Indole-3-carbinol attenuates the deleterious gestational effects of bisphenol A exposure on the prostate gland of male F1 rats

被引：34
作者：
Brandt, Joyce Zalotti [1 ]
Silveira, Livia Teresa R. [1 ]
Grassi, Tony Fernando [2 ]
Anselmo-Franci, Janete A. [3 ]
Favaro, Wagner Jose [4 ]
Felisbino, Sergio Luis [1 ]
Barbisan, Luis Fernando [1 ]
Scarano, Wellerson Rodrigo [1 ]
机构：
[1] Sao Paulo State Univ, Inst Biosci, Dept Morphol, UNESP, BR-18618970 Botucatu, SP, Brazil
[2] UNESP, Sch Med, Dept Pathol, BR-18618970 Botucatu, SP, Brazil
[3] Univ Sao Paulo FORP USP, Fac Dent, BR-14040904 Ribeirao Preto, SP, Brazil
[4] Univ Estadual Campinas, UNICAMP, Inst Biol, BR-13083862 Campinas, SP, Brazil
来源：
REPRODUCTIVE TOXICOLOGY | 2014年 / 43卷
基金：
巴西圣保罗研究基金会;
关键词：
Bisphenol A; Prostate; Inflammation; Indole-3-carbinol; Chemoprevention; Reproductive toxicology; DEVELOPMENTAL EXPOSURE; LATERAL PROSTATE; VENTRAL PROSTATE; ESTROGEN; EXPRESSION; ESTRADIOL; CARCINOGENESIS; MODELS; LUNG; HYPERPLASIA;
D O I：
10.1016/j.reprotox.2013.11.001
中图分类号：
Q [生物科学];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
Bisphenol A (BPA) is a chemical that has been investigated for it potential to cause prostate diseases. In this study, pregnant Sprague-Dawley rats were treated with 25 or 250 mu g/kg BPA from gestational day (GD) 10 to GD21 with or without concurrent indole-3-carbinol (I3C) feeding. I3C is a phytochemical, and it affords chemoprotection against many types of neoplasia. Male F1 rats from different litters were euthanized on post-natal day (PND) 21 and PND180. BPA-treated groups showed a significant increase in histopathological lesions, but I3C feeding reversed many of these changes, mainly at PND180. Maternal I3C feeding increased prostate epithelial apoptosis in the BPA-treated groups and across age groups. Furthermore, I3C induced partial normalization of the prostate histoarchitecture. The results pointed to a protective effect of maternal I3C feeding during pregnancy in the BPA-exposed male offspring, thereby indicating reduction in the harmful effects of gestational BPA imprinting on the prostate. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码：56 / 66
页数：11
相关论文
共 72 条
[1]   Molecular targets and anticancer potential of indole-3-carbinol and its derivatives [J].
Aggarwal, BB ;
Ichikawa, H .
CELL CYCLE, 2005, 4 (09) :1201-1215
[2]   Age-dependent and lobe-specific spontaneous hyperplasia in the brown Norway rat prostate [J].
Banerjee, PP ;
Banerjee, S ;
Lai, JM ;
Strandberg, JD ;
Zirkin, BR ;
Brown, TR .
BIOLOGY OF REPRODUCTION, 1998, 59 (05) :1163-1170
[3]   The developmental origins of adult disease [J].
Barker, DJP .
JOURNAL OF THE AMERICAN COLLEGE OF NUTRITION, 2004, 23 (06) :588S-595S
[4]   Histopathological evidence for an association of inflammation with ductal pin-like lesions but not with ductal adenocarcinoma in the prostate of the noble rat [J].
Bernoulli, Jenni ;
Yatkin, Emrah ;
Laakso, Arto ;
Anttinen, Mikael ;
Bosland, Maarten ;
Vega, Katherine ;
Kallajoki, Markku ;
Santti, Risto ;
Pylkkaenen, Liisa .
PROSTATE, 2008, 68 (07) :728-739
[5]   Use of animal models in defining efficacy of chemoprevention agents against prostate cancer [J].
Bosland, MC .
EUROPEAN UROLOGY, 1999, 35 (5-6) :459-463
[6]  
Broadbent TA, 1998, CURR MED CHEM, V5, P469
[7]   3,3′-Diindolylmethane Inhibits Prostate Cancer Development in the Transgenic Adenocarcinoma Mouse Prostate Model [J].
Cho, Han Jin ;
Park, So Young ;
Kim, Eun Ji ;
Kim, Jin-Kyung ;
Park, Jung Han Yoon .
MOLECULAR CARCINOGENESIS, 2011, 50 (02) :100-112
[8]   Profound effects of the weak environmental estrogen-like chemical bisphenol A on the growth of the mammary gland of noble rats [J].
Colerangle, JB ;
Roy, D .
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY, 1997, 60 (1-2) :153-160
[9]   The soy isoflavone genistein promotes apoptosis in mammary epithelial cells by inducing the tumor suppressor PTEN [J].
Dave, B ;
Eason, RR ;
Till, SR ;
Geng, Y ;
Velarde, MC ;
Badger, TM ;
Simmen, RCM .
CARCINOGENESIS, 2005, 26 (10) :1793-1803
[10]   Proliferative inflammatory atrophy of the prostate - Implications for prostatic carcinogenesis [J].
De Marzo, AM ;
Marchi, VL ;
Epstein, JI ;
Nelson, WG .
AMERICAN JOURNAL OF PATHOLOGY, 1999, 155 (06) :1985-1992
12345678