Abstract: Objective We investigated the mechanism of apoptosis induced by selenite from the perspective of mitochondrial damage, aiming to provide evidence to support therapeutic role of selenite in colorectal cancer. Methods Divide SW480 into 2 groups，investigate the ROS level，apoptosis and mitochondrial damage induced by selenite via confocal microscope, flowcytometry (FCM) and so on. Using MnTMPyP inhibits ROS level to analysis the process, detcect the function of cytochrome C in the process. Results Selenite increases ROS level in SW480 cells, induces mitochondrial damage, decreases mitochondrial membrane potential, leading to mitochondria fragmentation, release of cytochrome C and apoptosis. Superoxide anion inhibitor MnTMPyP could inhibit the process. Conclusion Selenite can induce mitochondrial damage and apoptosis in SW480 via oxidative stress. Selenite has potential therapeutic effect in treatment of colorectal cancer.

Key words: Selenite , Mitochondrial damage , Apoptosis , Colorectal cancer