Hydroxyl radical generations form the physiologically relevant Fenton-like reactions

Area of Science:

• Biochemistry
• Oxidative Stress Research
• Medical Chemistry

Background:

• Iron(II) species catalyze Fenton and Fenton-like reactions, producing hydroxyl radicals.
• Hydroxyl radicals can cause oxidative damage to biomolecules, contributing to diseases like neurodegeneration, cardiovascular disease, and cancer.
• Recent proposals question hydroxyl radical generation in physiological conditions, potentially impacting disease understanding and therapies.

Purpose of the Study:

• To review evidence for hydroxyl radical generation via physiologically relevant Fenton-like reactions.
• To examine the role of iron(II) complexes with physiological ligands in human blood plasma.
• To challenge the recent proposal that hydroxyl radicals are not generated under physiological conditions.

Main Methods:

• Review of up-to-date scientific literature.
• Focus on Fenton-like reactions involving iron(II) complexes with histidine, citrate, and phosphate.
• Summary of oxidative damage to biomolecules and cells.

Main Results:

• Convincing evidence supports hydroxyl radical generation from physiologically relevant Fenton-like reactions in human blood plasma.
• Iron(II) complexes with ligands like histidine, citrate, and phosphate facilitate this radical generation.
• Oxidative damage to biomolecules and cells by hydroxyl radicals is confirmed.

Conclusions:

• The findings strongly challenge the recent proposal that hydroxyl radicals are not generated under physiological conditions.
• Hydroxyl radical generation in biological systems remains a significant factor in oxidative stress.
• This has implications for understanding disease mechanisms and developing therapeutic strategies.