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Abstract

Iron plays a crucial role in redox reactions, influencing cellular metabolism, oxygen transport, and enzymatic processes. However, its ability to cycle between ferrous (Fe²+) and ferric (Fe³+) states also contributes to oxidative stress when dysregulated. Excess iron catalyzes the formation of reactive oxygen species (ROS) through Fenton reactions, leading to oxidative damage in biomolecules, including lipids, proteins, and DNA. This oxidative stress is implicated in the pathogenesis of various diseases, such as neurodegenerative disorders, cardiovascular diseases, and cancer. Understanding the interplay between iron homeostasis, redox biology, and disease mechanisms may aid in developing targeted therapeutic strategies. Future research should focus on iron chelation therapies and antioxidant interventions to mitigate iron-induced oxidative stress.