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Compound reference

Glutathione

Cellular & Longevity Research · vial. For laboratory research use only. Not for human or veterinary consumption, diagnostic use, therapeutic use, or clinical use.

Chemistry identity

Reference identifiers

CAS 70-18-8Formula C10H17N3O6SMW 307.33 g/mol (average MW)PubChem CID 124886Amino acids 3

Published literature

Research context

Peer-reviewed literature referencing this compound, provided for research context.

Polyethylene microplastics as emerging reproductive toxicants: Evidence from an oocyte-based mammalian model2026

Nikoloff N, Fabra MC, Campagna AA, Sella ME, Taminelli GL, Carranza-Martin AC

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

In a bovine oocyte in-vitro maturation model, researchers used intracellular glutathione (GSH) content as a redox-status biomarker to characterize how polyethylene microplastic exposure disrupted mitochondrial organization and antioxidant balance during meiotic maturation, without compromising overall oocyte viability.

Research progress of ferroptosis in cervical cancer treatment2026

Wang F, Wang L, Bai Y

Annals of medicine

This narrative review surveys the cystine/glutathione axis (system Xc−–GPX4) as a regulator of iron-dependent lipid peroxidation (ferroptosis) being investigated as a research strategy against chemoresistant cervical cancer cell models, characterizing glutathione's role as the GPX4 cofactor governing lipid-peroxide detoxification within redox-homeostasis signaling and its crosstalk with p53/NRF2 pathways.

Upregulation of Peroxiredoxin 3 Protects Afg3l2-KO Cortical Neurons In Vitro from Oxidative Stress: A Paradigm for Neuronal Cell Survival under Neurodegenerative Conditions2019

Bettegazzi B, Pelizzoni I, Salerno Scarzella F, Restelli LM, Zacchetti D, Maltecca F, et al.

Oxidative medicine and cellular longevity

In a mouse AFG3L2 knockout model (embryonic fibroblasts and cortical neurons), researchers used pharmacologic glutathione depletion to show that elevated basal glutathione was necessary for the enhanced oxidative-stress tolerance of AFG3L2-deficient fibroblasts, isolating glutathione's specific contribution to cellular antioxidant defense from other compensatory pathways (peroxiredoxin 3, SOD2).

Ferroptosis Contributes to Neuronal Death and Functional Outcome After Traumatic Brain Injury2019

Kenny EM, Fidan E, Yang Q, Anthonymuthu TS, New LA, Meyer EA, et al.

Critical care medicine

Using an HT22 neuronal cell line and a mouse controlled-cortical-impact traumatic brain injury model, this study measured cortical glutathione depletion alongside 15-lipoxygenase-driven lipid peroxidation as markers of ferroptotic cell death, and showed that pharmacological inhibition of the lipoxygenase pathway reduced oxidized-phospholipid lipid-peroxidation products and hippocampal TUNEL-positive cell-death markers, with improved spatial-memory performance in the injured mice.

Induction of Nrf2-mediated cellular defenses and alteration of phase I activities as mechanisms of chemoprotective effects of coffee in the liver2008

Cavin C, Marin-Kuan M, Langouët S, Bezençon C, Guignard G, Verguet C, et al.

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

In rat liver and primary hepatocyte models, this study characterized glutathione and glutathione S-transferase induction as downstream markers of Nrf2-antioxidant-response-element pathway activation, mapping how this endogenous glutathione-dependent detoxification system correlates with reduced carcinogen-DNA adduct formation in cell and tissue models.

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This product is intended strictly for research and laboratory use only. It is designated for in vitro testing and experimental purposes. Any use involving human or animal consumption is prohibited by law. All information provided on this website is for educational purposes only. This product must only be handled by licensed, qualified professionals. It is not intended for use as a drug, food, or cosmetic, and must not be misused, mislabeled, or misrepresented as such.