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An Overview on Arsenic Trioxide-Induced Cardiotoxicity
Vadavanath Prabhakaran Vineetha1, Kozhiparambil Gopalan Raghu2
1Department of Processing Technology, Kerala University of Fisheries and Ocean Studies (KUFOS), Panangad P.O., Kochi, 682506, India. vinnivp@gmail.com.
Cardiovascular Toxicology
|January 9, 2019
Summary
Arsenic trioxide (ATO) effectively treats acute promyelocytic leukemia but causes cardiotoxicity. This review explores ways to mitigate ATO
Area of Science:
- Oncology
- Cardiology
- Toxicology
Background:
- Arsenic trioxide (ATO) is a vital chemotherapy for acute promyelocytic leukemia.
- ATO's clinical utility is limited by cardiotoxicity, preventing its use in some patients.
- Reactive oxygen species contribute to various diseases, including cancer and cardiovascular disorders.
Purpose of the Study:
- To review the dual effects (beneficial and harmful) of arsenic and ATO.
- To elucidate the mechanisms behind ATO-induced toxicity.
- To explore strategies for circumventing ATO's cardiotoxicity.
Main Methods:
- Literature review of arsenic and ATO effects.
- Analysis of mechanisms underlying ATO toxicity.
- Identification of potential protective agents against reactive oxygen species.
Main Results:
- ATO demonstrates significant efficacy in treating relapsed/refractory acute promyelocytic leukemia.
- Cardiotoxicity is a major dose-limiting side effect of ATO.
- Reactive oxygen species play a role in ATO's toxicity and therapeutic effects.
Conclusions:
- Mitigating ATO-induced cardiotoxicity could expand its therapeutic application.
- Understanding ATO's mechanisms of action and toxicity is crucial for developing safer treatments.
- Agents that counteract reactive oxygen species may offer a protective strategy against ATO toxicity.
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