Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2009;23(1):61-8.
doi: 10.1016/j.jtemb.2008.10.001. Epub 2008 Dec 23.

Characterization of cytotoxicity induced by arsenic trioxide (a potent anti-APL drug) in rat cardiac myocytes

K G Raghu  1 , Ozhathil Lijo Cherian
Affiliations

Characterization of cytotoxicity induced by arsenic trioxide (a potent anti-APL drug) in rat cardiac myocytes

K G Raghu et al. J Trace Elem Med Biol. 2009.

Abstract

Arsenic, a known environmental toxicant, is ubiquitously present in the environment. Arsenic trioxide (ATO), an anti-acute promyelocytic leukemia (APL) drug, is associated with cardiac toxicity. It is reported to induce cardiac arrhythmia via altering various ion channels involved in the repolarization phase of cardiac action potential. The exact molecular mechanism of cardiovascular adverse effect due to ATO exposure has not been fully elucidated except for alteration on ion channels. To evaluate the cytotoxic effect of ATO on cardiac myocytes, primary culture of myocytes was treated with different doses (30, 60 and 90 microM) of ATO for various periods (24, 48 and 72 h). Cardiac toxicity was assessed by monitoring cell viability, mitochondrial and deoxyribonucleic acid (DNA) integrity, reactive oxygen species (ROS) generation, calcium overload and apoptosis. ATO exposure caused alteration in mitochondrial integrity, generation of ROS, calcium overload and apoptosis in cardiac cells in dose- and duration-dependent manner. There was no DNA fragmentation. Hence our results show that ATO causes apoptosis in cardiomyocytes by generation of ROS and the induction of calcium overload.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

LinkOut - more resources

-