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Role of heme in bromine‐induced lung injury
Author(s) -
Lam Adam,
Vetal Nilam,
Matalon Sadis,
Aggarwal Saurabh
Publication year - 2016
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.13086
Subject(s) - heme , heme oxygenase , lung , toxicity , hemopexin , medicine , inhalation , phosgene , oxidative stress , bronchoalveolar lavage , pharmacology , chemistry , immunology , biochemistry , anesthesia , enzyme , organic chemistry
Bromine (Br 2 ) gas inhalation poses an environmental and occupational hazard resulting in high morbidity and mortality. In this review, we underline the acute lung pathology (within 24 h of exposure) and potential therapeutic interventions that may be utilized to mitigate Br 2 ‐induced human toxicity. We discuss our latest published data, which suggest that an increase in heme‐dependent tissue injury underlies the pathogenesis of Br 2 toxicity. Our study was based on previous findings that demonstrated that Br 2 upregulates the heme‐degrading enzyme heme oxygenase‐1 (HO‐1), which converts toxic heme into bilverdin. Interestingly, following Br 2 inhalation, heme levels were indeed elevated in bronchoalveolar lavage fluid, plasma, and whole lung tissue in C57BL/6 mice. High heme levels correlated with increased lung oxidative stress, lung inflammation, respiratory acidosis, lung edema, higher airway resistance, and mortality. However, therapeutic reduction of heme levels, by either scavenging with hemopexin or degradation by HO‐1, improved lung function and survival. Therefore, heme attenuation may prove a useful adjuvant therapy to treat patients after Br 2 exposure.