Glutathione

Glutathione is a peptide studied for its effects on skin and hair, aging, and inflammation. Endogenous tripeptide antioxidant (glutamate-cysteine-glycine) supporting liver detox, skin brightening, and anti-aging. Permitted under WADA rules.

Glutathione (GSH) is a tripeptide made of the amino acids glutamate, cysteine, and glycine, and is the body's most abundant intracellular antioxidant. It is found in plants, animals, fungi, and some bacteria and archaea, and prevents damage to important cellular components caused by reactive oxygen species, free radicals, peroxides, lipid peroxides, and heavy metals. Beyond direct radical scavenging, glutathione supports phase-II liver detoxification, regenerates other antioxidants such as vitamins C and E, and maintains cellular redox balance.

Overview

Supplemental glutathione — oral (including liposomal), intravenous, intramuscular, or subcutaneous — is used for antioxidant support, liver health, and dermatological skin-brightening protocols, though oral bioavailability of standard formulations is limited.

Glutathione is permitted under World Anti-Doping Agency (WADA) rules as a substance; only high-volume intravenous infusion is restricted as a method, not glutathione itself.

Mechanism of action

The body's master intracellular antioxidant. Scavenges free radicals and supports liver phase-II detoxification. Regenerates vitamins C and E. Used for liver health, skin brightening, and anti-aging.

Reported effects

Effects reported in the literature and from preclinical models include:

• Oral glutathione at 250 mg once daily, 250 mg twice daily, or 500 mg once daily significantly reduced the skin melanin index compared with placebo in five randomized controlled trials. ^[4] Phase II
• Topical glutathione at 0.5% was significantly more effective for skin lightening than 0.1% glutathione and placebo. ^[4] Phase II
• Topical 2% glutathione combined with oral glutathione gave better skin lightening than either form used alone. ^[4] Phase II
• Glutathione acts as the essential reducing substrate for glutathione peroxidase 4 (GPX4), which removes toxic lipid peroxides to suppress ferroptotic cell death, and glutathione depletion is a defining feature of ferroptosis. ^[3][1][2] Preclinical
• In metabolic dysfunction-associated steatotic liver disease, falling glutathione levels promote hepatic lipid accumulation and oxidative injury, and glutathione chelates excess cuprous ions to limit copper-driven cell death. ^[3] Preclinical
• Mitochondrial glutathione metabolizes hydrogen peroxide inside mitochondria, and a long-term imbalance between mitochondrial reactive oxygen species and mitochondrial glutathione can cause cell dysfunction and ferroptosis. ^[5] Preclinical

Evidence grades: FDA approvedApproved (non-US)Phase IIIPhase IIPhase IPreclinicalAnecdotal

Dosage and administration

Oral

• General: 250-500mg daily, taken on an empty stomach (standard oral bioavailability is low)
• Liposomal: 500-1000mg daily (enhanced absorption versus standard oral)

Intravenous

• Antioxidant/skin protocols: 600-1200mg, 1-3 times weekly

Intramuscular

• 200-600mg, 1-3 times weekly

Subcutaneous

• 100-300mg, several times weekly

Cofactor support

• pair with vitamin C and N-acetylcysteine (NAC) to aid synthesis and recycling

Natty status

Glutathione is generally regarded as compatible with the natty designation, particularly when used for therapeutic healing purposes. Opinions vary across natural bodybuilding federations, and athletes who compete should consult the rulebook of their respective sanctioning body.^[6]

Research

The peptide has been the subject of 50 studies and reference works collected on this site. Additional bibliography is in § External links below.

Related compounds

Other peptides in this catalogue with overlapping mechanisms or status:

Frequently asked questions

What is Glutathione?

Endogenous tripeptide antioxidant (glutamate-cysteine-glycine) supporting liver detox, skin brightening, and anti-aging. Permitted under WADA rules.

What is Glutathione used for?

Glutathione is used to support the liver, to brighten skin, to slow visible aging, and to help protect cells against damage.

How does Glutathione work?

The body's main built-in antioxidant, made of three amino acids, taken by mouth or given by drip or injection. It neutralises harmful molecules and puts vitamins C and E back to work.

Is Glutathione natty?

Glutathione is generally regarded as compatible with natural bodybuilding. Most sanctioning bodies do not prohibit its therapeutic use, though rules vary by federation.

Is Glutathione banned by WADA?

No. Glutathione is permitted under World Anti-Doping Agency (WADA) rules. Intravenous infusion above the volume limit of WADA method M2.2 is restricted whatever is infused, and the list is revised every year, so check the current edition before competing.

How is Glutathione administered?

Glutathione is typically administered via: oral, intravenous injection, intramuscular injection, subcutaneous injection. Dosage and administration protocols vary; see the Dosage section for details.

References

1. ^ Bidirectional regulation between ferroptosis and tumor-associated macrophages: mechanisms, strategies, and therapeutic perspectives. Recent review
2. ^ Mechanism of Ferroptosis in Cardiovascular Disease and Its Regulation by Natural Compounds: A Narrative Review. Recent review
3. ^ a b [Role of glutathione in regulating ferroptosis and cuproptosis in metabolic dysfunction-associated steatotic liver disease]. Recent review
4. ^ a b c Glutathione as a skin-lightening agent and in melasma: a systematic review. Recent review
5. ^ Mitochondrial Glutathione in Cellular Redox Homeostasis and Disease Manifestation. Recent review
6. ^ a b World Anti-Doping Agency. (2026). Prohibited List 2026.

