Bisphenol-A affects spermatogenesis in the adult rat even at a low dose

被引:124
作者
Sakaue, M
Ohsako, S
Ishimura, R
Kurosawa, S
Kurohmaru, M
Hayashi, Y
Aoki, Y
Yonemoto, J
Tohyama, C
机构
[1] Univ Tokyo, Natl Inst Environm Studies, Environm Hlth Sci Div, Tsukuba, Ibaraki 3058506, Japan
[2] Univ Tokyo, Natl Inst Environm Studies, Endocrine Disrupters & Dioxin Res Project, Tsukuba, Ibaraki, Japan
[3] Univ Tokyo, Grad Sch Agr & Life Sci, Dept Vet Anat, Tsukuba, Ibaraki, Japan
关键词
bisphenol-A; low dose; adult rat; testis; spermatogenesis; daily sperm production; testicular weight; 2D-PAGE;
D O I
10.1539/joh.43.185
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
Bisphenol-A (BPA), a xenobiotic estrogenic compound widely used as a plastics monomer, has been suspected to have a so-called low dose effect on the reproductive system when administered transplacentally. In the present study, we investigated possible low-dose effects of BPA on spermatogenesis in adult rats. Male rats (13 weeks old; W13) were administrated a daily oral dose of BPA, ranging from 2 ng to 200 mg/kg, for 6 days and examined for testicular weight (TW) and daily sperm production (DSP) at W14 and W18. A BPA dose as low as 20 mug/kg tended to decrease TW and significantly reduced both DSP and the efficiency of spermatogenesis (DSP per gram testis) at W18, showing that BPA suppressed a normal increase in DSP and TW from W13 to W18. A single administration of 20 mug BPA/kg to W13 rats affected the intensity or mobility of several protein spots in the testicular cytosol fraction as shown by two-dimensional gel electrophoresis analysis. The present study showed that BPA at a low dose affects spermatogenesis in the adult rat.
引用
收藏
页码:185 / 190
页数:6
相关论文
共 29 条
[1]   A case of a laboratory animal feed with high estrogenic activity and its impact on in vivo responses to exogenously administered estrogens -: Commentary [J].
Boettger-Tong, H ;
Murthy, L ;
Chiappetta, C ;
Kirkland, JL ;
Goodwin, B ;
Adlercreutz, H ;
Stancel, GM ;
Mäkelä, S .
ENVIRONMENTAL HEALTH PERSPECTIVES, 1998, 106 (07) :369-373
[2]  
Brontons J A, 1995, ENV HLTH PERSPECT, V103, P608
[3]   Normal reproductive organ development in CF-1 mice following prenatal exposure to bisphenol A [J].
Cagen, SZ ;
Waechter, JM ;
Dimond, SS ;
Breslin, WJ ;
Butala, JH ;
Jekat, FW ;
Joiner, RL ;
Shiotsuka, RN ;
Veenstra, GE ;
Harris, LR .
TOXICOLOGICAL SCIENCES, 1999, 50 (01) :36-44
[4]   EVIDENCE FOR DECREASING QUALITY OF SEMEN DURING PAST 50 YEARS [J].
CARLSEN, E ;
GIWERCMAN, A ;
KEIDING, N ;
SKAKKEBAEK, NE .
BRITISH MEDICAL JOURNAL, 1992, 305 (6854) :609-613
[5]   Estrogenic induction of spermatogenesis in the hypogonadal mouse [J].
Ebling, FJP ;
Brooks, AN ;
Cronin, AS ;
Ford, H ;
Kerr, JB .
ENDOCRINOLOGY, 2000, 141 (08) :2861-2869
[6]   Targeted disruption of the estrogen receptor gene in male mice causes alteration of spermatogenesis and infertility [J].
Eddy, EM ;
Washburn, TF ;
Bunch, DO ;
Goulding, EH ;
Gladen, BC ;
Lubahn, DB ;
Korach, KS .
ENDOCRINOLOGY, 1996, 137 (11) :4796-4805
[7]   Immunolocalisation of oestrogen receptor-alpha within the testis and excurrent ducts of the rat and marmoset monkey from perinatal life to adulthood [J].
Fisher, JS ;
Millar, MR ;
Majdic, G ;
Saunders, PTK ;
Fraser, HM ;
Sharpe, RM .
JOURNAL OF ENDOCRINOLOGY, 1997, 153 (03) :485-495
[8]   Bisphenol A interacts with the estrogen receptor α in a distinct manner from estradiol [J].
Gould, JC ;
Leonard, LS ;
Maness, SC ;
Wagner, BL ;
Conner, K ;
Zacharewski, T ;
Safe, S ;
McDonnell, DP ;
Gaido, KW .
MOLECULAR AND CELLULAR ENDOCRINOLOGY, 1998, 142 (1-2) :203-214
[9]   A role for oestrogens in the male reproductive system [J].
Hess, RA ;
Bunick, D ;
Lee, KH ;
Bahr, J ;
Taylor, JA ;
Korach, KS ;
Lubahn, DB .
NATURE, 1997, 390 (6659) :509-512
[10]  
Hess RA, 1997, J ANDROL, V18, P602