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Effect of ascorbic acid on reactive oxygen species production in chemotherapy and hyperthermia in prostate cancer cells.

16:46 EDT 18th April 2014 | BioPortfolio

Summary of "Effect of ascorbic acid on reactive oxygen species production in chemotherapy and hyperthermia in prostate cancer cells."

Cellular reactive oxygen species (ROS) production is increased by both temperature and anticancer drugs. Antioxidants are known to suppress ROS production while cancer patients may take them as dietary supplement during chemotherapy and hyperthermic therapy. We examined changes in ROS production in prostate cancer cells in the presence of various anticancer drugs and antioxidants at different temperatures. ROS production was increased with temperature in cancer cells, but not in normal cells; this increase was potently inhibited by ascorbic acid. ROS production was also increased in the presence of some anticancer drugs, such as vinblastine, but not by others. Dietary antioxidant supplements, such as β-carotene, showed variable effects. Ascorbic acid potently inhibited ROS production, even in the presence of anticancer drugs, while β-carotene showed no inhibition. Accordingly, our results suggest that cancer patients should carefully choose antioxidants during their cancer chemotherapy and/or hyperthermic therapy.

Affiliation

Department of Orthopaedic Surgery, Yokohama City University School of Medicine, 3-9 Fukuura, Kanazawaku, Yokohama, 236-0004, Japan.

Journal Details

This article was published in the following journal.

Name: The journal of physiological sciences : JPS
ISSN: 1880-6562
Pages:

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Medical and Biotech [MESH] Definitions

Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.

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Metabolite of ASCORBIC ACID and the oxidized form of the lactone DEHYDROASCORBIC ACID.

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