doi:10.1155/2012/417652 Research Article Effect of Marine Omega 3 Fatty Acids on

Copyright © 2012 O. J. Nøstbakken et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Methylmercury (MeHg) is a ubiquitous environ...

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Bibliographic Details
Main Authors: Toxicity In Fish, Mammalian Cells Invitro
Other Authors: The Pennsylvania State University CiteSeerX Archives
Format: Text
Language:English
Published: 2012
Subjects:
Atlantic salmon
Online Access:http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.651.3165
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359764/pdf/JBB2012-417652.pdf
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Summary:Copyright © 2012 O. J. Nøstbakken et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Methylmercury (MeHg) is a ubiquitous environmental contaminant which bioaccumulates in marine biota. Fish constitute an important part of a balanced human diet contributing with health beneficial nutrients but may also contain contaminants such as MeHg. Interactions between the marine n-3 fatty acids eicosapentaenoic acid (20:5n-3, EPA) and docosahexaenoic acid (22:6n-3, DHA) with MeHg-induced toxicity were investigated. Different toxic and metabolic responses were studied in Atlantic salmon kidney (ASK) cell line and the mammalian kidney-derived HEK293 cell line. Both cell lines were preincubated with DHA or EPA prior to MeHg-exposure, and cell toxicity was assessed differently in the cell lines by MeHg-uptake in cells (ASK and HEK293), proliferation (HEK293 and ASK), apoptosis (ASK), oxidation of the red-ox probe roGFP (HEK293), and regulation of selected tox-icological andmetabolic transcriptional markers (ASK). DHAwas observed to decrease the uptake of MeHg in HEK293, but not in ASK cells. DHA also increased, while EPA decreased,MeHg-induced apoptosis in ASK.MeHg exposure induced changes in selected metabolic and knownMeHg biomarkers in ASK cells. Both DHA andMeHg, but not EPA, oxidized roGFP inHEK293 cells. In con-clusion, marine n-3 fatty acids may ameliorate MeHg toxicity, either by decreasing apoptosis (EPA) or by reducing MeHg uptake (DHA). However, DHA can also augment MeHg toxicity by increasing oxidative stress and apoptosis when combined with MeHg. 1.

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