{'fraction_non_alphanumeric': 0.04487179487179487, 'fraction_numerical': 0.01282051282051282, 'mean_word_length': 5.038674033149171, '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}}
Multiple sites of action of N-hydroxy-2-acetylaminofluorene rat hepatic nuclear transcription.

This study attempts to identify the site(s) of action of N-hydroxy-2-acetylaminofluorene (N-OH-AAF) in relation to its inhibition of rat hepatic nuclear RNA synthesis. Two hr after N-OH-AAF injection (3 mg/100 g body weight), rat hepatic nuclear synthesis and nucleolar RNA synthesis in vitro were inhibited by 60 and 80%, respectively. When total nuclear RNA polymerases were solubilized and assayed in the presence of alpha-amanitin (3.2 mug/ml), only alpha-amanitin-sensitive activity was reduced (50%) by N-OH-AAF. Diethylamino-ethyl-Sephadex column chromatography confirmed this finding and further demonstrated that RNA polymerase II was the activity selectively inhibited. Since N-OH-AAF dramatically inhibited nucleolar RNA synthesis but had little effect on RNA polymerase I activity, per se, we therefore concluded that, in addition to its direct inhibitory effect on the enzymic function of RNA polymerase II, N-OH-AAF must also cause impairment of the nucleolar DNA template function.