Oxidative stress, caused by an imbalance between reactive oxygen and nitrogen species (RONS) and antioxidant defenses, is a major contributor to aging and age-related diseases, including cancer. This review explores the molecular and cellular mechanisms linking oxidative stress, aging, and cancer, emphasizing the roles of RONS and antioxidants from diet and exercise in cellular senescence, immunity, and antitumor responses. ROS, while essential for normal cell signaling, can also cause cellular damage and disease when excessive. Oxidative stress drives DNA damage, mutations, and epigenetic changes, which are key factors in tumor initiation, angiogenesis, metastasis, and therapy resistance. Accumulation of genetic and epigenetic damage from oxidative stress leads to uncontrolled cell proliferation, reduced differentiation, and evasion of cell death, promoting tumorigenesis. Common age-related cancers, such as colorectal, breast, lung, prostate, and skin cancers, are influenced by oxidative stress in their pathogenesis and progression. The review also discusses the dual role of ROS as both physiological regulators and therapeutic targets in cancer treatment. Antioxidant genes, such as SOD, catalase, and Nrf2, play critical roles in neutralizing ROS and maintaining redox homeostasis. Oxidative stress contributes to mitochondrial dysfunction, telomere shortening, protein oxidation, and chronic inflammation, all of which accelerate aging and increase cancer risk. Antioxidants, including vitamins, carotenoids, polyphenols, and minerals, may help prevent and treat age-related cancers by reducing oxidative stress and modulating cellular processes. However, their efficacy in clinical trials is mixed, and high doses may have pro-oxidant effects. Imaging techniques like fluorescence, bioluminescence, MRI, and PET are used to study oxidative damage in vivo, providing insights into its pathological implications. Overall, managing oxidative stress is crucial for healthy aging and reducing the risk of age-related tumors.Oxidative stress, caused by an imbalance between reactive oxygen and nitrogen species (RONS) and antioxidant defenses, is a major contributor to aging and age-related diseases, including cancer. This review explores the molecular and cellular mechanisms linking oxidative stress, aging, and cancer, emphasizing the roles of RONS and antioxidants from diet and exercise in cellular senescence, immunity, and antitumor responses. ROS, while essential for normal cell signaling, can also cause cellular damage and disease when excessive. Oxidative stress drives DNA damage, mutations, and epigenetic changes, which are key factors in tumor initiation, angiogenesis, metastasis, and therapy resistance. Accumulation of genetic and epigenetic damage from oxidative stress leads to uncontrolled cell proliferation, reduced differentiation, and evasion of cell death, promoting tumorigenesis. Common age-related cancers, such as colorectal, breast, lung, prostate, and skin cancers, are influenced by oxidative stress in their pathogenesis and progression. The review also discusses the dual role of ROS as both physiological regulators and therapeutic targets in cancer treatment. Antioxidant genes, such as SOD, catalase, and Nrf2, play critical roles in neutralizing ROS and maintaining redox homeostasis. Oxidative stress contributes to mitochondrial dysfunction, telomere shortening, protein oxidation, and chronic inflammation, all of which accelerate aging and increase cancer risk. Antioxidants, including vitamins, carotenoids, polyphenols, and minerals, may help prevent and treat age-related cancers by reducing oxidative stress and modulating cellular processes. However, their efficacy in clinical trials is mixed, and high doses may have pro-oxidant effects. Imaging techniques like fluorescence, bioluminescence, MRI, and PET are used to study oxidative damage in vivo, providing insights into its pathological implications. Overall, managing oxidative stress is crucial for healthy aging and reducing the risk of age-related tumors.