Glutathione biochemistry in asthma

N.L. Reynaert*

*Corresponding author for this work

Research output: Contribution to journal(Systematic) Review article peer-review

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Abstract

Oxidative stress in an important hallmark of asthma and much research has therefore focused on the predominant antioxidant in the lungs, namely the tripeptide glutathione. In lung samples of patients with asthma increased levels of glutathione are typically observed which appear to relate to the level of pulmonary inflammation and are therefore regarded as an adaptive response to the associated oxidative stress. Also in blood samples increased total GSH levels have been reported, representing the systemic inflammatory component of the disease. In addition, a number of the antioxidant enzymes involved in the maintenance of the GSH/GSSG ratio as well as enzymes that utilize GSH have been found to be altered in the lungs and blood of asthmatics and will be summarized in this review. Very few studies have however linked enzymatic alterations to GSH levels or found that either of these correlated with disease severity. Some animal studies have started to investigate the pathophysiological role of GSH biochemistry in asthma and have yielded surprising results. Important in this respect is the physiological role of the GSH redox equilibrium in determining the outcome of immune responses which could be deregulated in asthmatics and contribute to the disease. Clinical data as well as animal and cell culture studies regarding these aspects of GSH in the context of asthma will be summarized and discussed in this review.
Original languageEnglish
Pages (from-to)1045-1051
Number of pages7
JournalBiochimica et Biophysica Acta-general Subjects
Volume1810
Issue number11
DOIs
Publication statusPublished - Nov 2011

Keywords

  • Glutathione
  • Asthma
  • Oxidative stress
  • Redox balance
  • Glutathione peroxidase
  • Glutathione reductase
  • Glutathione-S-transferase
  • Glutaredoxin
  • OBSTRUCTIVE PULMONARY-DISEASE
  • SERUM SELENIUM CONCENTRATION
  • INDUCED AIRWAY INFLAMMATION
  • INCREASED OXIDATIVE STRESS
  • MESSENGER-RNA EXPRESSION
  • EPITHELIAL LINING FLUID
  • PEROXIDASE ACTIVITY
  • INDUCED SPUTUM
  • INTRINSIC ASTHMA
  • BRONCHIAL-ASTHMA

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