Source:http://linkedlifedata.com/resource/pubmed/id/10966520
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2000-10-13
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pubmed:abstractText |
The antioxidant tripeptide glutathione has been proposed to be important in defense against oxidative stress and heavy metal toxicity. We evaluated alterations in glutathione regulation and synthesis associated with low-level chronic methylmercury (MeHg) exposure in the developing mouse fetus. Female C57Bl/6 mice were given 0, 3, or 10 ppm MeHg in the drinking water for 2 weeks prior to breeding and throughout pregnancy. Fetuses were collected on gestational days (gd) 12 and 16. Total glutathione, reduced glutathione (GSH), oxidized glutathione (GSSR), and glutamate-L-cysteine ligase (Glcl) activity were assessed in yolk sacs and fetuses at gd 16. Western and Northern blots for Glcl-catalytic (Glclc) and Glcl-regulatory (Glclr) subunits were performed on gd 12 and gd 16 fetuses. There were no changes in total glutathione in gd 16 mouse fetuses with exposure, but there were dose-related decreases in GSH and increases in GSSR. In contrast, visceral yolk sacs exhibited an increase in total glutathione in the low-dose groups, but no changes in the high-dose group. There were no changes in Glcl activity in fetuses, but there was a 2-fold increase in Glcl activity in yolk sacs from both low-dose and high-dose groups. There was a 2-fold induction in GLCLC: mRNA and protein in the gd 16 yolk sacs at both 3 and 10 ppm MeHg. No treatment-related changes in Glclr protein in either gd 12 or gd 16 yolk sacs or fetuses were found. Thus, the yolk sac is capable of up-regulating Glclc and GSH synthetic capacity in response to MeHg exposure. This increase appears to be sufficient to resist MeHg-induced GSH depletion in the yolk sac; however fetal glutathione redox status is compromised with exposure to 10 ppm MeHg.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1096-6080
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
57
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
141-6
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pubmed:dateRevised |
2010-9-17
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pubmed:meshHeading |
pubmed-meshheading:10966520-Animals,
pubmed-meshheading:10966520-Blotting, Northern,
pubmed-meshheading:10966520-Blotting, Western,
pubmed-meshheading:10966520-Chromatography, High Pressure Liquid,
pubmed-meshheading:10966520-Female,
pubmed-meshheading:10966520-Fetus,
pubmed-meshheading:10966520-Glutamate-Cysteine Ligase,
pubmed-meshheading:10966520-Glutathione,
pubmed-meshheading:10966520-Mercury,
pubmed-meshheading:10966520-Methylmercury Compounds,
pubmed-meshheading:10966520-Mice,
pubmed-meshheading:10966520-Mice, Inbred C57BL,
pubmed-meshheading:10966520-Pregnancy,
pubmed-meshheading:10966520-Yolk Sac
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pubmed:year |
2000
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pubmed:articleTitle |
Modulation of glutathione and glutamate-L-cysteine ligase by methylmercury during mouse development.
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pubmed:affiliation |
Department of Environmental Health, University of Washington, Seattle, Washington 98195, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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