No effect of route of exposure (oral; subcutaneous injection) on plasma bisphenol A throughout 24 h after administration in neonatal female mice

被引:90
作者
Taylor, Julia A. [1 ]
Welshons, Wade V. [2 ]
Saal, Frederick S. vom [1 ]
机构
[1] Univ Missouri, Div Biol Sci, Columbia, MO 65211 USA
[2] Univ Missouri, Dept Biomed Sci, Columbia, MO 65211 USA
关键词
bisphenol A; neonatal metabolism; pharmacokinetics; UDP-glucuronosyltransferase;
D O I
10.1016/j.reprotox.2008.01.001
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Route of administration of chemicals in adults is an important factor in pharmacokinetics of chemicals such as bisphenol A (BPA), the monomer with estrogenic activity used to make polycarbonate plastic products and to line food and beverage cans. Based on findings in adults it has been proposed (CERHR, 2007) that non-oral routes of administration in newborn rodents would also lead to high exposure relative to oral administration. However, in fetuses and neonates, the enzyme that conjugates BPA (UDP-glucuronosyltransferase) is expressed at low levels, suggesting that there may be no differences in pharmacokinetics between oral and non-oral dosing. We thus conducted an analysis of plasma concentrations of unconjugated H-3-BPA after HPLC separation in postnatal day 3 female mice throughout the 24 It after administering H-3-BPA orally or via subcutaneous injection at doses above and below the current EPA reference dose. We found no significant difference in plasma BPA based on route of administration in neonatal mice at either dose. However, compared to data from other studies conducted with adults, there was a markedly higher plasma BPA level after oral administration of BPA in newborn mice. This finding sets aside the belief that non-oral administration of BPA renders data as not suitable for consideration of the hazard posed by low-dose exposure to BPA during neonatal life. Therefore the large numbers of BPA studies that used non-oral administration at very low doses during the neonatal period should not be dismissed by scientists or the regulatory community based on route of administration. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:169 / 176
页数:8
相关论文
共 30 条
[1]   Exposure of the US population to bisphenol A and 4-tertiary-octylphenol:: 2003-2004 [J].
Calafat, Antonia M. ;
Ye, Xiaoyun ;
Wong, Lee-Yang ;
Reidy, John A. ;
Needham, Larry L. .
ENVIRONMENTAL HEALTH PERSPECTIVES, 2008, 116 (01) :39-44
[2]  
*CERHR NTP, 2007, NTP CERHR EXP PAN RE
[3]   Age and dose dependency of the pharmacokinetics and metabolism of bisphenol A in neonatal Sprague-Dawley rats following oral administration [J].
Domoradzki, JY ;
Thornton, CM ;
Pottenger, LH ;
Hansen, SC ;
Card, TL ;
Markham, DA ;
Dryzga, MD ;
Shiotsuka, RN ;
Waechter, JM .
TOXICOLOGICAL SCIENCES, 2004, 77 (02) :230-242
[4]   DEVELOPMENT IN NEWBORN RAT OF CONJUGATION AND DE-CONJUGATION PROCESSES INVOLVED IN ENTEROHEPATIC CIRCULATION OF DIETHYLSTILBESTROL [J].
FISCHER, LJ ;
WEISSINGER, JL .
XENOBIOTICA, 1972, 2 (04) :399-+
[5]   Developmental exposure to estradiol and bisphenol A increases susceptibility to prostate carcinogenesis and epigenetically regulates phosphodiesterase type 4 variant 4 [J].
Ho, Shuk-Mei ;
Tang, Wan-Yee ;
de Frausto, Jessica Belmonte ;
Prins, Gail S. .
CANCER RESEARCH, 2006, 66 (11) :5624-5632
[6]  
ICRAIN DA, 2007, REPROD TOXICOL, V24, P225
[7]  
*IRIS, 1988, 80057 CASRN USEPA
[8]   An evaluation of evidence for the carcinogenic activity of bisphenol A [J].
Keri, Ruth A. ;
Ho, Shuk-Mei ;
Hunt, Patricia A. ;
Knudsen, Karen E. ;
Soto, Ana M. ;
Prins, Gail S. .
REPRODUCTIVE TOXICOLOGY, 2007, 24 (02) :240-252
[9]   Developmental increases in rat hepatic microsomal UDP-glucuronosyltransferase activities toward xenoestrogens and decreases during pregnancy [J].
Matsumoto, J ;
Yokota, H ;
Yuasa, A .
ENVIRONMENTAL HEALTH PERSPECTIVES, 2002, 110 (02) :193-196
[10]   Developmental effects of estrogenic chemicals are predicted by an in vitro assay incorporating modification of cell uptake by serum [J].
Nagel, SC ;
vom Saal, FS ;
Welshons, WV .
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY, 1999, 69 (1-6) :343-357