• Reduced GSH is a linear tripeptide of L-glutamine, L-cysteine and glycine.^[1] It is found naturally in all human cells with intracellular depletion ultimately resulting in cell death.^[1] GSH exists in the body in two forms: the reduced form (GSH) and the oxidised form (GSSG).^[2]
• In supplemental form, reduced GSH is stable and oral administration may enhance GSH concentrations to support antioxidant defence systems. Reduced GSH has the potential to act as a powerful intracellular antioxidant,^[3] with GSH status a highly sensitive indicator of cell functionality and viability.^[1]
• Oral GSH may effectively increase GSH tissue concentrations.^[4] Research shows that GSH is effectively absorbed in the gastrointestinal tract via a specialised uptake mechanism.^{[1],[5],[6],[7]}  GSH is absorbed intact and results in a substantial increase in blood plasma GSH, indicating that oral supplementation may be useful to enhance tissue availability of GSH.^[1],[8]
• GSH levels are depleted in response to oxidative stress^[1] and ageing.^[9],[10] Cellular damage is associated with ageing as well as the development of chronic disease.^[11] Plasma GSH has a high turnover and around 85% of the total GSH in plasma is normally in the reduced form.^[11]
• Oxidative stress has been extensively studied in neurological health. GSH, one of the most important brain antioxidants, plays a possible preventative role in protecting against free radical damage associated with brain ageing and disease.^{[12],[13],[14]}
• GSH depletion at the cellular level initiates extensive damage to the mitochondria, the energy centres of the cell. An increasing number of toxic or pathological states are associated with a marked depletion of mitochondrial GSH.^[15]
• GSH levels can quickly become depleted in times of high oxidative stress associated with illness, infection, trauma or surgery.^[1] GSH is also depleted due to deficiencies of nutrient precursors and lowered protein intake.^[1]
• Most GSH originates in the liver, with low plasma levels reflecting depleted liver stores.^[1],[11] GSH is involved in both phase 1 and phase 2 detoxification reactions, and is therefore crucial to the body's ability to break down and eliminate potentially harmful toxins. Effective detoxification is dependent on the optimal balance of this two-step process. GSH is the most important antioxidant for neutralising the free radicals produced in phase I of liver detoxification. When a high level of toxic exposure uses up the GSH during phase 1 processes, the phase 2 pathways stop.^[16] This imbalance can lead to impaired detoxification and greater production of highly reactive intermediate metabolites.
• GSH levels can be low in individuals with cirrhosis, viral hepatitis, non-alcoholic liver disease or as a result of chronic alcohol intake.^[1]
• GSH status may provide protection against heavy metals such as arsenic, cadmium, lead, nickel, and mercury.^[17],[18] When GSH is elevated or increased by supplementation, tissues exposed to toxic heavy metals demonstrate a capacity to reduce damage created by lipid peroxides.^[18]
• GSH and vitamin C are key intracellular antioxidants. GSH activity is enhanced by vitamin C, a prominent antioxidant nutrient that has the ability to modulate GSH levels.^[19],[20] Chronic vitamin C deficiency states are associated with depleted GSH and an enhanced risk of oxidative stress.^[11],[21]  Vitamin C supplementation can assist GSH concentrations to help maintain overall antioxidant protection.^[22]
• Glutathione Cell Support™ does not contain animal products making it suitable for vegetarians.

Each Vcap® Contains

Reduced L-Glutathione (as L-glutamyl-L-cysteinylglycine)  100 mg

Vitamin C (as ascorbic acid)                                             125 mg

Adults: Take 1 -2 capsules a day away from meals or as directed by your healthcare practitioner.

Precautions & Considerations

• Do not exceed a daily dose of 200mg of vitamin C in individuals with haemochromatosis.
• Care should be taken with vitamin C in individuals with clotting disorders or those taking anticoagulant and anti-platelet medication.
• Studies have not been performed on Glutathione Cell Support™ in pregnancy and lactation. 

References

[1] No authors listed. Glutathione, reduced (GSH). Monograph. Altern Med Rev. 2001 Dec;6(6):601-7.

