Biphasic effects of dietary antioxidants on oxidative stress-mediated carcinogenesis.
There is now strong evidence implicating the generation of reactive oxygen species (ROS) and the corresponding response to oxidative stress as key factors in the pathogenesis of several human diseases including cancer, atherosclerosis, and neurodegenerative disorders, and in ageing. The carcinogenicity of oxidative stress is primarily attributable to the genotoxicity of ROS, but ROS can promote cancer through diverse cellular processes. Therefore, dietary or pharmaceutical augmentation of the endogenous antioxidant defense capacity has been considered a plausible way to prevent ROS-mediated carcinogenicity, but actual antioxidant therapies have been equivocal at best. In fact, most free-radical scavengers act in reversible oxidation-reduction reactions, and some antioxidants can act both as antioxidants and prooxidants, depending on their structures and the conditions. This article summarizes the possible cancer-preventive and -enhancing mechanisms of dietary antioxidants, with an emphasis on epigenetic mechanisms.
Lee
Ki Won
KW
Department of Food Science and Technology, School of Agricultural Biotechnology and Center for Agricultural Biomaterials, Seoul National University, Republic of Korea.
Lee
Hyong Joo
HJ
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D000975:Antioxidants / Q000737:chemistry / Q000378:metabolism*; D002273:Carcinogens / Q000378:metabolism; D044127:Epigenesis, Genetic; D016166:Free Radical Scavengers; D006801:Humans; D008954:Models, Biological; D009369:Neoplasms / Q000139:chemically induced / Q000209:etiology / Q000378:metabolism*; D016877:Oxidants / Q000378:metabolism; D018384:Oxidative Stress; D019800:Phenol / Q000737:chemistry; D017382:Reactive Oxygen Species
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D002273:Carcinogens; D016166:Free Radical Scavengers; D016877:Oxidants; D017382:Reactive Oxygen Species; D019800:Phenol