Document Detail

Impaired development of mitochondria plays a role in the central nervous system defects of fetal alcohol syndrome.
MedLine Citation:
PMID:  15690350     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Alcohol consumption during pregnancy can induce a wide spectrum of adverse effects in offspring. Microcephaly and mental retardation are two major defects of central nervous system (CNS). Most mechanism studies of alcohol-related CNS defects have been focused on the morphologically abnormal tissues, and more attention has been paid to nuclear alteration as opposed to organelle development. METHODS: A mouse model of fetal alcohol syndrome (FAS) was used to investigate the effect of alcohol on fetal cerebral mitochondria development. Pregnant mice were given different doses of ethanol intragastrically from GD6 to GD15. Fetal cerebral mitochondria were isolated and analyzed on GD18. RESULTS: Excessive cell apoptosis was found in the cerebra of prenatal alcohol exposure fetuses. Proliferation and differentiation of fetal cerebral mitochondria were inhibited by alcohol. Affected mitochondrial volume constriction and adenosine triphosphate (ATP) accumulation, reduced activities of respiratory chain complex I and IV and ATP synthase were detected in the cerebral tissue without obvious malformed appearance. CONCLUSIONS: Impaired mitochondria development plays a role in the CNS defects induced by prenatal alcohol exposure.
Yajun Xu; Peng Liu; Yong Li
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Birth defects research. Part A, Clinical and molecular teratology     Volume:  73     ISSN:  1542-0752     ISO Abbreviation:  Birth Defects Res. Part A Clin. Mol. Teratol.     Publication Date:  2005 Feb 
Date Detail:
Created Date:  2005-02-16     Completed Date:  2005-11-28     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  101155107     Medline TA:  Birth Defects Res A Clin Mol Teratol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  83-91     Citation Subset:  IM    
Department of Nutrition and Food Hygiene, School of Public Health, Laboratory of Molecular Toxicology and Developmental Molecular Biology, Peking University, Beijing, China.
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MeSH Terms
Cerebellum / pathology,  physiopathology*
Ethanol / toxicity*
Fetal Alcohol Syndrome / physiopathology*
Mental Retardation / chemically induced,  physiopathology
Microcephaly / chemically induced,  physiopathology
Mitochondria / metabolism*,  pathology
Multienzyme Complexes / metabolism*
Pregnancy, Animal
Reg. No./Substance:
0/Multienzyme Complexes; 64-17-5/Ethanol

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