Oxidative stress by different oxygen concentrations can cause damage to the immature intestinal tract of newborns and preterm infants.Newborns, especially premature infants, have underdeveloped intestinal tracts, immature immune function, increased susceptibility to oxidative stress, and are prone to intestinal inflammatory diseases.Both hypoxia and hyperoxia can trigger oxidative stress, leading to intestinal damage.Histological changes include damage to the intestinal barrier, watery degeneration of the intestinal epithelium, and reduced goblet cells and villi.Hypoxia-induced intestinal injury is affected by a variety of signaling pathways including CRF-TLR4, Grx1-HIF-VEGF, NLRP3-Caspase-1, and miRNA-SIRT axis.The intestinal injury induced by hyperoxia is closely related to TLR4/NF-κB signaling pathway, Nrf2/IL-17D axis, and ASK1-MAPK cascade.This review focuses on the histological changes and molecular pathways of hypoxic or hyperoxic-induced intestinal injury to establish a framework for potential interventions.