Background Reactive oxygen species (ROS) and antioxidant ingredients are a series of crucial signaling molecules in oxidative stress response.Under some stress conditions such as ischemia/hypoxia and starvation, the relative excessive accumulation of ROS could break cellular homeostasis and induce oxidative damages, finally resulting in programmed cell death (PCD) such as autophagy.In this process, ROS could promote the formation of autophagy.Autophagy, in turn, may contribute to reduce ROS levels.The internal regulatory mechanisms of autophagy by ROS can be summarized as transcriptional and post-transcriptional regulation.Autophagy also may regulate ROS levels through several pathways.