Abstract
Mice deficient in selenoprotein P exhibit a disturbed selenium distribution and reduced activities of other selenoenzymes and display defects in growth and motor co-ordination. We have normalized selenoenzyme activities and rescued the phenotype of mutant mice by supplementing their nursing mothers with sodium selenite. Our results indicate that selenium from inorganic sources can be transferred efficiently via mother's milk to the developing offspring in a form that is both highly bioavailable by target tissues and yet sufficiently safe to prevent overdosages.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Administration, Oral
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Animals
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Behavior, Animal
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Deficiency Diseases / metabolism
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Deficiency Diseases / therapy
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Dose-Response Relationship, Drug
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Drinking
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Female
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Glutathione Peroxidase / blood
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Mice
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Mice, Knockout
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Milk / chemistry
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Movement Disorders / therapy
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Phenotype
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Pregnancy
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Proteins / genetics*
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Selenium / analysis
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Selenium / blood
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Selenium / deficiency*
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Selenoprotein P
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Selenoproteins
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Sodium Selenite / administration & dosage
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Sodium Selenite / therapeutic use
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Weight Gain
Substances
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Proteins
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Selenoprotein P
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Selenoproteins
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Glutathione Peroxidase
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Selenium
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Sodium Selenite