| pubmed-article:20026259 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20026259 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:20026259 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
| pubmed-article:20026259 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:20026259 | lifeskim:mentions | umls-concept:C0013935 | lld:lifeskim |
| pubmed-article:20026259 | lifeskim:mentions | umls-concept:C0014442 | lld:lifeskim |
| pubmed-article:20026259 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:20026259 | lifeskim:mentions | umls-concept:C0242606 | lld:lifeskim |
| pubmed-article:20026259 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:20026259 | pubmed:dateCreated | 2010-2-15 | lld:pubmed |
| pubmed-article:20026259 | pubmed:abstractText | 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. | lld:pubmed |
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| pubmed-article:20026259 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20026259 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20026259 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20026259 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20026259 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20026259 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:20026259 | pubmed:issn | 1879-3169 | lld:pubmed |
| pubmed-article:20026259 | pubmed:author | pubmed-author:DongJianJ | lld:pubmed |
| pubmed-article:20026259 | pubmed:author | pubmed-author:SulikKathleen... | lld:pubmed |
| pubmed-article:20026259 | pubmed:author | pubmed-author:ChenShao-yuSY | lld:pubmed |
| pubmed-article:20026259 | pubmed:copyrightInfo | Copyright 2009 Elsevier Ireland Ltd. All rights reserved. | lld:pubmed |
| pubmed-article:20026259 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20026259 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:20026259 | pubmed:volume | 193 | lld:pubmed |
| pubmed-article:20026259 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20026259 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20026259 | pubmed:pagination | 94-100 | lld:pubmed |
