Skip Navigation


ToxSci Advance Access originally published online on August 29, 2007
Toxicological Sciences 2007 100(2):423-432; doi:10.1093/toxsci/kfm224
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
100/2/423    most recent
kfm224v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Kaur, P.
Right arrow Articles by Syversen, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kaur, P.
Right arrow Articles by Syversen, T.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2007. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Role of Docosahexaenoic Acid in Modulating Methylmercury-Induced Neurotoxicity

Parvinder Kaur*,1, Kristina Schulz*, Michael Aschner{dagger} and Tore Syversen*

* Department of Neuroscience, Norwegian University of Science and Technology, N-7489 Trondheim, Norway {dagger} Departments of Pediatrics and Pharmacology, and the Kennedy Center, Vanderbilt University Medical Center, B-3307 Medical Center North, Nashville, Tennessee 37232-2495

1 To whom correspondence should be addressed at the Department of Neuroscience, Norwegian University of Science and Technology, Faculty of Medicine, Olav Kyrresgt, 3, N-7489 Trondheim, Norway. Fax: +47-73598655. E-mail: parvinder.kaur{at}ntnu.no.

Received July 11, 2007; accepted August 21, 2007


  Abstract

The effect of docosahexaenoic acid (DHA) in modulating methylmercury (MeHg)-induced neurotoxicity was investigated in C6-glial and B35-neuronal cell lines. Gas chromatography measurements indicated increased DHA content in both the cell lines after 24 h supplementation. Mitochondrial activity evaluated by 3-(4, 5-dimethylthiazol-2-yl)-2, 5 diphenyltetrazolium bromide (MTT) reduction indicated that 10µM MeHg treatment for 50 min led to a significant (p < 0.001) and similar decrease in MTT activity in both the cell lines. However, DHA pretreatment led to more pronounced depletion (p < 0.05) in the MTT activity in C6 cells as compared to B35 cells. The depletion of glutathione (GSH) content measured with the fluorescent indicator monochlorobimane was more apparent (p < 0.001) in C6 cells treated with DHA and MeHg. The amount of reactive oxygen species (ROS) detected with the fluorescent indicator—chloromethyl derivative of dichloro dihydro fluorescein diacetate (CMH2DCFDA)—indicated a fourfold increase in C6 cells (p < 0.001) as compared to twofold increase in B35 cells (p < 0.001) upon DHA and MeHg exposure. However, the cell-associated MeHg measurement using 14C-labeled MeHg indicated a decrease (p < 0.05) in MeHg accumulation upon DHA exposure in both the cell lines. These findings provide experimental evidence that although pretreatment with DHA reduces cell-associated MeHg, it causes an increased ROS (p < 0.001) and GSH depletion (p < 0.05) in C6 cells.

Key Words: neurotoxicology; in vitro; cell culture; glutathione; reactive oxygen species.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.