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Carcinogenesis Advance Access published online on June 9, 2008
Carcinogenesis, doi:10.1093/carcin/bgn142
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Laboratory and Clinical Studies of Cancer Chemoprevention by Antioxidants in Berries

Gary D. Stoner1, Li-Shu Wang1 and Bruce C. Casto2

1 Department of Internal Medicine, College of Medicine
2 Division of Environmental Health Sciences, College of Public Health, The Ohio State University, Columbus, Ohio 43210

Address correspondence to: Gary D. Stoner, Ph.D., Department of Internal Medicine, Innovation Centre, 2001 Polaris Parkway, Columbus, OH 43240, E-Mail: gary.stoner{at}osumc.edu. Phone : (614)293-3268; FAX : (614)293-5952

Reactive oxygen species [ROS] are a major cause of cellular injury in an increasing number of diseases, including cancer. Most ROS are created in the cell through normal cellular metabolism. They can be produced by environmental insults such as ultraviolet light and toxic chemicals, as well as by the inflammatory process. Interception of ROS or limiting their cellular effects is a major role of antioxidants. Due to their content of phenolic and flavonoid compounds, berries exhibit high antioxidant potential, exceeding that of many other foodstuffs. Through their ability to scavenge ROS and reduce oxidative DNA damage, stimulate antioxidant enzymes, inhibit carcinogen-induced DNA adduct formation and enhance DNA repair, berry compounds have been shown to inhibit mutagenesis and cancer initiation. Berry constituents also influence cellular processes associated with cancer progression including signaling pathways associated with cell proliferation, differentiation, apoptosis and angiogenesis. This review article summarizes laboratory and human studies, demonstrating the protective effects of berries and berry constituents on oxidative and other cellular processes leading to cancer development.

Received March 29, 2008; revised May 30, 2008; accepted May 1, 2008.


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