Protective Effects of Crocetin on Arsenic Trioxide-induced Oxidative Stress in Human Umbilical Vein Endothelial Cells

Abstract

Background/aim: The clinical use of arsenic trioxide (As₂O₃) is hampered due to its cardiotoxicity. Therefore, it is critical to prevent As₂O₃-induced loss of endothelial integrity. The purpose of this study was to examine As₂O₃-induced endothelial dysfunction and evaluate the efficacy of crocetin on reversing As₂O₃-induced cardiotoxicity.

Materials and methods: Cultured human umbilical vein endothelial cells (HUVECs) were used to examine As₂O₃-induced oxidative stress, apoptosis, production of reactive oxygen species (ROS) and DNA adducts. In addition, the impact of crocetin on As₂O₃-induced cardiotoxicity was evaluated.

Results: As₂O₃ decreased the viability of HUVEC cells and led to apoptosis. Additionally, As₂O₃ elevated NADPH oxidase activity, and the levels of intracellular ROS. Furthermore, the formamidopyrimidine DNA-glycosylase- and endonuclease III-digestible adducts were induced by As₂O₃ Crocetin treatment reversed the As₂O₃-induced reduction in cell viability, the induction of apoptosis, the activation of NADPH oxidase activity, ROS levels and DNA adducts.

Conclusion: Crocetin protects from As₂O₃-induced cardio-toxicity.

Keywords: Apoptosis; arsenic trioxide; crocetin; human umbilical vein endothelial cells; oxidative adducts; oxidative damage; reactive oxygen species.