Glutathione redox system in oxidative lung injury

Qamar Rahman*, Parveen Abidi, Farrukh Afaq, D. Schiffmann, Brooke T. Mossman, David W. Kamp, Mohammad Athar

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

143 Scopus citations


Glutathione (GSH) is a ubiquitous intracellular thiol present in all tissues, including lung. Besides maintaining cellular integrity by creating a reduced environment, GSH has multiple functions, including detoxification of xenobiotics, synthesis of proteins, nucleic acids, and leukotrienes. Present in high concentrations in bronchoalveolar lavage fluid (BALF), GSH provides protection to the lung from oxidative injury induced by different endogenous or exogenous pulmonary toxicants. Its depletion in the lung has been associated with the increased risk of lung damage and disease. The redox system of GSH consists of primary and secondary antioxidants, including glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S- transferase (GST), and glucose 6-phosphate dehydrogenase (G6PD). Alterations in the activities of there enzymes may reflect reduced cellular defense and may serve as surrogate markers of many lung diseases. As GSH is also involved in the regulation of expression of protooncogenes and apoptosis (programmed cell death), the development of diseases such as cancer and human immune deficiency may be affected by depleting or elevating cellular GSH levels. Exogenous delivery of GSH or its precursor N-acetyl cysteine (NAC) is being used as chemotherapeutic approach.

Original languageEnglish (US)
Pages (from-to)543-568
Number of pages26
JournalCritical Reviews in Toxicology
Issue number6
StatePublished - 1999


  • Antioxidant
  • Gene regulation
  • Glutathione
  • Lung
  • Lung injury
  • Redox system enzymes
  • Therapeutics

ASJC Scopus subject areas

  • Toxicology


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