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Review
. 2016 Jun;1374(1):159-67.
doi: 10.1111/nyas.13091. Epub 2016 Jun 15.

Chlorine-induced cardiopulmonary injury

Matthew Carlisle  1   2 , Adam Lam  1   2 , Erik R Svendsen  3   4 , Saurabh Aggarwal  1   2 , Sadis Matalon  1   2
Affiliations
Review

Chlorine-induced cardiopulmonary injury

Matthew Carlisle et al. Ann N Y Acad Sci. 2016 Jun.

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.

Keywords: autophagy; cardiac injury; chlorine; lung injury; mitochondrial dysfunction.

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Figures

Figure 1
Figure 1
Role of autophagy on chlorine (Cl2)-induced mitochondrial dysfunction. Mitochondria are the key regulators of cell survival in response to Cl2-induced cellular stress. Healthy mitochondria produce reactive oxygen species (ROS) that serve a cell signaling function; however, damaged mitochondria produce excessive amounts of ROS and become a major contributor of cellular and organ injury leading to mitochondrial DNA damage, formation of mitochondrial permeability transition (MPT) pores, and cell death. Mitochondria modified by ROS are targeted for removal by mitophagy, a critical step in maintaining mitochondrial quality control and limit cellular and organ injury. Upregulation of mitophagy by rapamycin or trehalose prevents mitochondrial oxidative damage and is beneficial in ameliorating Cl2 toxicity. Alternatively, decreasing mitophagy with 3-methyladenine (3-MA) enhances Cl2-induced injury.
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