Chlorine inhalation induces acute chest syndrome in humanized sickle cell mouse model and ameliorated by postexposure hemopexin

Autor: Noor A. Ahmed, Namasivayam Ambalavanan, Muna Sapkota, Tamas Jilling, Adam Molyvdas, Kelsey Maclin, Carolyn J. Albert, Israr Ahmad, Saurabh Aggarwal, David A. Ford, Sadis Matalon, Ammar Saadoon Alishlash, Stephen F. Doran
Rok vydání: 2021
Předmět:
Zdroj: Redox Biology
Redox Biology, Vol 44, Iss, Pp 102009-(2021)
ISSN: 2213-2317
Popis: Triggering factors of Acute Chest Syndrome (ACS) is a leading cause of death in patients with Sickle Cell Disease (SCD) and targeted therapies are limited. Chlorine (Cl2) inhalation happens frequently, but its role as a potential trigger of ACS has not been determined. In this study, we hypothesized that Cl2 exposure resembling that in the vicinity of industrial accidents induces acute hemolysis with acute lung injury, reminiscent of ACS in humanized SCD mice. When exposed to Cl2 (500 ppm for 30 min), 64% of SCD mice succumbed within 6 h while none of the control mice expressing normal human hemoglobin died (p
Graphical abstract Image 1
Highlights • Chlorine inhalation induces exaggerated hemolysis in sickle mice. • Free heme results in fatal acute chest syndrome in sickle versus control mice. • Chlorinated lipids mediate the effects of chlorine on the red blood cells. • Hemopexin alleviates chlorine induced hypoxia, and acute lung injury. • Therefore, postexposure hemopexin injection improves the survival of sickle mice.
Databáze: OpenAIRE