Abstract:
Experiments are described which show that copper acetate has a powerful retarding effect on hepatic tumor development in rats with 4’-Ethyl-Dimethylaminoazobenzene treatment. Thus, of 5 rats which survived the treatment with copper acetate and 4’-Ethyl-Dimethylaminoazobenzene for longer than 3 months, no animal developed a tumor. This can be contracted with a control group receiving 4’-Ethyl-Dimethylaminoazobenzene alone, in which 4 rats all developed tumors in an average time of 84.8 days.
An assessment of liver damage based on the development of cirrhosis and regenerative hyperplasia is described.
Possible mechanisms through which the protective effect right he mediated are briefly discussed, it has been established that there is no alteration or destruction of the carcinogen when mixed and stored with copper acetate.
Thus it can be seen that copper could alter azo-dye carcinogenesis by a variety of means, and since it is an essential part of many enzyme and biosynthetic reactions it is conceivable that enzymes and reactions which involve copper diet modifies this, alternatively a high copper diet and the consequent tissue storage may itself inactivate some enzyme systems which are involved in the metabolism of the dye and so prevent tumor development.
