GLUTATHIONE CONTENT, GLUTATHIONE TRANSFERASE-ACTIVITY AND LIPID-PEROXIDATION IN ACRYLAMIDE-TREATED NEUROBLASTOMA N1E-115 CELLS

Acrylamide is a well known neurotoxic compound that produces central a nd peripheral distal axonopathy. Degenerative changes of this type can be induced in the neuroblastoma cell line C 1300, clone N1E 115 and h ave been extensively studied in our laboratory particularly with regar d to the interference by acrylamide with cellular metabolism. In the p resent study the mechanism of acrylamide-induced neurite degeneration in N1E 115 cells is elucidated further. Acrylamide concentrations were selected that were not cytotoxic but caused an increasingly severe ne urite degeneration. The rate of protein synthesis was decreased in a c oncentration-dependent manner in response to acrylamide exposure (0-2. 5 mM). Detoxification of acrylamide in vivo occurs mainly through conj ugation with glutathione, (GSH) both non-enzymatically and enzymatical ly by glutathione S-transferases (GST). Cells grown in the presence of acrylamide showed a concentration-dependent decrease in GSH content. At the highest acrylamide concentration tested this was accompanied by an increased GST activity. Despite the reduced level of GSH and possi ble impaired protection of the plasma membrane against oxidative stres s no elevated level of lipid peroxidation could be observed in the acr ylamide-treated cells.