Glutathione Breakthrough: Advancement in Antioxidant Science

Glutathione (GSH) is one of the most critical molecules of the entire body. GSH plays an important role in antioxidant defense, nutrient metabolism and is key in a vast number of cellular processes including gene expression, DNA and protein synthesis, cell proliferation and apoptosis, signal transduction, cytokine production, immune response, and protein glutathionylation. GSH is ubiquitous in the regulation of pathways essential for whole body homeostasis. To date there are over 76,000 medical articles about the health benefits of Glutathione.

As the most important intracellular antioxidant, GSH regulates all other antioxidants while preventing damage to important cellular components caused by reactive oxygen species, such as free radicals and peroxides.

Metabolic imbalance, allergies, asthma, inflammation, immunodeficiency, and diseases such as cancer, cardiovascular disease, seizure, Alzheimer’s disease, Parkinson’s disease, sickle cell anemia, liver disease, cystic fibrosis, HIV, AIDS, infection, heart attack, stroke, and diabetes are associated with low GSH levels and high oxidative stress levels.

Despite the overwhelming benefits, there has been only limited clinical use of glutathione in medicine because of its unstable nature. The cysteine moiety of the GSH tripeptide makes its use in clinical medicine difficult at best. Oral preparations of GSH have been found to be unpalatable due to the sulfur taste and GSH is easily inactivated by stomach acid before it can be absorbed.  Transdermal preparations are sticky and smell of sulfur. IV-supplementation is effective, but invasive and not readily available to most patients due to the expense and limited access to an educated practitioner. Even when GSH is given intravenously, much of the GSH is oxidized into GSSG in the IV-bag during storage, transport or while being infused. Nebulized forms of GSH have also been used but the smell and taste result in poor patient compliance and it is counterintuitive to suggest that aerosolizing a compound that is highly reactive in the presence of atmospheric oxygen is an effective strategy.

Advanced Cellular Glutathione (ACG)

ACG Glutathione® Case Studies

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GSH is Critical in Many Cellular Reactions

1. GSH reacts with various physiological metabolites such as, estrogen, prostaglandins, leukotrienes, and chemicals, such as bromobenzene and counteracts acetaminophen overdose
2. GSH interacts with Nitric oxide and both have critical roles regulating lipids, glucose, and amino acid utilization
3. GSH is involved with the removal of the carcinogen, Formaldehyde, from the body
4. GSH is required for the prostaglandin H2 pathways
5. GSH inhibits Influenza virus infection
6. GSH is involved in many other important metabolic pathways, including protein metabolism
7. GSH is required for the proliferation of cells, including lymphocytes and intestinal epithelial cells
8. GSH plays an important role in spermatogenesis and sperm maturation
9. GSH is essential for the activation of T-lymphocytes and polymorphonuclear leukocytes, and is required for cytokine production. GSH is important for successful immune responses when the host is immunologically challenged
10. GSH is involved in the process of maintaining Vitamin C and E in the active metabolic forms

Enhance Your Practice with Superior Patient Outcomes

Literature Cited

1. Ballatori et al (2009) Glutathione dysregulation and the etiology and progression of human diseases. Biol Chem. 2009 March; 390(3): 191–214.
2. Sies, H. (1999) Glutathione and its cellular functions. Free Radic. Biol. Med. 27:916-921.
3. Guoyao Wu2, Yun-Zhong Fang, Sheng Yang, Joanne R. Lupton, and Nancy D. Turner. (2004) Glutathione Metabolism and Its Implications for Health.  Am. Soc. Nut. Sci.
4. Townsend, D. M., Tew, K. D. & Tapiero, H. (2003) The importance of glutathione in human disease. Biomed. Pharmacother. 57:145-155.
5. Badaloo, A., Reid, M., Forrester, T., Heird, W. C. & Jahoor, F. (2002) Cysteine supplementation improves the erythrocyte glutathione synthesis rate in children with severe edematous malnutrition. Glutathione Metabolism and Its Implications for Health.Am. J. Clin. Nutr. 76:646-652.
6. Jones, D. P. (2002) Redox potential of GSH/GSSG couple: assay and biological significance. Methods Enzymol. 348:93-112.
7. Lyons, J., Rauh-Pfeiffer, A., Yu, Y. M., Lu, X. M., Zurakowski, D., Tompkins, R. G., Ajami, A. M., Young, V. R. & Castillo, L. (2000) Blood glutathione synthesis rates in healthy adults receiving a sulfur amino acid-free diet. Proc. Natl. Acad. Sci. U.S.A. 97:5071-5076.
8. Yu, Y. M., Ryan, C. M., Fei, Z. W., Lu, X. M., Castillo, L., Schultz, J. T., Tompkins, R. G. & Young, V. R. (2002) Plasma L-5-oxoproline kinetics and whole blood glutathione synthesis rates in severely burned adult humans. Am. J. Physiol. 282:E247-E258.
9. Lu, S. C. (2000) Regulation of glutathione synthesis. Curr. Top. Cell Regul. 36:95-116.
10. Griffith, O. W. (1999) Biologic and pharmacologic regulation of mammalian glutathione synthesis. Free Radic. Biol. Med. 27:922-935.
11. Canals, S., Casarejos, M. J., de Bernardo, S., Rodriguez-Martin, E. & Mena, M. A. (2003) Nitric oxide triggers the toxicity due to glutathione depletion in midbrain cultures through 12-lipoxygenase. J. Biol. Chem. 278:21542-21549.
12. Johnson, A. T., Kaufmann, Y. C., Luo, S., Todorova, V. & Klimberg, V. S. (2003) Effect of glutamine on glutathione, IGF-1, and TGF-β1. J. Surg. Res. 111:222-228.
13. Fang, Y. Z., Yang, S. & Wu, G. (2002) Free radicals, antioxidants, and nutrition. Nutrition 18:872-879.
14. Lei, X. G. (2002) In vivo antioxidant role of glutathione peroxidase: evidence from knockout mice. Methods Enzymol. 347:213-225.
15. Cai, J., Chen, Y., Seth, S., Furukawa, S., Compans, R. W. & Jones, D. P. (2003) Inhibition of influenza infection by glutathione. Free Radic. Biol. Med. 34:928-936

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