Skip to content
2000
Volume 17, Issue 11
  • ISSN: 1389-5575
  • E-ISSN: 1875-5607

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.

Loading

Article metrics loading...

/content/journals/mrmc/10.2174/1389557517666170228115324
2017-07-01
2025-01-24
Loading full text...

Full text loading...

/content/journals/mrmc/10.2174/1389557517666170228115324
Loading
This is a required field
Please enter a valid email address
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error
Please enter a valid_number test