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Effects on Hepatic Microsomal N-and C-oxygenation of Aromatic Amines by in Vivo Corticosteroid or Aminofluorene Treatment, Diet, or Stress¹

The Wenner-Gren Institute for Experimental Biology, University of Stockholm, Stockholm, Sweden

Various environmental, endocrine, and inherent conditions, which enhance the tumor-inducing capacity of carcinogenic aromatic amines, are associated with an increased N-oxygenation of these compounds in vivo. The impairment of protein-synthesizing functions of liver ribosomes by reactive metabolites of the carcinogenic amines is, to a certain extent, correlated with these functions.

Here the effect of similar conditions on microsomal N-oxygenation and C-oxygenation in vitro was studied, using N-oxide formation and N-demethylation of N,N-dimethylaniline as test reactions. Increased microsomal N-oxygenation, and to a considerably smaller extent N-demethylation was obtained by in vivo treatment with corticosteroid or 2-aminofluorene. Vitamin E depletion, protein deficiency, or stress caused an increase in N-oxygenation accompanied by decreased N-demethylation. These conditions thus gave rise to an increase in the N-oxygenation/C-oxygenation ratio.

Guinea pig liver microsomes showed a higher N-demethylating capacity and a lower N-oxygenation than did rat liver microsomes.

The N-oxygenation of N, N-dimethylaniline by liver microsomes thus seems to be well correlated with the tumor-inducing properties and ribosome-impairing capacity of carcinogenic aromatic amines under various in vivo conditions.

¹ This work was supported by research grants from the Swedish Cancer Society.

Received 5/ 8/67. Accepted 10/ 7/67.