IN a previous paper (Barnes and Magee, 1954) some toxic properties of dimethylnitrosamine (DMN) were described. It was found that rats and other animals suffer severe liver damage after the administration of DMN in doses of the order of 25 mg. per kilogram body weight, either orally or parenterally. The liver lesion was an extensive centrilobular type of necrosis, involving all lobules; followed by evidence of regeneration in surviving animals. An outstanding feature of the necrosis was its very haemorrhagic character and the liver lesion was frequently accompanied by massive haemorrhagic ascites and bleeding into the gastro intestinal tract.These features of the acute liver necrosis were similar to those produced by the senecio alkaloids in rats (Davidson, 1935). A recent paper (Schoental, Head and Peacock, 1954) showed that senecio alkaloids also produced liver tumours if they were administered over longer periods. It seemed possible, therefore, that the chemically much simpler molecule DMN might also produce liver tumours in rats. The present paper describes the results of a long-term feeding experiment in which the compound was added to the diet of rats. A smaller and shorter experiment on rabbits was also performed. In the rats a very high incidence of hepatic tumours occurred, many with metastatic spread, but in the rabbits no tumours were observed. In no instance were primary tumours found in organs other than the liver.MATERIAL AND METHODS Male and female albino rats and cross-bred male rabbits were used. The basal diets were M.R.C. Diet 41 (Bruce and Parkes, 1949) for the rats and M.R.C. Diet 18 (Bruce, 1947) for the rabbits. The diet was given in powder form. DMN was made up as a solution in arachis oil so that 10 ml. added to 1 kg. of powder gave the required concentration.The food intake of the rats was measured for each cage of 5 animals by filling the container each day and measuring the unconsumed residue.The animals were weighed weekly and observed each day when their food was being measured. Post mortems were carried out on all animals that were either found dead or killed by coal gas when seriously ill. Tissues were fixed in Helly's fluid and formol-saline, embedded in paraffin and sectioned at 5,s. All sections were stained with haematoxylin and eosin as a routine and selected material was stained by Mallory's connective tissue method, Gomori's silver impregnation, and

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Acrylamide produces ataxia and limb weakness in rats when given in repeated oral doses of 25 100 mg./kg. at various intervals or mixed with the diet in concentrations of 100 to 400 p.p.m. An electrophysiological and histological study of peripheral nerves has been carried out in chronical poisoned rats. In animals with severe clinical abnormalities, motor nerve conduction velocity in the fibr supplying the small muscles of the hind paw was reduced to approximately 80% of the control value. Histologically, degeneration of axis cylinders and myelin sheaths was found in peripheral nerve affecting predominantly the distal parts of the longest fibres. When paralysed animals were no longer given acrylamide, they recovered clinically, conduction velocity returned to the normal range, and there was histological evidence of regeneration of nerve fibres.