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Evidence-Based Supplement Research
Evidence-Based Supplement Research

Selenium accumulation in prostate tissue during a randomized, controlled short-term trial of l-selenomethionine: a Southwest Oncology Group Study.

  • 2006-04-01
  • Clinical cancer research : an official journal of the American Association for Cancer Research 12(7)
    • Anita L Sabichi
    • J Jack Lee
    • Robert J Taylor
    • Ian M Thompson
    • Brian J Miles
    • Catherine M Tangen
    • Lori M Minasian
    • Louis L Pisters
    • John R Caton
    • Joseph W Basler
    • Seth P Lerner
    • David G Menter
    • James R Marshall
    • E David Crawford
    • Scott M Lippman

Study Design

Type
Randomized Controlled Trial (RCT)
Sample size
n = 34
Population
men with organ-confined prostate cancer
Methods
randomized, controlled, short-term trial of l-selenomethionine (SeMet) versus observation
Blinding
Open-label
Funding
Unclear

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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