Abstract
BACKGROUND/AIM: The clinical use of arsenic trioxide (As(2)O(3)) is hampered due to its cardiotoxicity. Therefore, it is critical to prevent As(2)O(3)-induced loss of endothelial integrity. The purpose of this study was to examine As(2)O(3)-induced endothelial dysfunction and evaluate the efficacy of crocetin on reversing As(2)O(3)-induced cardiotoxicity. MATERIALS AND METHODS: Cultured human umbilical vein endothelial cells (HUVECs) were used to examine As(2)O(3)-induced oxidative stress, apoptosis, production of reactive oxygen species (ROS) and DNA adducts. In addition, the impact of crocetin on As(2)O(3)-induced cardiotoxicity was evaluated. RESULTS: As(2)O(3) decreased the viability of HUVEC cells and led to apoptosis. Additionally, As(2)O(3) elevated NADPH oxidase activity, and the levels of intracellular ROS. Furthermore, the formamidopyrimidine DNA-glycosylase- and endonuclease III-digestible adducts were induced by As(2)O(3) Crocetin treatment reversed the As(2)O(3)-induced reduction in cell viability, the induction of apoptosis, the activation of NADPH oxidase activity, ROS levels and DNA adducts. CONCLUSION: Crocetin protects from As(2)O(3)-induced cardio-toxicity.