Document Detail

Lipid peroxidation and superoxide dismutase-1 and glutathione peroxidase activities in trisomy 16 fetal mice and human trisomy 21 fibroblasts.
MedLine Citation:
PMID:  2948148     Owner:  NLM     Status:  MEDLINE    
An increase in lipid peroxidation has been reported in fetal human trisomy 21 brains. To determine whether this change can be regarded as a consequence of the increase in soluble Cu, Zn-superoxide dismutase (SOD-1) activity caused by the trisomy, we have made use of the trisomy 16 mouse, a model for human trisomy 21. Lipid peroxidation, as malonaldehyde, and the activities of SOD-1 and glutathione peroxidase were studied in diploid and trisomy 16 mouse fetuses and fetal brains and, for comparison, in diploid and trisomy 21 human fibroblasts. SOD-1 activity in diploid mouse brain increased during fetal and postnatal development, but glutathione peroxidase activity was unchanged. Mean SOD-1 activity was almost exactly 50% increased in trisomy 16 fetuses and fetal brains and in human trisomy 21 fibroblasts, confirming the gene dosage effect in both species. The SOD-1 activity in the trisomic fetuses was correlated with that in their matched diploid littermates, suggesting that factors other than the gene dosage also determine activity. Mean glutathione peroxidase activity was not increased in trisomy 16 fetuses or brains and only slightly increased in human trisomy 21 fibroblasts. Mean lipid peroxidation was decreased in fetal trisomy 16 brains but was increased in human trisomy 21 fibroblasts. These results do not lend support to the notion that increased SOD-1 activity is developmentally deleterious and necessarily increases lipid peroxidation and, secondarily, the activity of glutathione peroxidase. The difference between the human and mouse data concerning lipid peroxidation in trisomic brains may be related to structural differences in the lipids which provide the substrate for lipid peroxidation.
K G Annerén; C J Epstein
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Pediatric research     Volume:  21     ISSN:  0031-3998     ISO Abbreviation:  Pediatr. Res.     Publication Date:  1987 Jan 
Date Detail:
Created Date:  1987-02-19     Completed Date:  1987-02-19     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0100714     Medline TA:  Pediatr Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  88-92     Citation Subset:  IM    
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MeSH Terms
Brain / embryology,  enzymology
Chromosomes, Human, Pair 16*
Down Syndrome / enzymology*
Glutathione Peroxidase / metabolism*
Lipid Peroxides / metabolism*
Superoxide Dismutase / metabolism*
Grant Support
Reg. No./Substance:
0/Lipid Peroxides; EC Peroxidase; EC Dismutase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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