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Cancer Epidemiology Biomarkers & Prevention Vol. 13, 391-397, March 2004
© 2004 American Association for Cancer Research

DNA Stability and Serum Selenium Levels in a High-Risk Group for Prostate Cancer

Nishi Karunasinghe1, Jacqueline Ryan2, John Tuckey2, Jonathan Masters2, Michael Jamieson3, Larry C. Clarke, James R. Marshall4 and Lynnette R. Ferguson1

1 Discipline of Nutrition, The University of Auckland, Auckland, New Zealand; 2 Urology Department, Auckland Hospital, Auckland, New Zealand; 3 Oncology Department, Waikato Hospital, Hamilton, New Zealand; and 4 Roswell Park Cancer Institute, Buffalo, NY

Requests for reprints: Lynnette R. Ferguson, Discipline of Nutrition, Faculty of Medical and Health Sciences, The University of Auckland, Private Bag 92019, Auckland, New Zealand. Phone: 64-9-373-7599 ext. 86372; Fax: 64-9-373-7502. E-mail: l.ferguson{at}auckland.ac.nz

The essential micronutrient, selenium, is at low levels in the New Zealand diet. Selenium is a component of a number of proteins involved in the maintenance of genomic stability, and recommended daily allowances (RDA) are set on saturation levels for glutathione peroxidase (GPx), a key enzyme in surveillance against oxidative stress. It has been assumed but not proven that this level will be adequate for other key selenoenzymes. The "Negative Biopsy Trial" identifies a group of New Zealand individuals at high risk of prostate cancer, whose serum selenium levels will be monitored and who will be supplemented with a yeast-based tablet, with or without selenium, over an extended time. Access to patients on this trial provides the opportunity to ask the more generic question as to whether selenium levels in this population are adequate to maintain genomic stability. The single cell gel electrophoresis (comet) assay was used to study DNA damage in blood leukocytes harvested from these volunteers. Average serum selenium levels before randomization was 97.8 ± 16.6 ng/ml, low by international standards. For the half of the population below this mean value, lower serum selenium levels showed a statistically significant inverse relationship (P = 0.02) with overall accumulated DNA damage. Although other interpretations cannot be excluded, the data suggest that the selenium intake in half of this population is marginal for adequate repair of DNA damage, increasing susceptibility to cancer and other degenerative diseases. It also raises the question as to whether glutathione peroxidase saturation levels are appropriate indicators of the optimal selenium levels for a given population.




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Copyright © 2004 by the American Association for Cancer Research.