Reactive oxygen species generated in different compartments induce cell death, survival, or senescence

► Steady-state level and site of reactive oxygen species generation dictate cellular consequences. ► Low level of exogenously produced H2O2 triggers G2/M arrest and cell senescence. ► Mitochondria-produced H2O2 induces reversible ATP drop, G1/S arrest, and senescence. ► RIP1 kinase inhibition blocks death induced by high level of H2O2.