title: Effect of perinatal and postnatal bisphenol A exposure to the regulatory circuits at the hypothalamus-pituitary-gonadal axis of CD-1 mice.
abstract: Bisphenol A (BPA) is used in the manufacture of many products and is ubiquitous in the environment. Adverse effects of BPA on animal reproductive health have been reported, however most of the studies relied on the approaches in the assessment of conventional histology and anatomical features. The mechanistic actions of BPA are not clear. In the present study, a murine model was used to study potential effects of BPA exposure during perinatal and postnatal periods on endocrine functions of hypothalamic-pituitary-gonadal (HPG)-axis. At the hypothalamic-pituitary level, BPA exposure resulted in the up-regulation of the expression levels of KiSS-1, GnRH and FSH mRNA in both male and female pups. At the gonadal levels, BPA caused inhibition in the expressions of testicular steroidogenic enzymes and the synthesis of testosterone in the male pups. Conversely exposure to BPA resulted in a greater aromatase expression level and the synthesis of estrogen in the female pups. BPA is a weak estrogen agonist and its effects reported on animal studies are difficult to reconcile with mechanistic action of estrogen. In this study we hypothesized that the effects of BPA on reproductive dysfunction may be due to its actions on gonadal steroidogenesis and so the anomalous releases of endogenous steroid hormones. This non-ER-mediated effect is more potent in affecting the feedback regulatory circuits in the HPG-axis.
authors.affiliation: Croucher Institute of Environmental Sciences, Department of Biology, Hong Kong Baptist University, Kowloon, Hong Kong.
authors.forename: Wei
authors.initials: W
authors.lastname: Xi
authors.forename: C K F
authors.initials: CK
authors.lastname: Lee
authors.forename: W S B
authors.initials: WS
authors.lastname: Yeung
authors.forename: John P
authors.initials: JP
authors.lastname: Giesy
authors.forename: M H
authors.initials: MH
authors.lastname: Wong
authors.forename: Xiaowei
authors.initials: X
authors.lastname: Zhang
authors.forename: Markus
authors.initials: M
authors.lastname: Hecker
authors.forename: Chris K C
authors.initials: CK
authors.lastname: Wong
mesh_terms: D000367:Age Factors; D000375:Aging; D000704:Analysis of Variance; D000818:Animals; D001559:Benzhydryl Compounds; D004305:Dose-Response Relationship, Drug; D052244:Endocrine Disruptors / Q000633:toxicity*; D004785:Environmental Pollutants / Q000633:toxicity*; D005260:Female; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D005865:Gestational Age; D012739:Gonadal Steroid Hormones / Q000096:biosynthesis; D006065:Gonadotropins, Pituitary / Q000378:metabolism; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism; D008297:Male; D051379:Mice; D019055:No-Observed-Adverse-Effect Level; D010053:Ovary / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism; D010636:Phenols / Q000633:toxicity*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012333:RNA, Messenger / Q000378:metabolism; D043562:Receptors, G-Protein-Coupled / Q000187:drug effects / Q000235:genetics; D018000:Receptors, Peptide / Q000187:drug effects / Q000235:genetics; D011987:Receptors, Steroid / Q000187:drug effects / Q000235:genetics; D012098:Reproduction / Q000187:drug effects*; D013737:Testis / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D052244:Endocrine Disruptors; D004785:Environmental Pollutants; D012739:Gonadal Steroid Hormones; D006065:Gonadotropins, Pituitary; D010636:Phenols; D012333:RNA, Messenger; D043562:Receptors, G-Protein-Coupled; D018000:Receptors, Peptide; D011987:Receptors, Steroid; C006780:bisphenol A; D000098826:Bisphenol A Compounds