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Selenium Accumulation in Prostate Tissue During a Randomized, Controlled Short-term Trial of l-Selenomethionine: a Southwest Oncology Group Study

Authors' Affiliations: ¹ University of Texas M.D. Anderson Cancer Center, ² Baylor College of Medicine, Houston, ³ Texas A&M University, College Station, ⁴ University of Texas Health Science Center, ⁵ Brook Army Medical Center/Wilford Hall Medical Center, San Antonio, Texas, ⁶ Southwest Oncology Group Statistical Center, Seattle, Washington, ⁷ National Cancer Institute of Health, Bethesda, Maryland, ⁸ Roswell Park Cancer Institute, Buffalo, New York, and ⁹ University of Colorado Health Sciences Center, Denver, Colorado

Requests for reprints: Anita L. Sabichi, Department of Clinical Cancer Prevention, Unit 1360, University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, P.O. Box 301439, Houston, TX 77230-1439. Phone: 713-745-4928; Fax: 713-794-4403; E-mail: asabichi{at}mdanderson.org.

Purpose: Epidemiologic and clinical data suggest that selenium could prevent prostate cancer, but it has not been shown that supplemental selenium leads to an increased concentration of selenium in prostate tissue compared with adjacent tissue.

Experimental Design: We conducted a randomized, controlled, short-term trial of l-selenomethionine (SeMet) versus observation in men with organ-confined prostate cancer. The primary endpoint was the measurement of selenium concentration in prostate tissue and seminal vesicle (SV). We assessed baseline selenium levels in serum and in toenail specimens (reflecting long-term intake) and post-intervention selenium levels in serum, and in prostate and SV tissues using hydride generation atomic fluorescence spectroscopy.

Results: Sixty-six eligible patients were randomly assigned to the SeMet (n = 34) or observation (n = 32) arm; both arms had similar baseline patient characteristics. Baseline serum selenium was similar in the two groups (P = 0.64). Baseline toenail selenium levels were slightly higher in the SeMet group than in the control group (P = 0.07). After the intervention, the mean serum selenium level increased 15% in the SeMet arm and was higher than in the observation arm (P = 0.001). The selenium concentration in prostate tissue was 22% higher in the SeMet arm (n = 26) than in the observation arm (n = 25; 1.80 versus 1.47 ppm; P = 0.003, Wilcoxon rank sum test) and remained significantly higher after adjusting for chronic selenium intake (P = 0.021, ANCOVA). SV selenium concentration was similar in both groups (P = 0.384) and was lower than in prostate tissue.

Conclusions: The present study is the first to show that selenium taken as oral supplementation accumulates preferentially in the human prostate gland as opposed to the SV. These findings support the hypothesis that oral selenium supplementation may contribute to the cancer preventive effects of selenium.

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				D. N. Syed, N. Khan, F. Afaq, and H. Mukhtar Chemoprevention of Prostate Cancer through Dietary Agents: Progress and Promise Cancer Epidemiol. Biomarkers Prev., November 1, 2007; 16(11): 2193 - 2203. [Abstract] [Full Text] [PDF]