Oxygen is often required to treat newborns with respiratory disorders, and prolonged exposure to high oxygen concentrations impairs lung development. Ferroptosis plays a vital role in the development of many diseases and has become the focus of treatment and prognosis improvement for related diseases, such as neurological diseases, infections, cancers, and ischemia-reperfusion injury. Whether ferroptosis participates in the pathogenesis of hyperoxia-induced lung injury remains unknown. The aims of this study are to determine the effects of hyperoxia on lung ferroptosis and development in neonatal mice. Newborn C57BL/6 mice were reared in either room air (RA) or hyperoxia (85% O2) at postnatal days 1-7. On postnatal days 3 and 7, the lungs were harvested for histological and biochemical analysis. The mice reared in hyperoxia exhibited significantly higher Fe2+, malondialdehyde, and iron deposition and significantly lower glutathione, glutathione peroxidase 4, and vascular density than did those reared in RA on postnatal days 3 and 7. The mice reared in hyperoxia exhibited a comparable mean linear intercept on postnatal day 3 and a significantly higher mean linear intercept than the mice reared in RA on postnatal day 7. These findings demonstrate that ferroptosis was induced at a time point preceding impaired lung development, adding credence to the hypothesis that ferroptosis is involved in the pathogenesis of hyperoxia-induced lung injury and suggest that ferroptosis inhibitors might attenuate hyperoxia-induced lung injury.