RESUMO
The article "The Molecular Mechanism of Aluminum Phosphide poisoning in Cardiovascular Disease: Pathophysiology and Diagnostic Approach", written by Seyed Farzad Hosseini · Mehdi Forouzesh · Mohsen Maleknia · Samira Valiyari · Mahmood Maniati · Azin Samimi, was originally published electronically on the publisher's internet portal (currently SpringerLink) on 25th July 2020 with open access. With the author(s)' decision to step back from Open Choice, the copyright of the article changed on 29th July 2020 to © Springer Science+Business Media, LLC, part of Springer Nature 2020 and the article is forthwith distributed under the terms of copyright. The original article has been corrected.
RESUMO
Nowadays, poisoning with metal phosphides, especially aluminum phosphide (ALP), is one of the main health threats in human societies. Patients suffer from significant complications due to this type of poisoning, and the heart is one of the main organs targeted by ALP. Therefore, in this study, we discussed the effect of phosphine on cardiac function. This study is based on data obtained from PubMed, between 2002 and 2020. The key keywords included "Aluminum phosphide," "Oxidative Stress," "Mitochondria," "Cardiovascular disease," and "Treatment." The results showed that ALP produced reactive oxygen species (ROS) due to mitochondrial dysfunction. ROS production leads to red blood cell hemolysis, decreased ATP production, and induction of apoptosis in cardiomyocytes, which eventually results in cardiovascular disease. Since ALP has the most significant effect on cardiomyocytes, the use of appropriate treatment strategies to restore cell function can increase patients' survival.