Prostate cancer and oxidative stress

Abstract

The American Cancer Society estimates that more than 200,000 American men are diagnosed with prostate cancer (PCa) each year and more than 30,000 die from the disease. The major reasons for such high mortality rate are late detection, delayed and unsuccessful therapy leading to metastasis, and tumor recurrence. Also the disease impacts certain ethnicities, such as African-Americans (AA) and Hispanics, at a disproportionate rate. AA have twice the incidence and mortality of PCa than Caucasians. The causes of such ethnic disparity in the clinical manifestation and outcome of PCa are not well understood. Genetic influences, environmental exposures, aging, immunocompromise, and other factors such as increased oxidative stress contribute towards such disparity. Much of recent attention is focused on PCa prevention and control of metastasis without diminishing quality of life. Reactive oxygen species (ROS) are responsible for a multitude of functions including cell proliferation and control. The body utilizes many antioxidative enzymes, vitamins, and biomolecules to control ROS concentrations. Any upward deviation from ROS/antioxidant homeostasis results in a condition called oxidative stress (OS). Aging, smoking, fatty diets, environmental toxins, and prostate infection/inflammation result in decreased concentrations of antioxidants and increased OS. Such oxidative stress alters DNA, reduces apoptosis in favor of cell survival mechanisms, may induce epigenetic changes, and propagates mutant clones. Cells become cancerous and begin to proliferate resulting in metastasis. Many diverse natural and synthetic antioxidants have been described that can be incorporated into everyday diet as supplements for prevention and/or growth of certain cancers. In addition, new clinical assays will certainly help to predict PCa risk in patients, identify cancer onset sooner, arrest mutagenesis, help design better drugs and treatment modalities, and save precious lives.