Hydrogen peroxide is considered to be a dose- and time-dependent mediator in apoptotic and necrotic death. In this study, we examined the signaling of the E6 and E7 proteins with respect to apoptosis or necrosis after H₂O₂ injury using an in vitro model with overexpressed E6 or E7 genes. For this purpose, the E6 and E7 gene expressing astrocytes were exposed to 10 µM and 200 µM H₂O₂ solutions. Twenty-four hours after treatment with the lower dosage(10 µM H₂O₂), control, E6-expressing cells suffered about 45% injury and LXSN-expressi ng cells decreased by 67% as assessed by LDH release. However, E7-expressing cells showed less injury, resulting in 20-30% of LDH release. Astrocytes expressing E6, E7, LXSN and mock-infected cells showed a typical apoptotic death patter n on the DNA gel after treatment with a low-dose of H₂O₂ (10 µM), however the y died from necrotic death after a high-dose (200 µM) H₂O₂. Overexpression of HPV-E7 genes protected the cells from apoptotic death after a low-dose of H₂O₂ and from necrotic death after a high-dose of H₂O₂, while the overexpression of E 6 genes from the necrotic death. E7 expressing astrocytes showed higher catalas e activity and the levels of E2F protein surged more than 100-folds compared with the control astrocytes. We believe that the activity of E7 protein to protect astrocytes from H₂O₂ injury was at least partly due to increased catalase, a scavenger protein.