Effects of Xenoestrogens on the Differentiation of Behaviorally Relevant Neural Circuits in Higher Vertebrates

Panzica, Giancarlo; Mura, Elena; Miceli, D.; Martini, Mariangela; Gotti, Stefano; Viglietti‐Panzica, C.

doi:10.1111/j.1749-6632.2008.03628.x

Cited by 21 publications

(23 citation statements)

References 72 publications

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“…However, BPA when injected to immature male in the present study showed more activity in reducing circulatory testosterone levels and sexual behavior than in ova injection. Consequently, the permanent effects of the estrogen like compounds on sexual behavioral can be induced by administering during a sensitive developmental stage, such as the period of differentiation or maturation of the reproductive organs (Panzica et al, 2009). Whereas estrogen-induced morphological changes in the testis have been reported to disappear after hatching (Halldin et al, 1999(Halldin et al, , 2003 while the estrogen-induced effects on the male brain are rather permanent.…”

Section: Discussionmentioning

confidence: 99%

Testicular Functions and Sexual Behavior in Male Japanese Quail after Exposure to Bisphenol A

Hanafy¹,

Khalil²,

Abdel-Rahi³

et al. 2015

Asian J. of Poultry Science

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Recently, with the world progress of industries, several adverse factors such as Endocrine Disrupting Chemicals (EDCs) have appeared. These contaminants have negative devastating effects on the reproductive performance in a large number of domestic and wildlife animal species. Therefore, the objective of this study was to investigate the reproductive and physiological changes due to pre-pubertal exposure of Japanese quail males to Bisphenol A (BPA) as one of EDCs (BPA is a synthetic chemical acts as estrogenic effect). Three weeks old male quails were weekly injected intra-peritoneally (at 3, 4 and 5 weeks old) with BPA at doses of 0, 1, 5, or 10 mg kgG 1 b.wt. After 6 weeks exposure of BPA, time of sexual libido, semen characteristics, fertility percent, sexual organs development, histopathology of testes were examined and plasma testosterone concentrations were estimated. The results showed that BPA has adverse and deterioration effects on most of the studied traits. The males received 5 and 10 mg BPA showed significantly delayed time of sexual libido compared with control group. Also, males received 5 mg BPA showed significantly reduced semen volume and cloacal gland area compared with control males. The lowest initial motility and fertility percent (p#0.05) were detected in 10 mg group while the highest values were obtained in the control group. Males treated with 1 and 10 mg BPA had lower (p = 0.028) foam production than those produced in control males. Plasma concentrations of testosterone were significantly reduced (p<0.000) in all treated groups compared with control group. Histologically, the growth of the testes was negatively affected by exposure to/or over 1 mg kgG 1 BPA: Namely, the development of seminiferous tubules and spermatogenesis were severely inhibited compared with control testes. It could be concluded that exposure to estrogenic effects of environmental endocrine disruptors such as BPA before/at puberty lead to malformation of reproductive organs and reduction of reproductive capacity which appears not to regenerate in adult male quail.

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Section: Discussionmentioning

confidence: 99%

Testicular Functions and Sexual Behavior in Male Japanese Quail after Exposure to Bisphenol A

Hanafy¹,

Khalil²,

Abdel-Rahi³

et al. 2015

Asian J. of Poultry Science

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“…In this regard, some studies have demonstrated that MDCs can masculinize or feminize energy balancing traits depending upon type and dose of the tested chemical, the timing of exposure and the metabolic challenge. In experimental animals, sex-dependent differences in body weight in response to prenatal or early postnatal exposure to low doses of BPA or DES have been reported; both chemicals increased body weight in female rodents but decreased or did not affect it in males [328, 443]. A recent study has examined in detail the energy balance traits of mice prenatally exposed either to a low or a high dose of BPA or to DES showing that exposure to BPA but not to DES hypermasculinized male and masculinized female mice (see also [440]).…”

