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Selenium status and erythropoiesis in mice
Author(s) -
Kaushal Naveen,
Hegde Shailaja N,
Gandhi Ujjawal H,
Paulson Robert F,
Prabhu K. Sandeep
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.728.5
Subject(s) - erythropoiesis , selenium , oxidative stress , selenium deficiency , glutathione peroxidase , chemistry , hemoglobin , heinz body , medicine , glutathione , endocrinology , anemia , biology , biochemistry , catalase , enzyme , organic chemistry
Reduced hematocrit has been associated with selenium deficiency in many epidemiological studies in animal and human subjects. However, the events leading to such hematological changes are not well understood. Recent studies have shown that oxidative stress plays an important role in the regulation of erythropoiesis. Selenoproteins, such as glutathione peroxidases, can effectively scavenge peroxides and mitigate cellular oxidative stress. Foxo3, a key transcription factor of the forkhead family that regulates expression of selenium‐dependent glutathione peroxidase‐1, has been reported to be vital for erythroid development. Given the importance of antioxidants in the regulation of erythropoiesis, time seems propitious to study the role of selenium in erythroid development. As a consequence of increased oxidative stress in erythrocytes isolated from selenium‐deficient mice, a significantly higher levels of denatured hemoglobin (as Heinz bodies) were seen; however, such Heinz bodies were absent in the erythrocytes in selenium‐adequate (0.1 ppm) and selenium‐supplemented (0.4 ppm) mice. Our studies indicate that selenium is essential during erythrocyte development.