Exposure to bisphenol A during gestation and lactation causes loss of sex difference in corticotropin-releasing hormone-immunoreactive neurons in the bed nucleus of the stria terminalis of rats

Funabashi, Toshiya; Kawaguchi, Maiko; Furuta, Miyako; Fukushima, Atsushi; Kimura, Fukuko

doi:10.1016/s0306-4530(03)00055-6

Cited by 69 publications

(40 citation statements)

References 42 publications

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“…No effects on the volume of the SDN-POA of the hypothalamus were observed in offspring of rats orally exposed to bisphenol A doses ranging from 3.2-320 mg/kg bw/ day during the gestation and lactation period (Kwon et al, 2000). Single dose level rat studies demonstrated reduced sexually dimorphic difference in corticotropinreleasing hormone neurons in anterior stria terminalis at 2.5 mg/kg bw/day (Funabashi et al, 2004a). No changes in sexual behavior were reported for female rats exposed to 0.3-320 mg/kg bw/day or males exposed to r0.3 mg/ kg bw/day during the gestation and/or lactation period (Kwon et al, 2000).…”

Section: Experimental Animal Studies Considered Bymentioning

confidence: 92%

“…3.2.1.3 Neurodevelopmental endpoints: Funabashi et al (2004a), supported in part by Yokohama City University, examined the effects of bisphenol A on the numbers of corticotropin-releasing hormone neurons in the preoptic area and bed nucleus of the stria terminalis of rats exposed during development. [No information was provided about chow or composition of bedding and caging.]…”

Section: Experimental Animalmentioning

confidence: 99%

“…Neural and Behavioral Endpoints Following Oral Administration: Several studies addressing effects on neural and behavioral endpoints have been conducted following gestational and lactational exposure [rats: (Funabashi et al, 2004a;Negishi et al, 2004a;Della Seta et al, 2005)]; mice: [(Palanza et al, 2002;Nishizawa et al, 2003Nishizawa et al, , 2005bLaviola et al, 2005;Ryan and Vandenbergh, 2006)], pubertal exposure [rat: (Akingbemi et al, 2004;Della Seta et al, 2006;Ceccarelli et al, 2007)], and exposure during adulthood [gerbils: (Razzoli et al, 2005)]. …”

Section: Experimental Animal Studies Considered Bymentioning

confidence: 99%

“…Gestational and lactational exposures in rats have reported subtle effects on sexually-dimorphic brain nuclei (Funabashi et al, 2004a), hormonal receptors in brain (Nishizawa et al, , 2005b, and certain sexually-dimorphic or reproductively relevant behaviors (Negishi et al, 2004a;Ryan and Vandenbergh, 2006). Most of this work has utilized single doses across the range of 2-40 mg/kg, and none has been confirmed or linked to other functional or clearly adverse effects.…”

Section: Experimental Animal Studies Considered Bymentioning

confidence: 99%

See 3 more Smart Citations

NTP‐CERHR expert panel report on the reproductive and developmental toxicity of bisphenol A

Chapin

Adams

Boekelheide

et al. 2008

Birth Defects Research Pt B

401

304

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Section: Experimental Animal Studies Considered Bymentioning

confidence: 92%

Section: Experimental Animalmentioning

confidence: 99%

Section: Experimental Animal Studies Considered Bymentioning

confidence: 99%

Section: Experimental Animal Studies Considered Bymentioning

confidence: 99%

See 2 more Smart Citations

NTP‐CERHR expert panel report on the reproductive and developmental toxicity of bisphenol A

Chapin

Adams

Boekelheide

et al. 2008

Birth Defects Research Pt B

401

304

View full text Add to dashboard Cite

“…However, the safety of this dose has been strongly disputed due to the increasing number of animal studies reporting adverse effects upon low exposures (Welshons et al 2006). Importantly, developmental exposures have been reported to exert programming effects in the rodent brain, including alterations in sexually dimorphic brain areas , Funabashi et al 2004, behavior (Farabollini et al 1999, Kubo et al 2001, Kawai et al 2003, Rubin et al 2006, cognitive skills (Carr et al 2003, Miyagawa et al 2007, Xu et al 2007, and levels of estrogen receptors (Khurana et al 2000). Published human data are also associating neurobehavioral problems in children with maternal levels of BPA during pregnancy (Braun et al 2009, Perera et al 2012.…”

Section: Introductionmentioning

confidence: 99%

Perinatal exposure to low-dose bisphenol A affects the neuroendocrine stress response in rats

Panagiotidou¹,

Zerva²,

Mitsiou³

et al. 2013

Journal of Endocrinology

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Bisphenol A (BPA) is an estrogen-mimicking endocrine disruptor. Early-life exposures to low doses of BPA exert long-lasting effects on animals' reproductive and brain physiology. However, little is known about the effects of BPA on the stress-response system. Given the interaction of sex and stress hormones, we examined the effect of a low perinatal BPA exposure on the function of the hypothalamic-pituitary-adrenal (HPA) axis at rest and upon application of acute stress. Throughout pregnancy and lactation rats received daily 40 mg BPA/kg body weight orally via cornflakes. We studied the effect of this low but chronic exposure to BPA in the male and female offspring at puberty. BPA exposure led to abnormal adrenal histology including reduced zona reticularis especially in male offspring, hyperplasia of zona fasciculata in both sexes, and increased adrenal weight in female offspring. BPA-treated females had increased basal corticosterone and reduced hypothalamic glucocorticoid receptors (GR) levels. Stressed BPA-exposed females exhibited anxiety-like behavioral coping, a less rigorous corticosterone response, and did not downregulate GR in the hypothalamus, compared with control females. BPA-exposed males exhibited a heightened corticosterone stress response compared with females; they also displayed increased pro-opiomelanocortin mRNA levels and retained the prestress levels of pituitary corticotropin-releasing hormone-receptor 1, compared with control males. We found that perinatal chronic exposure to a low dose of BPA perturbs the basal and stress-induced activity of the HPA axis in a sexually dimorphic manner at adolescence. Exposure to BPA might contribute to increased susceptibility to stress-related disorders in later life.

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Endocrine Disruption in Toxic Responses

Kawa

Sugihara

Nakamura

et al. 2009

General, Applied and Systems Toxicology

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Many endocrine‐disrupting agents, including industrial materials, pesticides, pharmaceuticals and phytochemicals, have been identified with their use by in vitro assay systems and in vivo studies in laboratory animals. These chemicals are widely distributed in the environment, and are able to mimic or antagonize the biological functions of natural hormones. Indeed, abnormalities thought to be due to such agents have been found in animals throughout the world. There is also thought to be a risk to humans, for example, DES syndrome. Xenoestrogens can accumulate in our environment, and may play a role in the increasing incidences of breast cancer, testicular cancer and other problems of the reproductive system in humans. Risks due to endocrine disruptors in the environment are discussed in this chapter.

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Exposure to bisphenol A during gestation and lactation causes loss of sex difference in corticotropin-releasing hormone-immunoreactive neurons in the bed nucleus of the stria terminalis of rats

Cited by 69 publications

References 42 publications

NTP‐CERHR expert panel report on the reproductive and developmental toxicity of bisphenol A

NTP‐CERHR expert panel report on the reproductive and developmental toxicity of bisphenol A

Perinatal exposure to low-dose bisphenol A affects the neuroendocrine stress response in rats

Endocrine Disruption in Toxic Responses

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