Myocardial infarction, acute ischemic stroke, and hyperglycemia triggered by acute chlorine gas inhalation

Köse, Ataman; Köse, Beril; Açıkalın, Ayça; Günay, Nurullah; Yıldırım, Cuma

doi:10.1016/j.ajem.2008.12.029

Cited by 17 publications

(21 citation statements)

References 13 publications

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“…These studies proposed a role for particulate matter-induced cardiovascular inflammation and oxidative stress (29). Cardiac effects of chlorine, especially cardiomegaly, were reported in autopsies of human victims of acute high-concentration chlorine gas exposure (1,(22)(23)(24). Similarly, experimental dogs that died of acute chlorine exposure had dilated right ventricles (30).…”

Section: Discussionmentioning

confidence: 99%

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Sarcoendoplasmic Reticulum Ca²⁺ ATPase. A Critical Target in Chlorine Inhalation–Induced Cardiotoxicity

Ahmad

Hendry‐Hofer

et al. 2015

Am J Respir Cell Mol Biol

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Autopsy specimens from human victims or experimental animals that die due to acute chlorine gas exposure present features of cardiovascular pathology. We demonstrate acute chlorine inhalation-induced reduction in heart rate and oxygen saturation in rats. Chlorine inhalation elevated chlorine reactants, such as chlorotyrosine and chloramine, in blood plasma. Using heart tissue and primary cardiomyocytes, we demonstrated that acute highconcentration chlorine exposure in vivo (500 ppm for 30 min) caused decreased total ATP content and loss of sarcoendoplasmic reticulum calcium ATPase (SERCA) activity. Loss of SERCA activity was attributed to chlorination of tyrosine residues and oxidation of an important cysteine residue, cysteine-674, in SERCA, as demonstrated by immunoblots and mass spectrometry. Using cardiomyocytes, we found that chlorine-induced cell death and damage to SERCA could be decreased by thiocyanate, an important biological antioxidant, and by genetic SERCA2 overexpression. We also investigated a U.S. Food and Drug Administration-approved drug, ranolazine, used in treatment of cardiac diseases, and previously shown to stabilize SERCA in animal models of ischemia-reperfusion. Pretreatment with ranolazine or istaroxime, another SERCA activator, prevented chlorine-induced cardiomyocyte death. Further investigation of responsible mechanisms showed that ranolazine-and istaroximetreated cells preserved mitochondrial membrane potential and ATP after chlorine exposure. Thus, these studies demonstrate a novel critical target for chlorine in the heart and identify potentially useful therapies to mitigate toxicity of acute chlorine exposure. Clinical RelevanceThis study defines impact of inhalation of a toxic gas, chlorine, on a critical cardiac calcium pump, sarcoendoplasmic reticulum Ca 21 ATPase (SERCA). It also demonstrates that therapeutic strategies that protect or modify SERCA function could be useful approaches for emergent resuscitation of severe chlorine inhalation victims.Chlorine is a commonly used chemical in industry and society. Acute chlorine inhalation toxicity can occur due to accidents at swimming pools and/or involving water purification systems, after transportation accidents, upon industrial exposure, with misuse of domestic cleaners, during military operations, and, more recently, through chemical terrorism. In the

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Section: Discussionmentioning

confidence: 99%

“…Besides pulmonary edema and respiratory failure, more than 90% of fatalities due to acute high-level chlorine exposure may be due to cardiovascular complications (1,(22)(23)(24). Our earlier studies with environmental oxidant gas exposures revealed enhanced airway epithelial cell death and subsequent loss of SERCA activity (17,25).…”

Section: Discussionmentioning

confidence: 99%

Sarcoendoplasmic Reticulum Ca²⁺ ATPase. A Critical Target in Chlorine Inhalation–Induced Cardiotoxicity

Ahmad

Hendry‐Hofer

et al. 2015

Am J Respir Cell Mol Biol

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“…Do sada su zabeleženi pojedinačni slučajevi trovanja pesticidima, ugljovodonicima, jedinjenjima azota, biljkama koje sadrže glikozide, morfinom i insulinom koji su doveli do akutnog miokarditisa i infarkta miokarda (13)(14)(15)(16)(17)(18)(19)(20).…”

