Oxidative stress, resulting from an imbalance between reactive oxygen and nitrogen species (RONS) and antioxidant defenses, is a significant factor in aging and age-related diseases, including cancer. RONS, produced by endogenous and exogenous processes, can cause cellular damage, leading to DNA alterations, lipid peroxidation, protein oxidation, and mitochondrial dysfunction. This damage contributes to cellular senescence, immune system dysfunction, and increased susceptibility to age-related pathologies such as inflammatory disorders, cardiovascular diseases, neurodegenerative diseases, diabetes, and cancer. Oxidative stress-driven DNA damage and mutations are key determinants of tumor initiation, angiogenesis, metastasis, and therapy resistance. The accumulation of genetic and epigenetic damage leads to unrestrained cell proliferation, inhibited cell differentiation, and evasion of cell death, facilitating tumorigenesis. Key genes involved in oxidative stress include NADPH oxidases, nitric oxide synthases, arachidonate lipoxygenases, cytochrome P450 enzymes, xanthine dehydrogenase/xanthine oxidoreductase, and hypoxia-inducible factor 1 alpha. Antioxidant genes, such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, nuclear factor erythroid 2-related factor 2, heme oxygenase-1, and peroxiredoxins, protect cells from oxidative damage. Oxidative stress plays a dual role in normal cell signal transduction and homeostasis, acting as a regulator of various cellular processes. In aging, oxidative stress promotes cellular and DNA damage, mitochondrial dysfunction, telomere shortening, protein aggregation, chronic inflammation, cellular senescence, and impaired autophagy. In tumorigenesis, oxidative stress contributes to DNA damage, inflammation, cellular senescence, mitochondrial dysfunction, and impaired antioxidant defenses, leading to uncontrolled cell proliferation, angiogenesis, invasion, metastasis, and therapy resistance. Antioxidant compounds have shown potential in cancer prevention and treatment by neutralizing free radicals and reducing oxidative stress. However, their effects are complex and not fully understood, and their use in cancer therapy requires careful consideration. Imaging techniques, such as fluorescence and bioluminescence imaging, are used to study oxidative damage in vivo. Overproduction of ROS is being explored as an anti-cancer therapy, particularly in combination with other treatments to enhance cancer cell killing.Oxidative stress, resulting from an imbalance between reactive oxygen and nitrogen species (RONS) and antioxidant defenses, is a significant factor in aging and age-related diseases, including cancer. RONS, produced by endogenous and exogenous processes, can cause cellular damage, leading to DNA alterations, lipid peroxidation, protein oxidation, and mitochondrial dysfunction. This damage contributes to cellular senescence, immune system dysfunction, and increased susceptibility to age-related pathologies such as inflammatory disorders, cardiovascular diseases, neurodegenerative diseases, diabetes, and cancer. Oxidative stress-driven DNA damage and mutations are key determinants of tumor initiation, angiogenesis, metastasis, and therapy resistance. The accumulation of genetic and epigenetic damage leads to unrestrained cell proliferation, inhibited cell differentiation, and evasion of cell death, facilitating tumorigenesis. Key genes involved in oxidative stress include NADPH oxidases, nitric oxide synthases, arachidonate lipoxygenases, cytochrome P450 enzymes, xanthine dehydrogenase/xanthine oxidoreductase, and hypoxia-inducible factor 1 alpha. Antioxidant genes, such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, nuclear factor erythroid 2-related factor 2, heme oxygenase-1, and peroxiredoxins, protect cells from oxidative damage. Oxidative stress plays a dual role in normal cell signal transduction and homeostasis, acting as a regulator of various cellular processes. In aging, oxidative stress promotes cellular and DNA damage, mitochondrial dysfunction, telomere shortening, protein aggregation, chronic inflammation, cellular senescence, and impaired autophagy. In tumorigenesis, oxidative stress contributes to DNA damage, inflammation, cellular senescence, mitochondrial dysfunction, and impaired antioxidant defenses, leading to uncontrolled cell proliferation, angiogenesis, invasion, metastasis, and therapy resistance. Antioxidant compounds have shown potential in cancer prevention and treatment by neutralizing free radicals and reducing oxidative stress. However, their effects are complex and not fully understood, and their use in cancer therapy requires careful consideration. Imaging techniques, such as fluorescence and bioluminescence imaging, are used to study oxidative damage in vivo. Overproduction of ROS is being explored as an anti-cancer therapy, particularly in combination with other treatments to enhance cancer cell killing.