Glutathione
The cell's principal thiol antioxidant — and the reason route of administration decides everything.
Skin & dermal · 7 min read · updated 13 Aug 2026
Research use only. The ranges below are what published studies and community protocols report. They are reference material for laboratory research, not medical advice or a recommendation for human or veterinary use.
The compound
Glutathione
View- Type
- Antioxidant Peptide
- CAS
- 70-18-8
- Formula
- C₁₀H₁₇N₃O₆S
- Mass
- 307.32 g/mol
At a glance
- Class
- Endogenous thiol tripeptide
- Sequence
- γ-Glu-Cys-Gly — note the unusual γ-linkage
- Molecular weight
- 307.32 g/mol
- CAS
- 70-18-8
- Intracellular concentration
- Millimolar — among the most abundant cellular metabolites
- Vial size stocked
- 1500 mg
Glutathione is a tripeptide with a structural quirk that matters: the bond between glutamate and cysteine is a γ-linkage, formed through the glutamate side chain rather than its α-carboxyl. Ordinary peptidases cannot cleave it. That single feature is why glutathione survives inside the cell at millimolar concentration while ordinary tripeptides are degraded within minutes.
Its jobs are the reduction of peroxides via glutathione peroxidase, the conjugation of electrophiles in phase II detoxification via glutathione S-transferase, the maintenance of protein thiols in the reduced state, and the recycling of vitamins C and E. The ratio of reduced (GSH) to oxidised (GSSG) glutathione is one of the standard readouts of cellular redox state.
The dermatological interest is separate and comes from a different mechanism: glutathione inhibits tyrosinase and shifts melanin synthesis from eumelanin toward the lighter pheomelanin. This is the basis of the skin-lightening literature, which is where most of the human intravenous dosing data actually comes from.
The oral absorption problem
This is the central fact about glutathione and it is routinely glossed over. Orally administered glutathione is extensively hydrolysed in the gut by γ-glutamyltransferase and absorbed as its constituent amino acids, not as the intact tripeptide. Plasma glutathione after an oral dose largely reflects resynthesis from those amino acids, and the rate-limiting step of that resynthesis is cysteine availability, not glutathione availability.
This is why N-acetylcysteine is often a more efficient way to raise cellular glutathione than glutathione itself, and why liposomal and sublingual formulations exist. It is also why parenteral routes — intravenous and subcutaneous — dominate the research protocols: they are the only routes that deliver intact glutathione to the circulation.
Where it is studied
- Dermatological pigmentation — the intravenous and oral skin-lightening literature, mostly from Southeast Asia, which is the source of the 600–1200 mg dose figures.
- Oxidative stress models across hepatology, neurology and pulmonology, where glutathione depletion is a shared feature.
- Detoxification research — paracetamol toxicity is the textbook case of glutathione depletion driving injury, and it is why NAC is the antidote.
- Redox biology generally, where the GSH:GSSG ratio serves as the readout rather than the intervention.
Rate and dilution
Like NAD+, glutathione is administered slowly. Rapid intravenous push is associated with flushing and discomfort, and subcutaneous injection of concentrated solution stings. A 1500 mg vial is a large amount of material — the fill volume should be chosen so the delivered concentration is comfortable, not so the syringe volume is small.
Storage
- Lyophilised: 2–8 °C or −20 °C, kept dry and protected from light and air.
- Reconstituted: 2–8 °C, used within days rather than weeks. Oxidation, not microbial growth, is the limiting process.
- Once a vial is opened, exposure to air begins the oxidation clock regardless of temperature.
Cautions
- The intravenous skin-lightening protocols are widely practised and thinly evidenced; regulators in several countries have issued warnings about high-dose intravenous glutathione for cosmetic purposes.
- Reported adverse events with intravenous use include hypersensitivity reactions and, rarely, more serious dermatological events such as Stevens-Johnson syndrome.
- Rate-related discomfort — flushing, chest tightness — mirrors the NAD+ pattern.
- Sulphur-containing compounds are a recognised allergen class; a reaction history matters.
References & credit
- 1Weschawalit S et al., Clin Cosmet Investig Dermatol 2017 — Glutathione and skin pigmentation — one of the controlled dermatological studies.
- 2Wu G et al., Journal of Nutrition 2004 — Glutathione metabolism and its implications for health — the synthesis and cysteine-limitation biology.
- 3Allen J, Bradley RD — J Altern Complement Med 2011 — Oral glutathione supplementation and oxidative stress biomarkers.
This article was written in-house. Where a dose range reflects community practice rather than a published trial, the community references we consulted are credited above and the article says which is which.