Section: Slika 1 Inicijalni Ekg: Sinusna Tahikardija; Bez Patološkihunclassified

Fatal myocardial infarction after intentional ingestion of sulfuric acid

Radovanovic¹,

Stojanović-Marjanović²,

Goran³

et al. 2012

Medicinski casopis

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UVODTrovanja korozivnim supstancama čine petinu svih intoksikacija koje se beleže u našoj zemlji, čime zauzimaju drugo mesto -odmah iza medikamentoznih intoksikacija (1). Kiseline izazivaju koagulacionu nekrozu na mestima kontakta s tkivom i to izraženije što je kiselina koncentrovanija. Zadesna i suicidalna ingestija jakih neorganskih kiselina rezultuje teškim oštećenjem gastrointestinalnog sistema i sistemskim efektima kao što su cirkulatorni kolaps, metabolička acidoza, hipoksija, respiratorna insuficijencija, intravaskularna koagulacija, nekroza bubrežnih tubula i akutna bubrežna insuficijencija (2). Kiseline izazivaju jak bol na mestu dodira sa tkivom, kašalj, promuklost, nemogućnost gutanja, slabljenje pulsa, prestanak lučenja mokraće. Smrt može nastupiti unutar dva sata zbog edema glotisa i šoka, a kod protrahiranog toka nakon dva do četiri dana zbog perforacije želuca, akutne bubrežne slabosti i diseminovane intravaskularna koagulacije (3). Težina trovanja zavisi od količine i koncentracije kiseline unete u organizam.

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“…Among these emitted contaminants, Cl 2 is known for its acute health effect on the respiratory system (Agabiti et al, 2001;Rabinowitz and Siegel, 2002;Uyan et al, 2009) and acute ischemic stroke (Kose et al, 2009). HCl g is an upper respiratory tract irritant because of its high water-solubility (Salem, 2005).…”

Section: Introductionmentioning

confidence: 99%

Acid Gas, Acid Aerosol and Chlorine Emissions from Trichlorosilane Burning Processes

Soo

Chen

et al. 2011

Aerosol Air Qual. Res.

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This study was set out to investigate the emission characteristics of HCl (in both particle (HCl p ) and gaseous (HCl g ) forms), and Cl 2 during the trichlorosilane (TCS) burning process under various relative humidity conditions (RH; range = 55%-90%) which might exist at its storage area. All experiments were conducted in a test chamber. We found that , emitted from the TCS burning process for the all selected RH conditions. The particle sizes of HCl p fell to the range of the accumulation mode (MMADs = 0.808-1.04 μm; GSDs = 2.13-3.50). Fractions of emitted HCl p reaching to the alveolar region (= 85.8-88.8%) were much higher than that of the tracheobronchial region (= 6.53-8.80%) and head region (= 4.67-5.40%). It is concluded that more ill-health effects on the deep lung region can be expected than other regions as workers exposed to the contaminants emitted from TCS burning processes.

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Myocardial infarction, acute ischemic stroke, and hyperglycemia triggered by acute chlorine gas inhalation

Cited by 17 publications

References 13 publications

Sarcoendoplasmic Reticulum Ca²⁺ ATPase. A Critical Target in Chlorine Inhalation–Induced Cardiotoxicity

Sarcoendoplasmic Reticulum Ca²⁺ ATPase. A Critical Target in Chlorine Inhalation–Induced Cardiotoxicity

Fatal myocardial infarction after intentional ingestion of sulfuric acid

Acid Gas, Acid Aerosol and Chlorine Emissions from Trichlorosilane Burning Processes

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Myocardial infarction, acute ischemic stroke, and hyperglycemia triggered by acute chlorine gas inhalation

Cited by 17 publications

References 13 publications

Sarcoendoplasmic Reticulum Ca2+ ATPase. A Critical Target in Chlorine Inhalation–Induced Cardiotoxicity

Sarcoendoplasmic Reticulum Ca2+ ATPase. A Critical Target in Chlorine Inhalation–Induced Cardiotoxicity

Fatal myocardial infarction after intentional ingestion of sulfuric acid

Acid Gas, Acid Aerosol and Chlorine Emissions from Trichlorosilane Burning Processes

Contact Info

Product

Resources

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Sarcoendoplasmic Reticulum Ca²⁺ ATPase. A Critical Target in Chlorine Inhalation–Induced Cardiotoxicity

Sarcoendoplasmic Reticulum Ca²⁺ ATPase. A Critical Target in Chlorine Inhalation–Induced Cardiotoxicity