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J. Biol. Chem., Vol. 278, Issue 16, 13640-13646, April 18, 2003
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From the Selenoprotein P (Se-P) contains most of the
selenium in plasma. Its function is not known. Mice with the Se-P gene
deleted (Sepp
Deletion of Selenoprotein P Alters Distribution of Selenium
in the Mouse*
,,,
, and**
Division of Gastroenterology, Department of
Medicine, Vanderbilt University School of Medicine, Nashville,
Tennessee 37232 and § Eccles Institute of Human Genetics,
The University of Utah, Salt Lake City, Utah 84112
/) were generated. Two
phenotypes were observed: 1) Sepp/
mice lost weight and developed poor motor coordination when fed diets
with selenium below 0.1 mg/kg, and 2) male
Sepp/ mice had sharply reduced fertility.
Weanling male Sepp+/+,
Sepp+/, and Sepp/
mice were fed diets for 8 weeks containing <0.02-2 mg selenium/kg. Sepp+/+ and Sepp+/
mice had similar selenium concentrations in all tissues except plasma
where a gene-dose effect on Se-P was observed. Liver selenium was
unaffected by Se-P deletion except that it increased when dietary
selenium was below 0.1 mg/kg. Selenium in other tissues exhibited a
continuum of responses to Se-P deletion. Testis selenium was depressed
to 19% in mice fed an 0.1 mg selenium/kg diet and did not rise to
Sepp+/+ levels even with a dietary selenium of
2 mg/kg. Brain selenium was depressed to 43%, but feeding 2 mg
selenium/kg diet raised it to Sepp+/+ levels.
Kidney was depressed to 76% and reached
Sepp+/+ levels on an 0.25 mg selenium/kg diet.
Heart selenium was not affected. These results suggest that the
Sepp/ phenotypes were caused by low
selenium in testis and brain. They strongly suggest that Se-P from
liver provides selenium to several tissues, especially testis and
brain. Further, they indicate that transport forms of selenium other
than Se-P exist because selenium levels of all tissues except testis
responded to increases of dietary selenium in
Sepp/ mice.
*
This work was supported by National Institutes of Health
Grants R01 ES02497 and P30 ES00267. It was presented at
Experimental Biology 2002, the annual meeting of the Federation
of American Societies for Experimental Biology, on April 22, 2002 and
published in abstract form (Hill, K. E., Zhou, J., McMahan, W. J.,
Motley, A. K., Atkins, J. F., Gesteland, R. F., and Burk, R. F. (2002) FASEB J. 16, A605 (abstr.)).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported by National Institutes of Health Grant GM61200.
**
To whom correspondence should be addressed: Medical Center
North, C-2104, Vanderbilt Medical Center, Nashville, TN 37232-2279. Tel.: 615-343-7740; Fax: 615-343-6229; E-mail:
raymond.burk@vanderbilt.edu.
Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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