TY - JOUR T1 - Protective Effects of Crocetin on Arsenic Trioxide-induced Oxidative Stress in Human Umbilical Vein Endothelial Cells JF - In Vivo JO - In Vivo SP - 3157 LP - 3163 DO - 10.21873/invivo.12610 VL - 35 IS - 6 AU - CHUNG-LIN TSAI AU - CHIA-WEN TSAI AU - WEN-SHIN CHANG AU - JIUNN-CHERNG LIN AU - LIANG-CHUN SHIH AU - JIE-LONG HE AU - DA-TIAN BAU Y1 - 2021/11/01 UR - http://iv.iiarjournals.org/content/35/6/3157.abstract N2 - 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. ER -