Raising the iron curtain: Lactate's secret role in oxidative stress defense
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<sup>2+</sup> within the labile iron pool, thereby establishing a metabolite-based H<sub>2</sub>O<sub>2</sub> detoxification system. In this scenario, the Fenton reaction between Fe<sup>2+</sup> and H<sub>2</sub>O<sub>2</sub> 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 H<sub>2</sub>O<sub>2</sub> and prevent damage to crucial biomolecules. If this system is compromised, for instance by inadequate HO•-scavenging or impaired Fe<sup>2+</sup> recycling, cells may become prone to ferroptosis.
Authors
- Renáta Váraljai (ORCID: https://orcid.org/0000-0001-6852-6859)
- Shirley K. Knauer (ORCID: https://orcid.org/0000-0003-4321-0924)
- Astrid Hensel
Institutions
- Essen University Hospital (DE)
- West German Heart and Vascular Center Essen (DE)
- University of Duisburg-Essen (DE)
Publication Details
- Journal
- Redox Biology
- Published
- 2025-07-05
- DOI
- https://doi.org/10.1016/j.redox.2025.103754
- Citations
- 2
- Primary Topic
- Iron Metabolism and Disorders
- Type
- article
- Field-Weighted Citation Impact
- 3.54
Funders
- Universität Duisburg-Essen
- National Institutes of Health
- National Heart, Lung, and Blood Institute
- National Institute of Mental Health
- National Institute on Drug Abuse
- National Human Genome Research Institute
- National Cancer Institute
- National Institute of Neurological Disorders and Stroke