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ToxSci Advance Access first published online on January 4, 2007
This version published online on January 17, 2007
Toxicological Sciences, doi:10.1093/toxsci/kfl200
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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

Diethanolamine Alters Proliferation and Choline Metabolism in Mouse Neural Precursor Cells

Mihai D. Niculescu*, Renan Wu{dagger}, Zhong Guo*, Kerry da Costa* and Steven H. Zeisel*,1

* Department of Nutrition, School of Public Health and School of Medicine, University of North Carolina at Chapel Hill, North Carolina, 27599-7461 USA {dagger} College of Chemistry and Material Engineering, Wenzhou University, Wenzhou, Zhejiang Province, P.R.China, 325000

1 Corresponding author: Department of Nutrition, School of Public Health and School of Medicine, University of North Carolina at Chapel Hill, North Carolina, 27599-7461 USA. steven_zeisel{at}unc.edu

Received November 9, 2006; accepted December 22, 2006


  Abstract

Diethanolamine (DEA) is a widely used ingredient in many consumer products and in a number of industrial applications. It has been previously reported that dermal administration of DEA to mice diminished hepatic stores of choline and altered brain development in the fetus. The aim of this study was to use mouse neural precursor cells in vitro to assess the mechanism underlying the effects of DEA. Cells exposed to DEA treatment (3 mM) proliferated less (by BrdU incorporation) at 48 h (24% of control), and had increased apoptosis at 72 h (308% of control). Uptake of choline into cells was reduced by DEA treatment (to 52% of control), resulting in diminished intracellular concentrations of choline and phosphocholine (55% and 12% of control, respectively). When choline concentration in the growth medium was increased 3-fold (to 210 µM), the effects of DEA exposure on cell proliferation and apoptosis were prevented, however, intracellular phosphocholine concentrations remained low. In choline kinase assays, we observed that DEA can be phosphorylated to phospho-DEA at the expense of choline. Thus, the effects of DEA are likely mediated by inhibition of choline transport into neural precursor cells and by altered metabolism of choline. Our study suggests that prenatal exposure to DEA may have a detrimental effect on brain development.

Key Words: diethanolamine; choline; neural precursor cells; cell proliferation; apoptosis.

The author's names have been corrected


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[Abstract] [Full Text] [PDF]


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