{'fraction_non_alphanumeric': 0.028272251308900525, 'fraction_numerical': 0.018848167539267015, 'mean_word_length': 5.828571428571428, '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}}
Triiodothyronine rapidly stimulates mitochondrial respiration in isolated hepatocytes.

Isolated hepatocytes from euthyroid or hypothyroid (thyroidectomized) rats showed a 20 to 30% stimulation of respiratory activity when treated with triiodothyronine (T3). Maximal stimulation was obtained in the presence of the uncoupler carbonylcyanide m-chlorophenyl-hydrazone (CCCP) suggesting a direct effect on the respiratory chain. Physiological concentrations of T3 (10-11-10-9) induced maximal stimulation after a short incubation (75% of maximum in 3 min) and the effect persisted for over 1 h of incubation. Mitochondria, rapidly isolated from T3-treated hepatocytes, retained stimulated respiratory activity in both coupled and uncoupled states. These results are consistent with the hypothesis that the mitochondrion is a primary target for thyroid hormones, and the present system appears to be suitable for the systematic investigation of these effects.