Authors
Hadis Fathizadeh, Hamidreza Rezaeipour, Fatemeh Nouri, Mahsa Mohajeri
Published in
Inflammopharmacology. Jul 14, 2026. Epub Jul 14, 2026.
Abstract
Glutathione (GSH) plays an important role in the antioxidant defense and body detoxification system. It is a tripeptide molecule consisting of glutamine, cysteine and glycine. It is mainly produced by the liver and is a powerful antioxidant that neutralizes free radicals and prevent cellules from damage. This review study was performed to explore the possible benefits and limitations of oral GSH supplementation in different conditions. The studies results indicated that GSH may considerably reduce oxidative stress. GSH's ability to eliminate free radicals and improve insulin sensitivity may contribute to its beneficial effect on diabetes management. Another result is that GSH could reduce oxidative damage, inflammation and improve the gastric mucosal repair Helicobacter-induced gastrointestinal diseases. Moreover, GSH supplementation exerts neuroprotective effects after a brief brain ischemic insult through the reduction of inflammation and oxidative stress. People with cystic fibrosis often have low GSH levels, which may lead to increased oxidative stress and lung inflammation. Oral GSH supplementation has been shown that could improve respiratory function, reduce lung damage and enhance antioxidant defense in cystic fibrosis patients. Also, GSH is gaining popularity as a skin-whitening ingredient because it can inhibit the production of melanin. Our results suggested that oral GSH supplementation may be beneficial for skin tone improvement and hyperpigmentation reduction. In conclusion, oral GSH supplementation can be useful for the treatment of neurodegenerative diseases, diabetic mellitus, stomach pathologies caused by Helicobacter, cystic fibrosis, transient cerebral ischemia attack, and skin-whitening conditions. Further research is needed to determine the best dosages, potential long-term benefits, and possible side effects of GSH supplementation in these conditions.
PMID:
42446814
Bibliographic data and abstract were imported from PubMed on 14 Jul 2026.
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