Section: Mdcs and Metabolism-relevant Diseasesmentioning

confidence: 99%

Metabolism disrupting chemicals and metabolic disorders

Heindel

Blumberg

Cave

et al. 2017

Reproductive Toxicology

846

651

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The recent epidemics of metabolic diseases, obesity, type 2 diabetes(T2D), liver lipid disorders and metabolic syndrome have largely been attributed to genetic background and changes in diet, exercise and aging. However, there is now considerable evidence that other environmental factors may contribute to the rapid increase in the incidence of these metabolic diseases. This review will examine changes to the incidence of obesity, T2D and non-alcoholic fatty liver disease (NAFLD), the contribution of genetics to these disorders and describe the role of the endocrine system in these metabolic disorders. It will then specifically focus on the role of endocrine disrupting chemicals (EDCs) in the etiology of obesity, T2D and NAFLD while finally integrating the information on EDCs on multiple metabolic disorders that could lead to metabolic syndrome. We will specifically examine evidence linking EDC exposures during critical periods of development with metabolic diseases that manifest later in life and across generations.

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“…Nearly all Kiss1 neurons in the RP3V and ARC co-express ERα, and a subset of RP3V Kiss1 neurons co-express ERβ (Smith et al, 2005, Smith et al, 2006) suggesting that disruption of ER expression within this neuronal phenotype could affect its sex specific ontogeny and function. Gestational and/or postnatal BPA exposure has been shown to alter Kiss1 mRNA expression within whole hypothalamic micropunches (Navarro et al, 2009, Xi et al, 2010), and RP3V Kiss1-immunoreactivity (Bai et al, 2011, Panzica et al, 2009) during peripuberty and adulthood. Although RP3V Kiss1 expression is not apparent in either sex until approximately the second week of life (Cao and Patisaul, 2011, Clarkson et al, 2009) we have shown that neonatal exposure to estrogen or an ERα selective agonist (Bateman and Patisaul, 2008, Patisaul, Todd, 2009) can defeminize kisspeptin signaling pathways in the adult RP3V, suggesting that the first few days of life may be a critical window of BPA vulnerability, and that this disruption may be apparent prior to puberty.…”

Section: Introductionmentioning

confidence: 99%

Neonatal Bisphenol A exposure alters sexually dimorphic gene expression in the postnatal rat hypothalamus

et al. 2012

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Developmental exposure to Bisphenol A (BPA), a component of polycarbonate and epoxy resins, has been purported to adversely impact reproductive function in female rodents. Because neonatal life is a critical window for the sexual dimorphic organization of the hypothalamic-pituitary-gonadal (HPG) axis, interference with this process could underlie compromised adult reproductive physiology. The goal of the present study was to determine if neonatal BPA exposure interferes with sex specific gene expression of estrogen receptor alpha (ERα), ER beta (ERβ) and kisspeptin (Kiss1) in the anterior and mediobasal hypothalamus. Long Evans (LE) neonatal rats were exposed to vehicle, 10 µg estradiol benzoate (EB), 50 mg/kg BPA or 50µg/kg BPA by subcutaneous injection daily from postnatal day 0 (PND 0) to PND 2. Gene expression was assessed by in situ hybridization on PNDs 4 and 10. Within the anterior hypothalamus ERα expression was augmented by BPA in PND 4 females, then fell to male-typical levels by PND 10. ERβ expression was not altered by BPA on PND 4, but significantly decreased or eliminated in both sexes by PND 10. Kiss1 expression was diminished by BPA in the anterior hypothalamus, especially in females. There were no significant impacts of BPA in the mediobasal hypothalamus. Collectively, BPA effects did not mirror those of EB. The results show that neonatal hypothalamic ER and Kiss1 expression is sensitive to BPA exposure. This disruption may alter sexually dimorphic hypothalamic organization and underlie adult reproductive deficiencies. Additionally, the discordant effects of EB and BPA indicate that BPA likely disrupts hypothalamic organization by a mechanism other than simply acting as an estrogen mimic.

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Effects of Xenoestrogens on the Differentiation of Behaviorally Relevant Neural Circuits in Higher Vertebrates

Cited by 21 publications

References 72 publications

Testicular Functions and Sexual Behavior in Male Japanese Quail after Exposure to Bisphenol A

Testicular Functions and Sexual Behavior in Male Japanese Quail after Exposure to Bisphenol A

Metabolism disrupting chemicals and metabolic disorders

Neonatal Bisphenol A exposure alters sexually dimorphic gene expression in the postnatal rat hypothalamus

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