L-Glutathione (GSH), a tripeptide comprising cysteine, glycine, and glutamic acid, appears to play a pivotal role in cellular defense against oxidative stress induced by toxins and free radicals.(1) Beyond scavenging free radicals intracellularly, this peptide appears to stimulate the synthesis of key antioxidants like vitamin C, vitamin E, CoQ10, and alpha-lipoic acid.(2)

As a water-soluble antioxidant, L-Glutathione is speculated to not only aid in detoxification processes, but also possibly indicates some potential in supporting immune function, facilitating tissue repair, and mitigating inflammation.

Naturally occurring, L-Glutathione peptide has been isolated from animals and plants and manifests in different forms, including L-glutamine, N-acetyl cysteine, N-acetyl methionine, S-adenosylmethionine (SAMe), and L-methionine, all metabolized into glutathione within the organism.

Researchers hypothesize that there are inherent antioxidant characteristics of L-Glutathione, and the peptide is further speculated to arise from a redox reaction involving amino acids Glutamate and Cysteine. The sulfur ion within the cysteine structure appears to undergo this reaction, effectively eliminating free radicals, peroxides, nitrogen dioxide, and diverse toxins, thereby safeguarding cellular structures.(2)

Described as ‘the master antioxidant’ by Garrett Teskey et al., L-Glutathione peptide, or GSH, is emphasized for its multifaceted potential in antioxidant defense systems and various metabolic processes. The significance of GSH was underscored in this study, with its deficiency posing a cellular risk for oxidative damage. (3)


Mechanism of Action

Glutathione is hypothesized to assume a large role in facilitating proper protein folding within the endoplasmic reticulum. Scientific data indicates that Glutathione may actively contribute to the attainment of the correct three-dimensional conformation of proteins, enabling them to bind to receptors and function in a normative manner. Its particular significance, research suggests, lies in the formation of disulfide bonds. While not the exclusive mechanism governing cellular protein folding, Glutathione appears to stand as a pivotal component in this process, thereby significantly impacting cellular functionality.(4)(5)

Debates persist regarding Glutathione’s classification as a neurotransmitter. Notably, it is speculated to modulate the redox states of entities such as the NMDA receptor, a function characteristic of neuromodulators. Additionally, Glutathione appears to induce activation of ionotropic receptors and the purinergic P2X7 receptor on Muller cells located in the retina. Muller cells are instrumental in maintaining the structure and function of retinal cells, including the regulation of neurotransmitter levels. This collective data suggests that, even if not categorized as a neurotransmitter, Glutathione may potentially play a significant role in neurotransmitter regulation.

L-Glutathione Peptide and Cell Aging

Scientists consider oxidative cellular damage to stand as a prominent contributor to both the overt manifestations of physiological aging and intrinsic aging processes, encompassing senescence, hormonal shifts, metabolic alterations, and DNA damage, culminating in disease and dysfunction. Given the suggested role of Glutathione in mitigating oxidative damage, it is unsurprising that the peptide has been hypothesized to act by ameliorating the effects of cell aging.

L-Glutathione Peptide and Neuroprotection

Research suggests that diminished Glutathione levels may have a positive correlation to cell aging, alongside severe disorders such as neurodegenerative diseases. Glutathione pathology may assume a role in the initiation of Parkinson’s disease (PD). Emerging research underscores Glutathione as a potential mediator in iron-dependent cell death, specifically ferroptosis. In the absence of Glutathione, this form of programmed cell death may unfold unchecked within the central nervous system, inducing premature cell aging and senescence, and possibly contributing to the genesis of neurodegenerative diseases. Substantial data exists to underscore the potential efficacy of Glutathione supplementation or its precursors, like N-acetyl cysteine, in research studies of neurological decline.(6)

The hypothesized speculated decline in Glutathione levels underscores Glutathione’s potential in the brain. While Glutathione levels are suggested to undergo a decline, the most dramatic decline appears to occur in the brain. This may possibly render the brain more susceptible to conditions such as Parkinson’s disease and heightened vulnerability following insults like stroke.(7)

