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The hypothesis of failure of neuronal cell body metabolism as the principal cause of acrylamide neuropathy is re‐examined. Protein synthesis was studied in rats during chronic intoxication with acrylamide in spinal cord, brain stem and heart during three phases of the intoxication. The incorporation of radioactivity into proteins was measured in vivo after injection of radioactive leucine or after incubation in vitro of tissue slices with the labelled precursor. A highly significant depression of incorporation of precursor was found which suggests a relation between the rate of incorporation of amino acids into protein and progress of acrylamide neuropathy.

Behavioural, histological and metabolic studies were performed on acrylamide‐intoxicated rats. Treated rats showed disturbed food and water consumption accompanied by loss of body weight. In addition, in an open field test they displayed less ambulation and rearing activity than controls, and had severe difficulties in balancing on a rotating rod. The last test gives a reliable indication of the acryla‐mide‐induced disorder before the onset of histological changes. In the discussion it is suggested that the data question the neurotoxic selectivity of acrylamide.

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