748. antagonism of ethionine and trypan blue in rat-liver carcinogenesis: ito, n. & farber, e....

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L762 CANCER RESEARCH Finsen Institute, Copenhagen, on the use of chlornaphazine (2-naphthyl-bis-(fl-chloro- ethyl)amine) in the treatment of polycythaemia. Of 61 patients treated, 20 received a total dose exceeding 100 g, and in this group 7 cases of bladder tumour occurred. In 8 patients who received 175 g or more, 5 bladder tumours were reported. Chlornaphazin must there- fore be considered carcinogenic when administered in large doses over a long period. 748. Antagonism of ethionine and trypan blue in rat-liver carcinogenesis Ito, N. & Farber, E. (1964). Antagonistic effects of ethionine and trypan blue on liver carcinogenesis in the rat. Proc. Amer. Ass. Cancer Res. 5, 31. Both ethionine (I) and trypan blue (II) are known to induce liver tumours. Dietary I induces hepatocellular carcinoma and injection of II induces retieulum cell sarcoma. Previous work has shown that II inhibits the induction of liver turnouts by p-dimethyl- aminoazobenzene. The authors have found that I and II antagonize each other in regard to the development of parenchymal cell and reticulum cell neoplasias in the liver. Groups of rats were given dietary I (group A), weekly subcutaneous injections of II (group B), and both treatments simultaneously (group C). It was found that 75 ~o of group A rats developed hepatocellular carcinomas and 90 ~o of group B developed reticulum cell sarcomas. The incidence of liver carcinoma or reticulum cell sarcoma in group C was only 13 ~o but these rats developed severe cholangiofibrosis. 749. Carcinogenic effects of diethylnitrosamine Herrold, Katherine McD. (1964). Comparative carcinogenic effects of diethylnitrosamine by different routes of administration to Syrian hamsters. Proc. Amer. Ass. Cancer Res. 5, 26. Diethylnitrosamine (I) has been shown to induce tumours of the trachea, bronchi, nasal cavity and liver when given to hamsters by the intratracheal, intragastric or subcutaneous routes. The present study demonstrated that, when given intraperitoneally, intradermally or by skin application, fewer hepatocellular carcinomas were produced than when the subcu- taneous route was used. The carcinogenic effect was greatest on the trachea, bronchi and nasal cavity, and suggests that the major pathway of excretion of I or its metabolite is via the respiratory system. 750. Carcinogens and tissue binding Ray, F. E. & Wejebe, O. O. (1964). Relation between carcinogenicity and tissue affinity of chemical carcinogens. Proc. Amer. Ass. Cancer Res. 5, 52. Two related compounds, 2-aeetamidofluorene (I) and 2-acetamidofluorenone (II) were examined for their ability to bind to intraeellular protein and ribosomal RNA following oral and intraperitoneal administration. Tritium-labelled materials were used, and livers and other tissues were assayed at intervals of 6-24 hr. It is known that I binds to liver proteins and that it is a potent liver carcinogen. II pro- duees only very few liver tumours, and the study established the fact that it had a lesser affinity for liver tissues than did I.

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Page 1: 748. Antagonism of ethionine and trypan blue in rat-liver carcinogenesis: Ito, N. & Farber, E. (1964). Antagonistic effects of ethionine and trypan blue on liver carcinogenesis in

L762 CANCER RESEARCH

Finsen Institute, Copenhagen, on the use of chlornaphazine (2-naphthyl-bis-(fl-chloro- ethyl)amine) in the treatment of polycythaemia. Of 61 patients treated, 20 received a total dose exceeding 100 g, and in this group 7 cases of bladder tumour occurred. In 8 patients who received 175 g or more, 5 bladder tumours were reported. Chlornaphazin must there- fore be considered carcinogenic when administered in large doses over a long period.

748. Antagonism of ethionine and trypan blue in rat-liver carcinogenesis Ito, N. & Farber, E. (1964). Antagonistic effects of ethionine and trypan blue on liver carcinogenesis in the rat. Proc. Amer. Ass. Cancer Res. 5, 31.

Both ethionine (I) and trypan blue (II) are known to induce liver tumours. Dietary I induces hepatocellular carcinoma and injection of II induces retieulum cell sarcoma. Previous work has shown that II inhibits the induction of liver turnouts by p-dimethyl- aminoazobenzene. The authors have found that I and II antagonize each other in regard to the development of parenchymal cell and reticulum cell neoplasias in the liver.

Groups of rats were given dietary I (group A), weekly subcutaneous injections of II (group B), and both treatments simultaneously (group C). It was found that 75 ~o of group A rats developed hepatocellular carcinomas and 90 ~o of group B developed reticulum cell sarcomas. The incidence of liver carcinoma or reticulum cell sarcoma in group C was only 13 ~o but these rats developed severe cholangiofibrosis.

749. Carcinogenic effects of diethylnitrosamine Herrold, Katherine McD. (1964). Comparative carcinogenic effects of diethylnitrosamine by different routes of administration to Syrian hamsters. Proc. Amer. Ass. Cancer Res. 5, 26.

Diethylnitrosamine (I) has been shown to induce tumours of the trachea, bronchi, nasal cavity and liver when given to hamsters by the intratracheal, intragastric or subcutaneous routes. The present study demonstrated that, when given intraperitoneally, intradermally or by skin application, fewer hepatocellular carcinomas were produced than when the subcu- taneous route was used. The carcinogenic effect was greatest on the trachea, bronchi and nasal cavity, and suggests that the major pathway of excretion of I or its metabolite is via the respiratory system.

750. Carcinogens and tissue binding Ray, F. E. & Wejebe, O. O. (1964). Relation between carcinogenicity and tissue affinity of chemical carcinogens. Proc. Amer. Ass. Cancer Res. 5, 52.

Two related compounds, 2-aeetamidofluorene (I) and 2-acetamidofluorenone (II) were examined for their ability to bind to intraeellular protein and ribosomal RNA following oral and intraperitoneal administration. Tritium-labelled materials were used, and livers and other tissues were assayed at intervals of 6-24 hr.

It is known that I binds to liver proteins and that it is a potent liver carcinogen. II pro- duees only very few liver tumours, and the study established the fact that it had a lesser affinity for liver tissues than did I.