{'fraction_non_alphanumeric': 0.046, 'fraction_numerical': 0.027333333333333334, 'mean_word_length': 5.228215767634855, '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}}
Whole‐body autoradiographic disposition, elimination and placental transport of [14C]Tri‐o‐cresyl phosphate in mice

Tri‐o‐cresyl phosphate (TOCP) is used commercially as a plasticizer and flame retardant. The disposition, metabolism, elimination and transplacental uptake of [phenyl‐U‐14C]TOCP and/or its metabolites, in pregnant and non‐pregnant mice, were examined. Pregnant (18th‐day gestation) and non‐pregnant, ICR mice were given an i.v. dose of [14C]TOCP (557 μCi kg−1; Specified activity 4.83 μCi μmol−1). At various time intervals (1, 24, 48 and 72 h) the animals were processed for whole‐body autoradiography (WBA). Over 72 h the nonpregnant mice excreted 55% of the 14C in the urine and 9% in the feces, while excretion in the urine and feces by the pregnant mice was 50% and 9% of the total dose, respectively. The WBA and its computerassisted image analysis indicated extensive distribution of the 14C label originally dosed as [14C]TOCP in pregnant mice and their fetuses. The retention of radioactivity in organs such as lung, spleen, gall‐bladder and liver of mother and its fetuses suggest that these are the target sites of TOCP toxicity. The distribution in non‐pregnant and pregnant mice and in the fetal tissues followed a similar pattern in uptake and retention until 72 h. Brain and spinal cord had the least amount of [14C]TOCP. This finding may support reports that explain the insensitivity of the mice towards organophosphate‐induced delayed neurotoxicity (OPIDN) of TOCP.