Description
Glutathione is a tripeptide made from three amino acids — glutamate, cysteine, and glycine — synthesised inside virtually every cell in the body. It is the most abundant antioxidant molecule in human cells, present at millimolar concentrations in the liver, lungs, and immune cells. Often called the body’s “master antioxidant,” it plays a central role in neutralising harmful reactive oxygen species, detoxifying drugs and environmental chemicals, and regulating immune function. Its concentrations decline with age and under conditions of chronic disease and oxidative stress.
What the research has found
Foundational research demonstrated that artificially depleting cellular glutathione renders cells dramatically more vulnerable to oxidative damage, confirming it as the primary line of defence against reactive oxygen species in virtually all cell types (Meister & Anderson, 1983). Studies on immune cell function showed that glutathione is essential for normal immune responses — lymphocyte proliferation, cytokine production, and natural killer cell activity were all significantly impaired when GSH was depleted, establishing it as a critical regulator of both innate and adaptive immunity (Hamilos & Wedner, 1985). Research into liver cell biology confirmed glutathione’s central role in Phase II detoxification — the process by which the liver neutralises and prepares harmful compounds for excretion (Hayes et al., 2005). Studies on mitochondrial glutathione identified it as a key determinant of whether cells survive or undergo programmed cell death under conditions of oxidative stress, with depleted mitochondrial GSH triggering the release of cytochrome c and activation of cell death pathways (Dalle-Donne et al., 2007).
For research use only. Not intended for use in humans or animals.
References
Dalle-Donne, I., et al. (2007). https://pubmed.ncbi.nlm.nih.gov/17197229/
Hamilos, D. L., & Wedner, H. J. (1985). https://pubmed.ncbi.nlm.nih.gov/3843082/
Hayes, J. D., et al. (2005). https://pubmed.ncbi.nlm.nih.gov/15822171/
Meister, A., & Anderson, M. E. (1983). https://pubmed.ncbi.nlm.nih.gov/6360752/
