<![CDATA[Free radicals are highly reactive chemical species containing one or more unpaired electrons that exert context-dependent effects on human physiology and disease. Although controlled levels of reactive oxygen and nitrogen species support cellular signalling, immune defence, and vascular regulation, their excessive production relative to antioxidant defences disrupts redox homeostasis and induces oxidative stress. This review synthesizes evidence on the sources, biological functions, and pathological effects of free radicals, with particular attention to their roles in human health and aging. It examines endogenous generation within mitochondria, peroxisomes, and the endoplasmic reticulum, together with exogenous sources such as radiation and environmental pollutants. The evidence indicates that excessive free-radical activity damages DNA, proteins, and lipids and contributes to processes associated with cancer, cardiovascular disease, neurodegenerative disorders, kidney dysfunction, and viral infections, including SARS-CoV-2 infection. Nevertheless, the physiological benefits of moderate reactive oxygen and nitrogen species concentrations demonstrate that these species are not inherently harmful and that their biological effects depend on concentration, location, and cellular context. The free radical theory of aging remains contested because available evidence both supports and challenges oxidative damage as a primary determinant of aging. Antioxidants, particularly flavonoids and vitamins, may mitigate oxidative injury; however, their effectiveness in delaying aging or disease progression remains inconclusive. This review underscores the need to understand free radicals within the broader framework of redox homeostasis rather than solely as harmful agents. It contributes a balanced synthesis of their beneficial and detrimental roles and highlights the need for further research to establish the efficacy and safety of natural antioxidant-based interventions.]]>
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