{'fraction_non_alphanumeric': 0.02780191138140747, 'fraction_numerical': 0.016507384882710686, 'mean_word_length': 5.582857142857143, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Metabolism of benz(a)anthracene catalyzed by liver microsomes of untreated and nicotine-pretreated rats.

The purpose of the present investigation was to determine whether nicotine causes an induction or alteration of rat liver microsomal monooxygenases (cytochromes P-450) involved in the metabolism and activation of polycyclic aromatic hydrocarbons. After 2, 4, and 10 days of continuous nicotine treatment (16.8 mg/day) neither an increase of benz(a)anthracene metabolism nor an alteration of the metabolite pattern could be observed in comparison to controls. Moreover, there was no significant change of cytochrome P-450 content or benzo(a)pyrene hydroxylation rates. In further control experiments the inducibility of the rats was tested by pretreatment with benzo(k)fluoranthene. As expected, this treatment resulted in a high increase of metabolism and the formation of the ultimate carcinogen as well as other metabolites of benz(a)anthracene due to the induction corresponding to isocytochrome P-450. For nicotine it can be concluded that this alkaloid cannot cause qualitative or quantitative changes of normal rat liver cytochromes P-450.