Cellular biological study on mechanisms of acrylamide toxicity and its prevention

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Utilizing ultra-high field magnetic resonance (MR), we found that acrylamide (50 mg/kg/day, 8 days, i.p.) causes morphological alterations in the rat brain (enlargement of ventricles and cisterns, thinning of cortex). Before this, we showed that MR is a very powerful tool to investigate changes in the rat brain caused by hexachlorophene. Since it was reported that acrylamide induced c-Fos, one of the immediate early genes, in the brain, we used pentylenetetrazol (PTZ), an established potent inducer of c-Fos, and found that PTZ causes increase of mRNA of c-Fos in the mouse brain and that it can be suppressed by L-carnitine. We also found that various chemicals activate mitogen activated protein kinase (MAPK) and that calcium is important in some cases. Based on these, we examined effects of acrylamide on human neuroblastoma SH/SY5Y cells. Acrylamide caused cell toxicity after incubation for 48-72 hours. Whereas it did not cause significant increase of c-Fos mRNA, exposure to acrylamide increased c-Jun mRNA. Nevertheless, no activation of MAPKs (ERK, JNK, p38) was found.