We previously obtained evidence that ferritin is a nuclear protein in embryonic avian corneal epithelial (CE) cells, and that the ferritin in this site protects DNA from UV-induced damage. UV irradiation is known to produce reactive oxygen species (ROS) and ferritin is known to ameliorate further oxidative damage by sequestering free iron, thus decreasing the formation of hydroxyl radicals through the Fenton reaction. Here we present evidence that nuclear ferritin can similarly prevent damage by the ROS, H2O2. These results, when coupled with our previous ones showing that nuclear ferritin appears in the CE early in its development, raises the possibility that this ferritin may serve two protective roles. The initial one would be during embryonic development to protect the CE from ROS endogenously produced by the embryo itself (e.g., H2O2; the latter one would be post-hatching to protect the CE from environmentally produced oxidative insults (e.g., from U.V. light).