[2] Kidd, P. Glutathione: systemic protectant against oxidative and free radical damage. Alternative Medicine Review. 2(3):155-176. 1997.

[3] Exner R, Wessner B, Manhart N, et al. Therapeutic potential of glutathione. Wien Klin Wochenschr. 2000 Jul 28;112(14):610-6.

[4] Aw TY, Wierzbicka G, Jones DP. Oral glutathione increases tissue glutathione in vivo. Chem Biol Interact. 1991;80(1):89-97.

[5] Vincenzini MT, Favilli F, Iantomasi T. Intestinal uptake and transmembrane transport systems of intact GSH; characteristics and possible biological role. Biochim Biophys Acta. 1992 Mar 26;1113(1):13-23.

[6] Favilli F, Marraccini P, Iantomasi T, et al. Effect of orally administered glutathione on glutathione levels in some organs of rats: role of specific transporters. Br J Nutr. 1997 Aug;78(2):293-300.

[7] Mårtensson J, Jain A, Meister A. Glutathione is required for intestinal function. Proc Natl Acad Sci U S A. 1990 Mar;87(5):1715-9.

[8] Hagen TM, Wierzbicka GT, Sillau AH, et al. Bioavailability of dietary glutathione: effect on plasma concentrations. Am J Physiol. 1990 Oct;259(4 Pt 1):G524-9.

[9] Julius M, Lang CA, Gleiberman L, et al. Glutathione and morbidity in a community-based sample of elderly. J Clin Epidemiol. 1994 Sep;47(9):1021-6.

[10] Lang CA, Naryshkin S, Schneider DL, et al. Low blood glutathione levels in healthy aging adults. J Lab Clin Med. 1992 Nov;120(5):720-5.

[11] Henning SM, Zhang JZ, McKee RW, et al. Glutathione blood levels and other oxidant defense indices in men fed diets low in vitamin C. J Nutri. 1991 Dec;121(12):1969-75

[12] Dringen R. Metabolism and functions of glutathione in brain. Prog Neurobiol. 2000 Dec;62(6):649-71.

[13] Singh I, Pahan K, Khan M, et al. Cytokine-mediated Induction of Ceramide Production Is Redox-sensitive. J Biol Chem, Vol. 273, Issue 32, 20354-20362, August 7, 1998.

[14] Barańczyk-Kuźma A, Kuźma M, Gutowicz M, et al. Glutathione S-transferase pi as a target for tricyclic antidepressants in human brain. Acta Biochim Pol. 2004;51(1):207-12.

[15] Lash LH. Mitochondrial Glutathione Transport: Physiological, Pathological and Toxicological Implications. Chem Biol Interact. 2006 Oct 27;163(1-2):54-67. Epub 2006 Apr 4.

[16] Murray, M. Pizzorno, J. Encyclopaedia of Natural Medicine. Revised 2nd Ed. Little, Brown Publishing. Great Britain. 2003.

[17] Valko M, Morris H, Cronin MT. Metals, toxicity and oxidative stress. Curr Med Chem. 2005;12(10):1161-208.

[18] No authors listed. Life Extension Foundation. Health Concerns; Heavy Metal Toxicity. Updated: 06/12/2003. http://www.lef.org/protocols/prtcl-156.shtml. Accessed January 2009.

[19] Lenton KJ, Therriault H, Cantin AM, et al. Direct correlation of glutathione and ascorbate and their dependence on age and season in human lymphocytes. Am J Clin Nutr. 2000 May;71(5):1194-1200.

[20] Lenton KJ, Sané AT, Therriault H, et al. Vitamin C augments lymphocyte glutathione in subjects with ascorbate deficiency. Am J Clin Nutr. 2003 Jan;77(1):189-95.

[21] Lenton KJ, Therriault H, Fülöp T, et al. Glutathione and ascorbate are negatively correlated with oxidative DNA damage in human lymphocytes. Carcinogenesis.1999 Apr;20(4):607-13.

[22] Johnston CS, Meyer CG, Srilakshmi JC. Vitamin C elevates red blood cell glutathione in healthy adults. Am J Clin Nutr. 1993 Jul;58(1):103-5.

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