Glutathione
also known as GSH, γ-L-Glutamyl-L-cysteinyl-glycine, L-Glutathione, reduced glutathione
Endogenous tripeptide (γ-glutamyl-cysteinyl-glycine) — master cellular thiol and principal non-enzymatic antioxidant. Synthesized via glutamate-cysteine ligase and glutathione synthetase. Functions as cofactor for glutathione peroxidase and transferase; conjugates electrophiles, reduces peroxides, maintains redox homeostasis. Investigated in IV, oral, and inhaled formulations for oxidative stress mitigation, hepatic detoxification, and metabolic support.
At a glance
IV · Oral · Inhaled
Primary target — Intracellular redox systems, glutathione peroxidase, glutathione transferase.
Pathway — Synthesized via glutamate-cysteine ligase (GCL) → γ-glutamylcysteine → glutathione synthetase (GS) → GSH.
Downstream effect — Reduction of reactive oxygen species, conjugation of electrophiles, maintenance of cellular thiol-disulfide balance, GPX4 activation for lipid peroxide reduction.
Origin — Endogenous tripeptide; predominantly synthesized in liver, exported to extracellular space and tissues [terrell-2025][hecht-2026].
| Parameter | Value |
|---|---|
| Endogenous synthesis | Hepatic synthesis ~10 g/day (basal rate)Tissue-specific; demand-driven upregulation via Nrf2 signaling. |
| Exogenous oral | 250–1000 mg/dayBioavailability limited; gastric hydrolysis reduces systemic uptake. |
| IV supplementation | 600–1200 mg (research protocols)Used in clinical oxidative stress and hepatic detoxification studies. |
| Precursor strategy | N-acetylcysteine (NAC) 600–1200 mg/dayProvides cysteine for endogenous GSH synthesis; bypasses GI degradation. |
| Evidence basis | Animal mechanistic + human mechanistic |
Reconstitution
A pure mass-to-volume utility. Enter what you have in the vial; the atlas computes the volume per dose. No prescription information.
- — Active malignancy (theoretical cysteine supply risk) [hecht-2026]
- — Severe asthma (inhaled formulations)
- 01Oral administration
Capsule or liquid form, 250–1000 mg once daily. Take on empty stomach for improved absorption, though GI hydrolysis limits bioavailability. NAC precursor strategy often preferred.
- 02Intravenous
Clinical protocols: 600–1200 mg slow infusion over 30–60 minutes. Used for acute oxidative stress, hepatic detoxification support. Administered in medical settings.
- 03Inhaled formulations
Nebulized GSH (research protocols). Monitor for bronchospasm in reactive airway patients. Used experimentally for pulmonary oxidative stress.
- 04Precursor supplementation
N-acetylcysteine (NAC) 600–1200 mg/day PO. Provides cysteine substrate for endogenous GSH synthesis. Bypasses gastric degradation, preferred for chronic supplementation.
Sources
of 39 rendered claims carry a resolvable citation.
- [aiana-2026]Aiana 2026 — Metabolic enhancement of glutathione biosynthesis via StGCL overexpression reduces acrylamide formation and improves salinity and osmotic stress resilience in potato tubers.
journal, 2026 - [hecht-2026]Hecht 2026 — Catabolism of extracellular glutathione supplies cysteine to support tumours.
journal, 2026 - [terrell-2025]Terrell 2025 — Extracellular Matrix Microstructures Directly Regulate Glutathione Bioavailability in Human Hepatocytes.
journal, 2025 - [wang-2026]Wang 2026 — Atmospherically relevant PM(2.5) promotes age-related muscle atrophy in an age-dependent manner.
journal, 2026