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Arsenic exposure in utero and nonepidermal proliferative response in adulthood in Tg.AC mice.

International Journal of Toxicology

chemically induced, Uterine Neoplasms, Urinary Bladder Neoplasms, toxicity, Tetradecanoylphorbol Acetate, administration & dosage, Sodium Compounds, Sex Characteristics, Random Allocation, Prenatal Exposure Delayed Effects, Pregnancy, Precancerous Conditions, Papilloma, Mice, adverse effects, Maternal Exposure, Male, Hyperplasia, Female, Dose-Response Relationship, Drug, Carcinogens, Arsenites, Arsenic, Animals, Aging, Adrenal Cortex Neoplasms, Adenoma

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      To expand our knowledge on the transplacental carcinogenic potential of inorganic arsenic, pregnant Tg.AC mice received drinking water with 0, 42.5, or 85 ppm arsenite from gestation day 8 to 18. After birth, groups (n = 25) of offspring received topical 12-O-tetradecanoyl phorbol-13-acetate (TPA) (2 microg twice a week) for 36 weeks and were killed; nonskin tumors were assessed. Arsenic increased adrenal cortical adenomas (ACAs; 25%-29%) compared with control (0%) independent of TPA in all male groups. Arsenic increased urinary bladder (UB) hyperplasia in males, but only with TPA. Arsenic induced ACAs in all female groups (control 0%; arsenic 17%-26%). Arsenic-treated females had UB hyperplasia in most groups (control 0%; arsenic 26%-32%), with 2 UB papillomas. All arsenic-treated females had uterine hyperplasia (26%-40%; control 4%) independent of TPA, and 3 had uterine tumors. Thus, arsenic in utero rapidly induces ACAs and uterine and UB preneoplasias in Tg.AC mice, showing transplacental carcinogenic potential in yet another strain of mice.

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