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
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
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