Selenium supplementation: plasma glutathione peroxidase an indicator of selenium intake. 1982

I Lombeck, and H Menzel, and G Steiner, and K Kasperek

Plasma glutathione peroxidase activity is markedly reduced in dietetically treated patients with PKU or MSUD in comparison to health children of the same age. This is due to the low selenium content of their diet. During supplementation with yeast rich in selenium (200 micrograms selenium per day) for 3 months 2 healthy adults did not show any significant change of their plasma GSHPx activity. 5 dietetically treated patients with PKU or MSUD and a reduced selenium state showed a rapid increase of the plasma GSHPx activity after selenium supplementation were started with 120 micrograms Se/m2 x d. The values doubled within the first two days and reached a plateau after 1--3 weeks. The patients showed no clinical anomalities before or during the selenium supplementation besides the inherited defect of amino acid metabolism. Plasma GSHPx activity seems to be a good indicator of short-term changes of selenium intake in patients with reduced selenium state.

UI MeSH Term Description Entries
D008375 Maple Syrup Urine Disease An autosomal recessive inherited disorder with multiple forms of phenotypic expression, caused by a defect in the oxidative decarboxylation of branched-chain amino acids (AMINO ACIDS, BRANCHED-CHAIN). These metabolites accumulate in body fluids and render a "maple syrup" odor. The disease is divided into classic, intermediate, intermittent, and thiamine responsive subtypes. The classic form presents in the first week of life with ketoacidosis, hypoglycemia, emesis, neonatal seizures, and hypertonia. The intermediate and intermittent forms present in childhood or later with acute episodes of ataxia and vomiting. (From Adams et al., Principles of Neurology, 6th ed, p936) Branched-Chain Ketoaciduria,Thiamine Responsive Maple Syrup Urine Disease,BCKD Deficiency,Branched-Chain alpha-Keto Acid Dehydrogenase Deficiency,Classic Maple Syrup Urine Disease,Classical Maple Syrup Urine Disease,Intermediate Maple Syrup Urine Disease,Intermittent Maple Syrup Urine Disease,Keto Acid Decarboxylase Deficiency,MSUD (Maple Syrup Urine Disease),Maple Syrup Urine Disease, Classic,Maple Syrup Urine Disease, Classical,Maple Syrup Urine Disease, Intermediate,Maple Syrup Urine Disease, Intermittent,Maple Syrup Urine Disease, Thiamine Responsive,Maple Syrup Urine Disease, Thiamine-Responsive,Branched Chain Ketoaciduria,Branched Chain alpha Keto Acid Dehydrogenase Deficiency,Branched-Chain Ketoacidurias,Ketoaciduria, Branched-Chain,Ketoacidurias, Branched-Chain
D010544 Peroxidases Ovoperoxidase
D010661 Phenylketonurias A group of autosomal recessive disorders marked by a deficiency of the hepatic enzyme PHENYLALANINE HYDROXYLASE or less frequently by reduced activity of DIHYDROPTERIDINE REDUCTASE (i.e., atypical phenylketonuria). Classical phenylketonuria is caused by a severe deficiency of phenylalanine hydroxylase and presents in infancy with developmental delay; SEIZURES; skin HYPOPIGMENTATION; ECZEMA; and demyelination in the central nervous system. (From Adams et al., Principles of Neurology, 6th ed, p952). Biopterin Deficiency,Dihydropteridine Reductase Deficiency Disease,Hyperphenylalaninemia, Non-Phenylketonuric,Phenylalanine Hydroxylase Deficiency Disease,BH4 Deficiency,DHPR Deficiency,Deficiency Disease, Dihydropteridine Reductase,Deficiency Disease, Phenylalanine Hydroxylase,Deficiency Disease, Phenylalanine Hydroxylase, Severe,Dihydropteridine Reductase Deficiency,Folling Disease,Folling's Disease,HPABH4C,Hyperphenylalaninaemia,Hyperphenylalaninemia Caused by a Defect in Biopterin Metabolism,Hyperphenylalaninemia, BH4-Deficient, C,Hyperphenylalaninemia, Tetrahydrobiopterin-Deficient, Due To DHPR Deficiency,Non-Phenylketonuric Hyperphenylalaninemia,Oligophrenia Phenylpyruvica,PAH Deficiency,PKU, Atypical,Phenylalanine Hydroxylase Deficiency,Phenylalanine Hydroxylase Deficiency Disease, Severe,Phenylketonuria,Phenylketonuria I,Phenylketonuria II,Phenylketonuria Type 2,Phenylketonuria, Atypical,Phenylketonuria, Classical,QDPR Deficiency,Quinoid Dihydropteridine Reductase Deficiency,Tetrahydrobiopterin Deficiency,Atypical PKU,Atypical Phenylketonuria,Biopterin Deficiencies,Classical Phenylketonuria,Deficiency, BH4,Deficiency, Biopterin,Deficiency, DHPR,Deficiency, Dihydropteridine Reductase,Deficiency, PAH,Deficiency, Phenylalanine Hydroxylase,Deficiency, QDPR,Deficiency, Tetrahydrobiopterin,Disease, Folling,Disease, Folling's,Hyperphenylalaninemia, Non Phenylketonuric,Non Phenylketonuric Hyperphenylalaninemia,Non-Phenylketonuric Hyperphenylalaninemias
D002648 Child A person 6 to 12 years of age. An individual 2 to 5 years old is CHILD, PRESCHOOL. Children
D002675 Child, Preschool A child between the ages of 2 and 5. Children, Preschool,Preschool Child,Preschool Children
D005979 Glutathione Peroxidase An enzyme catalyzing the oxidation of 2 moles of GLUTATHIONE in the presence of HYDROGEN PEROXIDE to yield oxidized glutathione and water. Cytosolic Glutathione Peroxidase,Glutathione Lipoperoxidase,Selenoglutathione Peroxidase,Glutathione Peroxidase, Cytosolic,Lipoperoxidase, Glutathione,Peroxidase, Glutathione,Peroxidase, Selenoglutathione
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D012643 Selenium An element with the atomic symbol Se, atomic number 34, and atomic weight 78.97. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of GLUTATHIONE PEROXIDASE. Selenium-80,Selenium 80

Related Publications

I Lombeck, and H Menzel, and G Steiner, and K Kasperek
January 1985, Acta veterinaria Scandinavica. Supplementum,
I Lombeck, and H Menzel, and G Steiner, and K Kasperek
January 1988, Biological trace element research,
I Lombeck, and H Menzel, and G Steiner, and K Kasperek
January 2004, Biological trace element research,
I Lombeck, and H Menzel, and G Steiner, and K Kasperek
September 1989, Journal of the South African Veterinary Association,
I Lombeck, and H Menzel, and G Steiner, and K Kasperek
January 1998, Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer,
I Lombeck, and H Menzel, and G Steiner, and K Kasperek
December 1984, Research communications in chemical pathology and pharmacology,
I Lombeck, and H Menzel, and G Steiner, and K Kasperek
July 1988, Tanpakushitsu kakusan koso. Protein, nucleic acid, enzyme,
I Lombeck, and H Menzel, and G Steiner, and K Kasperek
December 1996, Biological trace element research,
Copied contents to your clipboard!