Literature DB >> 25028454

Decreased glutathione and low catalase activity contribute to oxidative stress in children with α-1 antitrypsin deficiency.

Amparo Escribano1, Mónica Amor2, Sara Pastor3, Silvia Castillo1, Francisco Sanz4, Pilar Codoñer-Franch5, Francisco Dasí3.   

Abstract

BACKGROUND: Recent investigations in animal models have revealed oxidative stress and oxidative damage in the pathogenesis of alpha-1 antitrypsin deficiency (AATD). However, no data are available on the oxidative stress status and antioxidant enzyme activity in these patients. This study was aimed to analyse the oxidative stress profile and enzymatic antioxidant defence mechanisms in children with AATD.
METHODS: Oxidative stress parameters and the activity of the main antioxidant enzymes were prospectively measured in serum of fifty-one children diagnosed with AATD and thirty-eight control individuals.
RESULTS: Oxidative stress was increased in the serum of children with intermediate- (MZ; SZ) and high-risk (ZZ) phenotypes for developing AATD-related emphysema and/or liver disease. When compared with the control group, intermediate- and high-risk groups showed significantly lower total glutathione and reduced glutathione levels, decreased catalase activity and increased glutathione peroxidase activity leading to an accumulation of hydrogen peroxide that would explain the significantly increased levels of oxidative stress biomarkers observed in these patients. No differences were observed between the control (MM) and the low-risk (MS; SS) groups. A gradation in oxidative stress parameters was observed when patients were compared among themselves, in that the expression of the Z allele produces a higher oxidative stress status in homozygous (ZZ) than in heterozygous (MZ; SZ) patients.
CONCLUSIONS: Increased oxidative stress, together with reduced antioxidant defence are involved in the pathophysiology of AATD at early stages, opening up a new rationale for the use of antioxidant therapies in the treatment of the disease. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

Entities:  

Keywords:  COPD ÀÜ Mechanisms; Emphysema; Oxidative Stress; Rare lung diseases

Mesh:

Substances:

Year:  2014        PMID: 25028454     DOI: 10.1136/thoraxjnl-2014-205898

Source DB:  PubMed          Journal:  Thorax        ISSN: 0040-6376            Impact factor:   9.139


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