School of Pharmaceutical Sciences, Capital Medical University, Beijing, 100069, China; College of Life Science and Technology, Beijing University of Chemical Technology, Beijing, 100029, China.
Free Radic Biol Med. 2023 Nov 1;208:510-515. doi: 10.1016/j.freeradbiomed.2023.09.013. Epub 2023 Sep 17.
Iron(II) species can participate in the Fenton and Fenton-like reactions to generate the hydroxyl radical that can oxidatively damage biomolecules and induce oxidative stress in biological systems. Many diseases, including neurodegeneration, cardiovascular disease and cancer, are associated with oxidative stress. However, it is proposed recently that hydroxyl radical would not be generated from the Fenton reaction under physiological conditions and thus would not cause oxidative stress in biological systems. This proposal may cause confusion for understanding oxidative stress and can also have impact on therapeutic strategies for the diseases associated with oxidative stress. In this Mini-review, the up-to-date convincing evidences of hydroxyl radical generation from the physiologically relevant Fenton-like reactions of the iron(II) complexes with physiological ligands in human blood plasma, including histidine, citrate and phosphate, are succinctly reviewed. The oxidative damages caused by hydroxyl radical to biomolecules and cells are briefly summarized. These findings strongly challenge the above proposal.
亚铁离子可以参与 Fenton 及类 Fenton 反应生成羟基自由基，从而氧化损伤生物分子并诱导生物体系中的氧化应激。许多疾病，包括神经退行性疾病、心血管疾病和癌症，都与氧化应激有关。然而，最近有研究提出，在生理条件下，Fenton 反应不会产生羟基自由基，因此不会在生物体系中引起氧化应激。这一观点可能会导致人们对氧化应激的理解产生混淆，并且可能会对与氧化应激相关疾病的治疗策略产生影响。在这篇综述中，我们简要总结了羟基自由基在人血浆中与生理配体（包括组氨酸、柠檬酸和磷酸盐）反应生成亚铁离子配合物的生理相关的类 Fenton 反应中产生的最新令人信服的证据，简要综述了羟基自由基对生物分子和细胞造成的氧化损伤。这些发现强烈挑战了上述观点。
