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American Journal of Clinical Nutrition, Vol. 83, No. 2, 389, February 2006
© 2006 American Society for Clinical Nutrition

LETTER TO THE EDITOR

Assessment of biomarker selection in selenium-deficiency disease

Xia-Long Wang

Wildlife Medicine Department
Wildlife Resource College
Northeast Forestry University
26 He-xing Road
Harbin 150040
Heilongjiang Province
China
E-mail: wxlz1969{at}yahoo.com.cn or reptiles{at}21cn.com

Dear Sir:

Setting a standard for selenium status evaluation can be vexing. For example, in a recent article in the Journal, Xia et al (1) concluded that the use of glutathione peroxidase as an index of selenium status may not be appropriate. They found that full expression of selenoprotein P (SeP) requires a greater selenium dietary exposure than does full expression of plasma glutathione peroxidase activity. This implies that SeP is a better indicator of selenium nutritional status than is glutathione peroxidase (1). SeP is the transporter of selenium in serum (2, 3) and plays important roles in selenium tissue regulation (4-6). However, from the perspective of selenium-related disease assessments, even changes in SeP concentrations may not be useful. A low selenium status obtained with the use of glutathione peroxidase or SeP as indicators in clinical trials did not clearly predict Keshan disease in selenium-deficienct areas in China (7). Because SeP is more sensitive to selenium depletion than are other selenoproteins, it may be too sensitive for use as a standard. Turnover rates differ among selenoproteins (8, 9), which suggests that the regulating mechanisms also differ (10); in some tissues, the mechanisms of selenium use can be differentially sustained during dietary selenium depletion (11). Thus, evidence of selenium deficiency according to an arbitrary standard does not necessarily lead to a clinical prediction, even though the activity of a given selenium-containing enzyme may be reduced. Thus, the evaluation is less robust if it is based on only one criterion. Practical experience also showed that the assessment of selenium status should be carried out separately for different tissues (12). Adoption of SeP as the principal standard for selenium status evaluation does not adequately focus on the clinical specificities of different selenium-responsive diseases. In summary, biomarkers should be selected to match the characteristics of different selenium-responsive diseases.

ACKNOWLEDGMENTS

The author had no conflicts of interest.

REFERENCES

  1. Xia Y, Hill KE, Byrne DW, Xu J, Burk RF. Effectiveness of selenium supplements in a low-selenium area of China. Am J Clin Nutr 2005; 81: 829–34.[Abstract/Free Full Text]
  2. Hatfield DL, ed. Selenium: its molecular biology and role in human health. 2nd ed. Boston, MA: Kluwer Academic Publishers, 2003.
  3. Saito Y, Takahashi K. Characterization of selenoprotein P as a selenium supply protein. Eur J Biochem 2002; 269: 5746–51.[Medline]
  4. Richardson DR. More roles for selenoprotein P: local selenium storage and recycling protein in the brain. Biochem J 2005; 386: E5–7.[Medline]
  5. Yang JG, Hill KE, Burk RF. Dietary selenium intake controls rat plasma selenoprotein P concentration. J Nutr 1989; 119: 1010–2.[Abstract/Free Full Text]
  6. Burk RF, Hill KE. Selenoprotein P: an extracellular protein with unique physical characteristics and a role in selenium homeostasis. Annu Rev Nutr 2005; 25: 215–35.[Medline]
  7. Wang XL. A case report of white muscle disease. Chin J Endemiol 2003; 22: 288 (in Chinese).
  8. Pagmantidis V, Bermano G, Villette S, Broom I, Arthur J, Hesketh J. Effects of Se-depletion on glutathione peroxidase and selenoprotein W gene expression in the colon. FEBS Lett 2005; 579: 792–6.[Medline]
  9. Gu QP, Ream W, Whanger PD. Selenoprotein W gene regulation by selenium in L8 cells. Biometals 2002; 15: 411–20.[Medline]
  10. Yeh JY, Vendeland SC, Gu Q, Butler JA, Ou BR, Whanger PD. Dietary selenium increases selenoprotein W levels in rat tissues. J Nutr 1997; 127: 2165–72.[Abstract/Free Full Text]
  11. Yeh J-Y, Gu Q-P, Beilstein MA, Forsberg NE, Whanger PD. Selenium influences tissue levels of selenoprotein W in sheep. J Nutr 1997; 127: 394–402.[Abstract/Free Full Text]
  12. Sun Y, Butler JA, Whanger PD. Glutathione peroxidase activity and selenoprotein W levels in different brain regions of selenium-depleted rats (1). J Nutr Biochem 2001; 12: 88–94.[Medline]




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