BACKGROUND: Evidence for an association between selenium status and prostate 
cancer risk is still inconclusive. Anticarcinogenic effects of selenium are 
supposedly mediated through cellular protective and redox properties of 
selenoenzymes in vivo. We evaluated the association between serum selenium 
status and prostate cancer risk in a population with relative low selenium 
concentrations considering effect modification by genetic variants in 
selenoprotein genes.
MATERIALS AND METHODS: A case-control study of 248 incident prostate cancer 
cases and 492 matched controls was nested within the EPIC-Heidelberg cohort. 
Baseline blood samples were analyzed for serum selenium and selenoprotein P 
concentrations and glutathione peroxidase activity. Genotyping was carried out 
for SEP15 (rs5859, rs540049), SEPP1 (rs3877899, rs7579), GPX1 (rs1050450), and 
GPX4 (rs713041). Conditional logistic regression was used to calculate adjusted 
odds ratios (OR) and 95% confidence intervals (95% CI).
RESULTS: The OR for prostate cancer was 0.89 (95% CI, 0.79-1.01) per 10 μg/L 
increase of serum selenium concentration. This association was modified by 
rs1050450 (C>T) in GPX1 (P(interaction) = 0.03), with carriers of one or two T 
alleles having a significantly reduced OR of 0.87 (95% CI, 0.76-0.99). 
Furthermore, there was an association between rs7579 genotype in SEPP1 and 
prostate cancer risk (OR, 1.72; 95% CI, 0.99-2.98).
CONCLUSIONS: Our results support a role of selenium and polymorphisms in 
selenoenzymes in prostate cancer etiology, which warrants confirmation in future 
studies.
IMPACT: These findings might help to explain biological effects of selenium in 
prostate cancer development in order to overcome inconsistencies arising from 
former studies.