The variable criticality of Glutathione levels in the brain is speculated to intensify in states of stress. Typically, mild release of stress hormones may increase Glutathione production as a protective response against more severe stress. However, the potential age-associated decline in synthetic capacity appears to erode this adaptive response. Consequently, advancing age may amplify susceptibility to stress-induced neuronal damage

L-Glutathione Peptide and Cartilage

One of the underlying causes of osteoarthritis is considered by scientists to be the inability of cells that maintain cartilage structures to adapt to stress states within the organism.

Research suggests that Glutathione may play an important role in this process. Research in cows indicates that Glutathione supplementation and unloading the cartilage greatly impacted the cartilage structures. Researchers suggested that equalizing Glutathione with the organism may not fully support the cartilage development on its own; ensuring joint rest may be crucial for elevating the levels of Glutathione within them. Research so far indicates that inducing oxidant stress followed by periods of inactivity may support Glutathione levels in joints and may potentially delay the cell aging process in cartilage.(8)

L-Glutathione Peptide and Cancer Cells

Researchers have speculated that Glutathione appears to exert dual action in cancer cells, i.e., protecting and hindering the cells circumstantially. The peptide has been suggested to shield cancer cells from chemotherapy, acting as a scavenger against toxins and free radicals. Ongoing research explores selectively reducing Glutathione in tumor cells to enhance chemotherapy efficacy.(11) Studies also indicate the potential efficacy of Glutathione in preventing UV light-induced skin cancer in rats.

Glutathione’s potential in cancer studies has been suggested to be intricate, with both positive and pathogenic aspects. Findings suggest the peptide may be advantageous in preventing cancer cell proliferation by removing carcinogens and thereby potentially mitigating cancer development.

Conversely, once cancer manifests, Glutathione may foster tumor progression, possibly promoting metastasis by eliminating toxins generated in the process of killing cancer cells.(12)

L-Glutathione Peptide and Immune System

The immune system has been suggested by researchers to exhibit heightened sensitivity to Glutathione levels. Studies exploring the impact of increased Glutathione levels speculated that the peptide may remain inactive in states of normal immune system. However, its perceived activity becomes evident during disease, researchers speculate even in common viral illnesses.

This peculiar behavior likely stems from the immune system’s quiescent state during wellness, requiring minimal antioxidant capacity. In contrast, disease is considered to trigger a rapid escalation in the production of disease-fighting cells and antibodies, necessitating substantial antioxidant capacity, thereby potentially benefiting from elevated Glutathione levels.

Furthermore, studies suggest that Glutathione may increase storage levels, acting as a buffer against disease. A pilot study employing liposomal Glutathione reported heightened Glutathione stores, leading to a supposedly improved natural killer cell function (surveillance cells against disease) and increased lymphocyte proliferation.(14)


NOTE: These products are intended for laboratory research use only. This peptide is not intended for personal use. Please review and adhere to our Terms and Conditions before ordering.




