1. Malononitriles did not inhibit the rhodanese activity in tissue homogenates, nor did they competitively displace the cyanide.

  2. The rhodanese content of fetal tissue increased in amount with development and at birth. The rhodanese activity of the tissue of the mother was not significantly influenced by pregnancy.

  3. Animals fed 3′-methyl-4-dimethylaminoazobenzene showed a slight decrease in the rhodanese activity coincident with the development of hepatoma. The hepatoma itself showed a significantly damaged rhodanese activity, while the surrounding unimpaired liver tissues continued functioning normally.

  4. The Walker rat carcinoma 256 produced a general lowering of the rhodanese activity in the tissues, which could not be correlated with either loss of weight or a lowered food intake. This was not the case in the tissues of mice with transplanted tumors.

  5. A detailed analysis of different mouse transplanted tumors and the tissues of both the normal and tumor-bearing mice of strains A, C3H, and C57 revealed that the tumors do not have less rhodanese content than their homologous tissues or of some of the vital organs. Liver and kidney, in comparison, possess a disproportionately high activity of rhodanese that well fits in with their function of being the prime sites of cyanide detoxification.

  6. Administration of malononitrile and p-nitrobenzalmalononitrile to C3H-S-bearing mice for a period of 16 days did not influence the rhodanese activity of the tissues or that of the tumors.

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This work was supported in part by grants from the National Cancer Institute, United States Public Health Service.

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