Document Detail


Induction of apoptosis in the CNS during development by the combination of hyperoxia and inhibition of glutathione synthesis.
MedLine Citation:
PMID:  9840739     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Apoptosis in the central nervous system (in contrast to necrosis) is an endogenous cell suicide mechanism triggered in response to biological factors and genotoxic stimuli often resulting from oxidative stress. Excessive neural apoptosis may result in longterm brain dysfunction. A significant proportion of prematurely born infants are exposed to high oxygen and nutritional regimens deficient in antioxidant precursors. Such infants frequently display cognitive deficits when studied in later childhood. Studies in cell culture have characterized a close relationship between oxidative stress, glutathione availability and cell death. Here, we assessed this relationship in rat brain, as a model approximation of the situation that occurs in human infants. Two day old rats were exposed to an atmosphere of 95% oxygen and treated with buthionine sulfoximine (BSO), a glutathione synthesis inhibitor. Control groups consisted of rat-pups kept in air, air plus BSO, or oxygen alone. At the end of 5 days of treatment, brains were harvested, dissected and nerve growth factor protein (NGF), glutathione, and extent of apoptosis were measured. Hyperoxia induced a decrease in NGF protein while BSO induced a decrease in glutathione concentrations. Animals treated with both hyperoxia and BSO had a dramatic increase in the extent of brain apoptosis detected. We conclude from these studies that the brains of animals exposed to both oxidative stress and limited antioxidant protection are liable to pro-apoptotic changes. Increased cell death via apoptosis reflecting changes in neurotrophin and glutathione homeostasis may represent the mechanism responsible for the induction of the longterm cognitive deficits observed in some preterm infants.
Authors:
G Taglialatela; J R Perez-Polo; D K Rassin
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Free radical biology & medicine     Volume:  25     ISSN:  0891-5849     ISO Abbreviation:  Free Radic. Biol. Med.     Publication Date:  1998 Nov 
Date Detail:
Created Date:  1999-02-25     Completed Date:  1999-02-25     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  936-42     Citation Subset:  IM    
Affiliation:
The Department of Human Biological Chemistry, The University of Texas Medical Branch at Galveston, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn / growth & development*
Apoptosis*
Body Weight
Brain / cytology,  growth & development*,  metabolism
Buthionine Sulfoximine / pharmacology
Cataract / chemically induced
Cerebellum / cytology,  metabolism
Corpus Striatum / cytology,  metabolism
Enzyme Inhibitors / pharmacology
Female
Glutathione / antagonists & inhibitors*,  metabolism
Hippocampus / cytology,  metabolism
Nerve Growth Factors / metabolism
Oxygen / administration & dosage*
Pregnancy
Prosencephalon / cytology,  metabolism
Rats
Rats, Sprague-Dawley
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Nerve Growth Factors; 5072-26-4/Buthionine Sulfoximine; 70-18-8/Glutathione; 7782-44-7/Oxygen

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


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