External links

• Wikipedia article
• Metabolic Reprogramming in Renal Cell Carcinoma: A Scoping Review with Quantitative Integration of Metabolomic Studies.
• Bioactive plant metabolites with antihyperglycemic properties: prospects for the prevention and treatment of diabetes mellitus.
• Endothelial ferroptosis in blood-brain barrier dysfunction and neuroinflammation: mechanisms and immune-vascular crosstalk.
• Targeting mitochondria as a potential therapeutic strategy against radioresistance in cancer.
• Comprehensive analysis of pathogenic mechanisms of Enterobacter cancerogenus ECL9 in silkworms.
• Ostrich Meat: A Review on Nutritional Properties and Health Benefits.
• Redox-responsive nanomedicine beyond glutathione: harnessing reactive oxygen species and emerging endogenous triggers for precision drug delivery.
• Ferroptosis, lipid metabolism, and genetic regulation in postoperative rehabilitation of elderly hip fractures: from molecular mechanisms to clinical translation.
• Redox-responsive LNPs for therapeutics delivery.
• Targeting disulfidptosis: from molecular mechanisms to nanotechnology-mediated delivery strategies.
• The role of ferroptosis in the pathogenesis and treatment of breast cancer.
• Selective reduction of thalamic glutathione in migraine in the absence of detectable N-acetylaspartate alterations.
• Biogenic selenium nanoparticles: a multifunctional tool for combating oxidative stress and chronic diseases.
• Exercise-induced redox modulation of red blood cell function in health and disease: Mechanistic implications for hemoglobin cycling and microvascular regulation.
• An Intermediate-Centric View of Cascade Cancer Nanotherapeutics.
• The design of activatable photosensitizers and applications in precision immunomodulation.
• Beyond Antioxidant Activity, Towards Redox Modulation: N-Acetylcysteine (NAC) in Endometriosis and Uterine Leiomyomas.
• [Research progress on mechanisms and therapeutic potential of active components of TCM in intervening lipid metabolism reprogramming in colorectal cancer].
• Oxidative Stress in Childhood Nephrotic Syndrome: A Narrative Review From Mechanisms to Clinical Implications.
• Oxidative stress responses in human fungal pathogens: a review of molecular mechanisms.
• Plant stress physiology under environmental emerging contaminant exposure: from molecular responses to phytoremediation applications.
• The Redox Code of Diabetic Retinopathy: Decoding Metabolic Memory, Predicting Fate, and Targeting Heterogeneity.
• Targeting ferroptosis through kinase signaling: The roles of MAPK and AMPK pathways in cancer therapy.
• Unraveling the Crosstalk Between Ferroptosis and Cuproptosis for Rational Nanomedicine Design in Cancer.
• The NRF2 signaling pathway in hepatocellular carcinoma: dual roles, epigenetic reprogramming, and therapeutic opportunities in metabolic vulnerability.
• Breaking the cycle of fibrosis: Ferroptosis as a therapeutic target (Review).
• Role of arbutin and acetoside against Parkinson's disease.
• Selenium-centered radicals: generation, detection and their relevance in chemistry and biology.
• Engineered Nanozymes for Colorectal Cancer Therapy: Catalytic Reprogramming of the Tumor Microenvironment.
• Targeting ferroptosis and mitochondrial ROS: organoprotective mechanisms of anesthetic conditioning in liver transplantation.
• Targeting glutathione peroxidase 4 in ferroptosis: from immune regulation to pharmacological development and translational applications.
• From pumps to networks: ABC transporters in leukemia resistance and microenvironmental adaptation.
• Advances in ferroptosis mechanisms and therapeutic potential in head and neck squamous cell carcinoma.
• Organoselenium compounds as redox modulators of inflammation: Synthetic strategies, mechanistic insights, and therapeutic potential.
• Stimuli-Responsive Mesoporous Silica Nanoparticles for Precision Cancer Therapy: Design Principles, Cellular Uptake, and Translational Perspectives.
• The Auranofin-Colistin Combination Efficiency Against the Gram-Negative Strains: A Review.
• Metabolomics integrated with network pharmacology suggests the potential mechanisms of Chaibei Zhixian decoction in epilepsy.
• Pharmacological targeting of ferroptosis in cancer: mechanisms, tumor immunity, and translational challenges.
• Aflatoxin-associated hepatocarcinogenesis in a changing climate: the gut microbiome as a missing link in the One Health framework.
• NRF2-Regulated Ferroptosis in Breast Cancer: Mechanisms, Resistance, and Therapeutic Opportunities.
• Ferroptosis in retinal neurodegeneration: mechanistic vulnerability, therapeutic targeting, and translational barriers.
• Ferroptosis in major depressive disorder: Molecular mechanisms, cellular vulnerability, and therapeutic opportunities.
• Investigating the neurological function and anti-inflammatory effects of resveratrol in small mammal spinal cord injury models: A systematic review and meta-analysis.
• Glutathione and glutathione-dependent enzymes: From biochemistry to gerontology and successful aging.
• 1500mg Glutathione — commercial