Abstract:
:Acetaminophen is a widely used analgesic, which has exhibited evidence of estrogenic activity in estrogen-receptor positive human breast cancer cells. However, there is limited in vivo experimentation regarding the estrogenicity of acetaminophen. Therefore, the present study examined the in vivo estrogenic potential of acetaminophen using the immature female mouse model. Specifically, C57Bl/6 female mice were treated with acetaminophen (100, 200 and 250 mg/kg per day, i.p.) for 3 consecutive days. Positive controls received estradiol (10 microg/kg per day, i.p.) for 3 consecutive days. Markers of estrogenic activity examined were uterine weight, uterine peroxidase activity and progesterone receptor (PR) up-regulation. The results demonstrated that, at all three doses, acetaminophen did not significantly increase uterine weight, uterine peroxidase activity or PR levels. However, the co-administration of E(2) and acetaminophen (200 mg/kg per day, 3 days, i.p.) resulted in a decrease in the E(2)-induced upregulation of uterine and hepatic nuclear PR (uterine PR values of 39.7+/-6.6 and 23.7+/-3.4 fmol/mg for E(2)+vehicle and E(2)+acetaminophen, respectively, P<0.05). Additionally, the estradiol-induced increase in uterine peroxidase was decreased 75% by acetaminophen (200 mg/kg per day, 3 days, i.p.). Therefore, in the immature mouse model acetaminophen treatment did not elicit estrogenic activity. However, acetaminophen had a limited ability to antagonize the effects of E(2).
journal_name
Toxicol Lettjournal_title
Toxicology lettersauthors
Patel R,Rosengren RJdoi
10.1016/s0378-4274(01)00352-6keywords:
subject
Has Abstractpub_date
2001-05-31 00:00:00pages
89-96issue
1eissn
0378-4274issn
1879-3169pii
S0378427401003526journal_volume
122pub_type
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