Free radicals are chemical species containing one or more unpaired electrons in their outer shell, a characteristic that renders them highly reactive and intrinsically unstable in biological environments. At the cellular level, they rapidly interact with surrounding molecules in an effort to attain lower-energy, more stable configurations. This pronounced reactivity supports essential biological processes such as signal transduction, fine-tuning of immune responses and maintenance of redox homeostasis. However, when their production becomes dysregulated, these species initiate oxidative damage to lipids, proteins and nucleic acids, thereby compromising cellular structure and function.

Under physiological conditions, a dynamic equilibrium exists between free radical generation and antioxidant defense systems. As long as this balance is maintained, radical species act as regulatory intermediates in intracellular communication, host defense and adaptive response pathways. In contrast, increased radical burden arising from endogenous sources such as the mitochondrial respiratory chain, inflammation-activated oxidase systems and cytochrome P450 metabolism—or from exogenous factors including cigarette smoke, air pollution, pesticides, pharmaceuticals, ultraviolet light and ionizing radiation—leads to oxidative stress. This condition contributes to the development of numerous chronic disorders, particularly cancer, cardiovascular disease, metabolic syndrome and neurodegenerative conditions.

This chapter discusses the classification, chemical properties, major endogenous and exogenous sources and biological formation mechanisms of free radicals. Additionally, the beneficial and detrimental cellular effects of reactive oxygen and nitrogen species are examined within the framework of the “benefit–harm paradox,” based on current literature.