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Citation |
Carlisle M, Lam A, Svendsen ER, Aggarwal S, Matalon S. Ann. N. Y. Acad. Sci. 2016; 1374(1): 159-167. |
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Affiliation |
Division of Molecular and Translational Biomedicine, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama. |
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Copyright |
(Copyright © 2016, John Wiley and Sons) |
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DOI |
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PMID |
27303906 |
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Abstract |
Chlorine (Cl2 ) is utilized worldwide for a diverse range of industrial applications, including pulp bleaching, sanitation, and pharmaceutical development. Though Cl2 has widespread use, little is known regarding the mechanisms of toxicity associated with Cl2 exposure, which occurs during industrial accidents or acts of terrorism. Previous instances of Cl2 exposure have led to reported episodes of respiratory distress that result in high morbidity and mortality. Furthermore, studies suggest that acute Cl2 exposure also results in systemic vascular injury and subsequent myocardial contractile dysfunction. Here, we review both lung and cardiac pathology associated with acute Cl2 inhalation and discuss recently published data that suggest that mitochondrial dysfunction underlies the pathogenesis of Cl2 -induced toxicity. Last, we discuss our findings that suggest that upregulation of autophagy protects against Cl2 -induced lung inflammation and can be a potential therapeutic target for ameliorating the toxic effects of Cl2 exposure. Language: en |