The hypothesis presented here is that certain cell types under oxidative stress, such as cancer cells, reprogram their metabolism to accumulate lactate, along with cytosolic Fe within the labile iron pool, thereby establishing a metabolite-based HO detoxification system. In this scenario, the Fenton reaction between Fe and HO generates hydroxyl radicals (HO•), which are subsequently scavenged by abundant lactate. Thus, lactate production may function as a protective, iron-dependent antioxidant mechanism, enabling cells to decompose HO and prevent damage to crucial biomolecules. If this system is compromised, for instance by inadequate HO•-scavenging or impaired Fe recycling, cells may become prone to ferroptosis.