Emodin is one of the main active components (anthraquinones) contained in the root rhizome of Rheum palmatum L. Emodin exhibits a wide range of pharmacological effects, including anti-cancer, anti- inflammatory, diuretic and vasorelaxant. In this study, we examine the cytotoxic effects of emodin in mouse blastocysts and subsequent early development. Blastocysts treated with 50 or 75 μM emodin showed significant increases in apoptosis and significant decreases in total cell number. Experiments in blastocysts show that emodin induces apoptosis via ROS generation, loss of mitochondrial membrane potential, and activation of caspase-9 and caspase-3. These findings show for the first time that emodin induces ROS generation and mitochondria-dependent apoptotic processes and causes developmental injury in mouse blastocysts in vitro.