Impaired development of mitochondria plays a role in the central nervous system defects of fetal alcohol syndrome
✍ Scribed by Yajun Xu; Peng Liu; Yong Li
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- English
- Weight
- 295 KB
- Volume
- 73
- Category
- Article
- ISSN
- 1542-0752
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
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. Birth Defects Research (Part A) 2005. © 2005 Wiley‐Liss, Inc.