Free radicals (Salem Health: Cancer)
Exposure routes: The pathologically related free radicals originate within the body as a product of normal aerobic metabolic processes and inflammatory reactions, but some environmental agents, such as radiation and pollutants, with diverse routes of exposure, can increase the production of free radicals.
Where found: Free-radical-generating agents are diverse, as are their sources. The most common are tobacco smoke, sunlight, X rays, and automobile exhausts. Others include the carcinogens benzene, inorganic arsenic compounds, cadmium compounds, aflatoxins, and asbestos.
At risk: Populations at highest risk are those with a low dietary intake of antioxidants or genetic deficiencies in antioxidant enzymes (for example, glutathione peroxidase) or deoxyribonucleic acid (DNA) repair mechanisms, along with tobacco smokers, people who spend a long time in areas of heavy traffic or who are directly exposed to sunlight, and those with chronic inflammatory conditions.
Etiology and symptoms of associated cancers: The carcinogenic potential of free radicals arises from their ability to damage DNA, modify proteins by oxidation, and induce lipid peroxidation. The most frequently found form of oxidative DNA damage is hydroxylation of purine and pyrimidine bases. Other consequences of free radical actions for DNA are the generation of strand brakes, deamination, and...
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For Further Information (Salem Health: Cancer)
Halliwell, B. “Oxidative Stress and Cancer: Have We Moved Forward?” Biochemistry Journal 401 (2007): 1-11.
Hussain, S. P., L. J. Hofseth, and C. C. Harris. “Radical Causes of Cancer.” Nature Reviews. Cancer 3 (2003): 276-285.
Wu, W. S. “The Signaling Mechanism of ROS in Tumor Progression.” Cancer Metastasis Reviews 25 (2006): 695-705.
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