  1. Joseph Pizzorno, Glutathione!, IMCJ Integrative Medicine: A Clinician’s Journal, 2014 Feb, 13. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4684116/
  2. Henry Jay Forman et al., Glutathione: Overview of its protective roles, measurement, and biosynthesis, Mol Aspects Med.2009; 30(1-2); 1-12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2696075/
  3. Teskey G, Abrahem R, Cao R, Gyurjian K, Islamoglu H, Lucero M, Martinez A, Paredes E, Salaiz O, Robinson B, Venketaraman V. Glutathione as a Marker for Human Disease. Adv Clin Chem. 2018;87:141-159 https://pubmed.ncbi.nlm.nih.gov/30342710/
  4. Satoshi TsunodaEdward AvezovAlisa ZyryanovaTasuku KonnoLeonardo Mendes-SilvaEduardo Pinho MeloHeather P HardingDavid Ron (2014) Intact protein folding in the glutathione-depleted endoplasmic reticulum implicates alternative protein thiol reductants eLife 3:e03421. https://doi.org/10.7554/eLife.03421
  5. Hudson DA, Gannon SA, Thorpe C. Oxidative protein folding: from thiol-disulfide exchange reactions to the redox poise of the endoplasmic reticulum. Free Radic Biol Med. 2015 Mar;80:171-82. doi: 10.1016/j.freeradbiomed.2014.07.037. Epub 2014 Aug 1. PMID: 25091901; PMCID: PMC4312752. https://pubmed.ncbi.nlm.nih.gov/25091901/
  6. Homma T, Fujii J. Application of Glutathione as Anti-Oxidative and Anti-Aging Drugs. Curr Drug Metab. 2015;16(7):560-71. doi: 10.2174/1389200216666151015114515. PMID: 26467067. https://pubmed.ncbi.nlm.nih.gov/26467067/
  7. Maher P. The effects of stress and aging on glutathione metabolism. Ageing Res Rev. 2005 May;4(2):288-314. doi: 10.1016/j.arr.2005.02.005. PMID: 15936251. https://pubmed.ncbi.nlm.nih.gov/15936251/
  8. Zhu S, Makosa D, Miller B, Griffin TM. Glutathione as a mediator of cartilage oxidative stress resistance and resilience during aging and osteoarthritis. Connect Tissue Res. 2020 Jan;61(1):34-47. doi: 10.1080/03008207.2019.1665035. Epub 2019 Sep 15. PMID: 31522568; PMCID: PMC6884680. https://pubmed.ncbi.nlm.nih.gov/31522568/
  9. Weschawalit S, Thongthip S, Phutrakool P, Asawanonda P. Glutathione and its antiaging and antimelanogenic effects. Clin Cosmet Investig Dermatol. 2017 Apr 27;10:147-153. doi: 10.2147/CCID.S128339. PMID: 28490897; PMCID: PMC5413479. https://pubmed.ncbi.nlm.nih.gov/28490897/
  10. Dilokthornsakul W, Dhippayom T, Dilokthornsakul P. The clinical effect of glutathione on skin color and other related skin conditions: A systematic review. J Cosmet Dermatol. 2019 Jun;18(3):728-737. doi: 10.1111/jocd.12910. Epub 2019 Mar 20. PMID: 30895708. https://pubmed.ncbi.nlm.nih.gov/30895708/
  11. Wu JH, Batist G. Glutathione and glutathione analogues; therapeutic potentials. Biochim Biophys Acta. 2013 May;1830(5):3350-3. doi: 10.1016/j.bbagen.2012.11.016. Epub 2012 Nov 28. PMID: 23201199. https://pubmed.ncbi.nlm.nih.gov/23201199/
  12. Traverso N, Ricciarelli R, Nitti M, Marengo B, Furfaro AL, Pronzato MA, Marinari UM, Domenicotti C. Role of glutathione in cancer progression and chemoresistance. Oxid Med Cell Longev. 2013;2013:972913. doi: 10.1155/2013/972913. Epub 2013 May 20. PMID: 23766865; PMCID: PMC3673338. https://pubmed.ncbi.nlm.nih.gov/23766865/
  13. Dröge W, Breitkreutz R. Glutathione and immune function. Proc Nutr Soc. 2000 Nov;59(4):595-600. doi: 10.1017/s0029665100000847. PMID: 11115795. https://pubmed.ncbi.nlm.nih.gov/11115795/
  14. R. Sinha et al., “Oral supplementation with liposomal glutathione elevates body stores of glutathione and markers of immune function,” Eur. J. Clin. Nutr., vol. 72, no. 1, pp. 105–111, Jan. 2018, doi: 10.1038/ejcn.2017.132. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6389332/
    Your Cart
    Your cart is empty