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ToxSci Advance Access published online on August 29, 2007
Toxicological Sciences, doi:10.1093/toxsci/kfm224
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© 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*, Kristina Schulz*, Michael Aschner# and Tore Syversen*

* Department of Neuroscience, Norwegian University of Science and Technology, N-7489 Trondheim, Norway # Departments of Pediatrics and Pharmacology, and the Kennedy Center, Vanderbilt University Medical Center, B-3307 Medical Center North, 1162 21st Avenue, Nashville, TN 37232-2495, USA

Corresponding author: Parvinder Kaur, Department of Neuroscience, Faculty of Medicine, Olav Kyrresgt. 3, N-7489 Trondheim, Norway, Tel. +47-73551552; Fax +47-73598655, E-mail: parvinder.kaur{at}ntnu.no

Received July 11, 2007; revision received August 20, 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 hr supplementation. Mitochondrial activity evaluated by MTT reduction indicated that 10[mu]M 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 MCB-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 -chloro methyl derivative of di-chloro di-hydro fluorescein diacetate (CMH2DCFDA) indicated a four fold increase in C6 cells (p<0.001) as compared to two fold increase in B35 cells (p<0.001) upon DHA and MeHg exposure. However, the cell associated-MeHg measurement using 14C-labelled 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.


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