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Title: Reactive Oxygen and Nitrogen Species in Carcinogenesis: Implications of Oxidative Stress on the Progression and Development of Several Cancer Types. Author: Kruk J, Aboul-Enein HY. Journal: Mini Rev Med Chem; 2017; 17(11):904-919. PubMed ID: 28245782. Abstract: BACKGROUND: The body of evidence available from published literature during the past three decades indicates that reactive oxygen species and reactive nitrogen species can induce, promote and modulate carcinogenesis. OBJECTIVE: The purpose of this review was to present the current status of knowledge on the possible role of oxidative/nitrosative stress in the development and progression of several human cancers. Moreover, we discuss briefly the formation and decomposition of oxygen and nitrogen species within cells and their physiological and damaging influences. Given that some antitumor treatments are based on the formation of ROS, we also summarize what is currently known about supplementing the diet with antioxidants. METHODS: We conducted literature searches to review the recent progress toward the potential role of reactive oxygen and nitrogen species and associated oxidative stress in carcinogenesis. RESULTS: The epidemiological and laboratory studies showed that excessive production of reactive oxygen/ nitrogen species may lead to consequent alteration in the intracellular homeostasis and cause damage to all important cellular components when the excess of oxidants is not balanced by antioxidant defence and/or DNA repair mechanisms. Chronic oxidative stress can drive carcinogenesis by altering expression of cancer-related genes causing mutation and transformation. CONCLUSION: There is now common agreement that reactive oxygen and nitrogen species are involved in the development and progression of several human cancers like breast, prostate, colorectal, gynecological, cervical, eye, skin, leukemia, gastric. Antioxidant supplements at low doses can promote health, while excess supplementation can be harmful and even carcinogenic.[Abstract] [Full Text] [Related] [New Search]