Discrepancy between mRNA and protein expression of neutrophil gelatinase-associated lipocalin in bronchial epithelium induced by sulfur mustard

Majid Ebrahimi, Mehryar Habibi Roudkenar, Abbas Ali Imani Fooladi, Raheleh Halabian, Mostafa Ghanei, Hisatake Kondo, Mohammad Reza Nourani

    Research output: Contribution to journalArticlepeer-review

    25 Citations (Scopus)

    Abstract

    Sulfur mustard (SM) is a potent vesicant that has been employed as a chemical weapon in various conflicts during the 20th century. More recently, mustard was used in the Iraq conflict against Iranian troops and civilians. At the present time there are more than 40.000 people suffering from pulmonary lesions special bronchiolitis obliterans (BOs) due to mustard gas. SM increases the endogenous production of reactive oxygen species (ROS). Neutrophil Gelatinase-associated Lipocalin 2 (Lcn2, NGAL) is a member of the lipocalin superfamily for which a variety of functions such as cellular protection against oxidative stress have been reported. Ten normal and Twenty SM-induced COPD patient individuals were studied. Assessment of NGAL expressions in healthy and the patients endobrinchial biopsies were performed by semiquantitative RT-PCR, real-time RT-PCR, and Immunohistochemistry analysis. While Normal control samples expressed same level of mRNA NGAL, expression level of mRNA-NGAL was upregulated about 1.4- to 9.8-folds compared to normal samples. No significant immunoreactivity was revealed in both samples. As we are aware this is the first report of induction of NGAL in patients exposed to SM. NGAL may play an important role in cellular protection against oxidative stress toxicity induced by mustard gas in airway wall of patients.

    Original languageEnglish
    Article number823131
    JournalJournal of Biomedicine and Biotechnology
    Volume2010
    DOIs
    Publication statusPublished - 2010

    ASJC Scopus subject areas

    • Biotechnology
    • Molecular Medicine
    • Molecular Biology
    • Genetics
    • Health, Toxicology and Mutagenesis

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