved mitochondrial health is believed to support
overall health and energy.*
S-acetylglutathione has also been shown to decrease TNF-alpha, NFkappa beta, and F-2 isoprostane.[4,9-12] Additionally, there is mounting
evidence that intracellular glutathione levels in antigen-presenting
cells (e.g. macrophages) may influence the Th1/Th2 cytokine response
pattern and promote a balanced immune reaction.*[10]

References
1. Locigno R, Pincemail J, Henno A, et al. S-Acetyl-glutathione selectively induces
apoptosis in human lymphoma cells through a GSH-independent mechanism.
Int J Oncol. 2002 Jan;20(1):69-75. [PMID: 11743644]
2. Lomaestro BM, Malone M. Glutathione in health and disease:
pharmacotherapeutic issues. Ann Pharmacother. 1995 Dec;29(12):1263-73.
[PMID: 8672832]
3. Cacciatore I, Cornacchia C, Pinnen F, et al. Prodrug approach for increasing
cellular glutathione levels. Molecules. 2010 Mar 3;15(3):1242-64. [PMID:
20335977]
4. Vogel J, Cinatl J, Dauletbaev N, et al. Effects of S-acetylglutathione in cell and
animal model of herpes simplex virus type 1 infection. Med Microbiol Immunol.
2005 Jan;194(1-2):55-59. [PMID: 14624358]
5. Ballatori N, Krance SM, Notenboom S, et al. Glutathione dysregulation and the
etiology and progression of human diseases. Biol Chem. 2009 Mar;390(3):191-
214. [PMID: 19166318]
6. Richman PG, Meister A. Regulation of gamma-glutamyl-cysteine synthetase
by nonallosteric feedback inhibition by glutathione. J Biol Chem. 1975 Feb
25;250(4):1422-26. [PMID: 1112810]
7. Anderson ME, Powrie F, Puri RN, et al. Glutathione monoethyl ester: preparation,
uptake by tissues, and conversion to glutathione. Arch Biochem Biophys. 1985
Jun;239(2):538-48. [PMID: 4004275]
8. Anderson ME, Nilsson M, Sims NR. Glutathione monoethyl ester prevents
mitochondrial glutathione depletion during focal cerebral ischemia. Neurochem
Int. 2004 Feb;44(3):153-59. [PMID: 14568558]
9. Kretzschmar M. Regulation of hepatic glutathione metabolism and its role in
hepatotoxicity. Exp Toxicol Pathol. 1996 Jul;48(5):439-46. [PMID: 8765689]
10. Fraternale A, Paoletti MF, Casabianca A, et al. Antiviral and immunomodulatory
properties of new pro-glutathione (GSH) molecules. Curr Med Chem.
2006;13(15):1749-55. [PMID: 16787218]
11. Kretzschmar M, Klinger W. The hepatic glutathione system—influences of
xenobiotics. Exp Pathol. 1990;38(3):145-64. [PMID: 2192911]
12. Donnerstag B, Ohlenschlager G, Cinatl J, et al. Reduced glutathione and
S-acetylglutathione as selective apoptosis-inducing agents in cancer therapy.
Cancer Lett. 1996 Dec;110(1-2):63-70. [PMID: 9018082]