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HERO ID
874008
Reference Type
Journal Article
Title
The role of NOX enzymes in ethanol-induced oxidative stress and apoptosis in mouse embryos
Author(s)
Dong, J; Sulik, KK; Chen, SY
Year
2010
Is Peer Reviewed?
1
Journal
Toxicology Letters
ISSN:
0378-4274
EISSN:
1879-3169
Volume
193
Issue
1
Page Numbers
94-100
Language
English
PMID
20026259
DOI
10.1016/j.toxlet.2009.12.012
Web of Science Id
WOS:000275611900013
Abstract
Reactive oxygen species (ROS) play an important role in ethanol-induced apoptosis and teratogenesis. However, the major sources of ROS in ethanol-exposed embryos have remained undefined. This study was conducted to determine the role of NADPH oxidase (NOX) in ethanol-induced oxidative stress and apoptosis in mouse embryos. Analyses of mRNA expression indicated that ethanol treatment resulted in a significant increase in mRNA expression of NOX catalytic subunit Duox-1 in gestational day 9 (GD 9:0) mouse embryos. Ethanol exposure also resulted in significant increases in mRNA expression of NOX regulatory subunits, p22phox, p67phox, NOXA1 and NOXO1. In addition, a significant increase in NOX enzyme activity was found in the ethanol-exposed embryos as compared to controls. Co-treatment with the NOX inhibitor, diphenyleneiodonium (DPI), significantly prevented ethanol-induced increases in NOX enzyme activity, ROS generation and oxidative DNA damage in ethanol-exposed embryos. DPI treatment also resulted in a reduction in caspase-3 activation, decreased caspase-3 activity and diminished prevalence of apoptosis in ethanol-exposed embryos. These results support the hypothesis that NOX is a critical source of ROS in ethanol-exposed embryos and that it plays an important role in ethanol-induced oxidative stress and pathogenesis.
Keywords
NADPH oxidase; Fetal alcohol spectrum disorder; Reactive oxygen species; Embryo; Apoptosis
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