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Abstract

Summary

Cultures of the mouse neuroblastoma cell line C1300, clone N1E115 were exposed to acrylamide at 3.5 x 10^-4M for 14 days (subacute situation) or at 2.8 x 10^-3 M for 24 hr (acute situation).

In the subacute situation the total uptake of 2-deoxy-D-glucose was stimulated. This could be explained by an increase in both the non-specific diffusion and the specific transport. The activity of the glycolytic enzyme, enolase (EC4.2.1.11), was unaffected by exposure to acrylamide, whereas the activity of glyceraldehyde-3-phosphate-dehydrogenase (EC1.2.1.12) was inhibited. Acrylamide had a marked stimulating effect on the respiratory activity of the cells, whereas the incorporation of tritiated leucine remained unchanged. Furthermore, membrane integrity was maintained throughout the acrylamide exposure as judged by an unchanged rate of 2-deoxy-D-glucose-6-phosphate efflux. Corresponding results were obtained in the acute situation. In N1E115 cultures and under the experimental conditions used in this work acrylamide caused neurite degeneration resembling distal axonopathy in vivo. It is suggested that these degenerative changes are not due to a general intoxication of the cells, but rather to a specific effect. Consequently, the N1E115 cell line might be useful in studies of chemically-induced axonopathies.

Keywords

neuroblastoma cells acrylamide glucose uptake glucose metabolism leucine incorporation membrane integrity respiratory activity

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On the Application of Cultured Neuronal Cell Lines in Neurotoxicological Studies: Implications of Acrylamide-induced Neurite Disintegration

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