Display Settings:

Format

Send to:

Choose Destination
    Prostate. 2009 May 1;69(6):644-51.

    Suppression of prostate cancer in a transgenic rat model via gamma-tocopherol activation of caspase signaling.

    Source

    Department of Experimental Pathology and Tumor Biology, Mizuho-ku, Nagoya, Japan. sattak@med.nagoya-cu.ac.jp

    Abstract

    BACKGROUND:

    Epidemiological data indicate that intake of one form of vitamin E, gamma-tocopherol, may reduce prostate cancer risk, and several in vitro studies have demonstrated that gamma-tocopherol can inhibit prostate cancer cell growth. The purpose of the present study was to confirm effects of gamma-tocopherol on prostate cancer in the transgenic rat for adenocarcinoma of prostate (TRAP) model established in our laboratory.

    METHODS:

    In Experiment 1, heterozygous male TRAP rats 5 weeks of age received alpha-tocopherol at the concentration of 50 mg/kg in the diet, or gamma-tocopherol at 50 or 100 mg/kg for 10 weeks. In Experiment 2, TRAP rats of 3 weeks of age were given gamma-tocopherol at 50, 100, or 200 mg/kg diet for 7 weeks.

    RESULTS:

    gamma-Tocopherol did not affect body weight gain, organ weights or serum levels of either testosterone or estradiol. However, quantitative evaluation of prostatic lesions demonstrated significantly suppression of sequential progression from PIN to adenocarcinoma in a dose-dependent manner, along with clear activation of caspases 3 and 7 in the ventral lobe in both experiments.

    CONCLUSIONS:

    The present study clearly demonstrated that gamma-tocopherol suppresses prostate tumor progression in an in vivo TRAP model, and could be a candidate chemopreventive agent for human prostate cancer.

    (c) 2009 Wiley-Liss, Inc.

    PMID:
    19143023
    [PubMed - indexed for MEDLINE]

      Supplemental Content

      Icon for John Wiley & Sons, Inc.

      Save items

      loading

      Recent activity

      Your browsing activity is empty.

      Activity recording is turned off.

      Turn recording back on

      See more...
      Write to the Help Desk