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Effects of dietary saw palmetto on the prostate of transgenic adenocarcinoma of the mouse prostate model (TRAMP)
Author(s) -
Wadsworth Teri L.,
Worstell Teresa R.,
Greenberg Norman M.,
Roselli Charles E.
Publication year - 2007
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20552
Subject(s) - tramp , prostate , prostate cancer , dihydrotestosterone , medicine , apoptosis , endocrinology , adenocarcinoma , urology , androgen , cancer , chemistry , hormone , biochemistry
BACKGROUND Several of the proposed mechanisms for the actions of the liposterolic extract of saw palmetto (SPE) are exerted on known risk factors for prostate cancer (CaP). This study investigated whether SPE could prevent the progression of CaP in a transgenic adenocarcinoma of the mouse prostate (TRAMP) model. METHODS Two different doses of SPE designed to deliver 50 mg/kg/day SPE and 300 mg/kg/day SPE were administered in a custom diet to TRAMP mice for 12 or 24 weeks. Body and organ weights were used to evaluate toxicity, and radioimmunoassay was used to measure plasma and tissue androgen levels to monitor effects of SPE on 5α reductase activity. Prostate tissues were evaluated histologically to determine the effect of treatment on tumor grade, cell proliferation, and apoptosis. RESULTS Treatment with 300 mg/kg/day SPE from 4 to 24 weeks of age significantly reduced the concentration of 5α‐dihydrotestosterone (DHT) in the prostate and resulted in a significant increase in apoptosis and significant decrease in pathological tumor grade and frank tumor incidence. CONCLUSIONS Dietary supplementation with SPE may be effective in controlling CaP tumorigenesis. SPE suppression of prostatic DHT levels lends support to the hypothesis that inhibition of the enzyme 5α‐reductase is a mechanism of action of this substance. Prostate 67: 661–673, 2007. © 2007 Wiley‐Liss, Inc.