{'fraction_non_alphanumeric': 0.032377428307123035, 'fraction_numerical': 0.02960222016651249, 'mean_word_length': 5.402366863905326, '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}}
Influence of age and 3‐methylcholanthrene on azo‐dye carcinogenesis and metabolism of p‐dimethylaminoazobenzene in rat liver

Two groups of male Sprague‐Dawley rats of different ages received a carcinogenic diet containing 0.06% dimethylaminoazobenzene (DAB). Out of a group of 4‐ to 6‐ week‐old rats, 20% developed hepatomas 31/2 months after the beginning of the diet, and after 10 months the percentage of tumors reached 56%. Rats aged 10–11 weeks old did not present hepatomas before 6 months of DAB feeding; the yield was only 28% after 10 months of carcinogen ingestion. In control rats, in vitro DAB metabolites binding to DNA and proteins proceeding from microsomal activation of carcinogen decreased by 70% between 4 and 12 weeks; within the same time azoreductase activity remained constant. A single injection of 3‐methylcholanthrene (20 mg/kg) greatly increased binding but not azoreductase activity. Time‐effect was similar in treated and control rats. Results were discussed looking for age and methylcholanthrene effect on carcinogenesis‐DAB metabolism relationship.