Effects of early prepubertal exposure to bisphenol A on the onset of puberty, ovarian weights, and estrous cycle in female mice

Nah, Won Heum; Park, Mi Jung; Gye, Myung Chan

doi:10.5653/cerm.2011.38.2.75

Cited by 110 publications

(92 citation statements)

References 54 publications

(46 reference statements)

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“…The observations that females developmentally exposed to BPA exhibited normal estrus cyclicity, ovarian and uterine weights, and were able to ovulate and produce offspring indicate that BPA-induced alterations did not interfere with the normal functioning of the HPG axis. A normal length of estrus cycle was also described in studies using ICR and CD1 mice exposed to BPA during the postnatal period (Nikaido et al 2005, Nah et al 2011 or during both gestation and lactation (Tyl et al 2008) whereas BPA exposure during the prenatal period has been shown to increase estrus cycle length (Honma et al 2002, Nikaido et al 2004). This indicates again that the time window of BPA exposure could result in different effects.…”

Section: Discussionmentioning

confidence: 99%

“…The studies investigating the effects of BPA on reproductive physiology report various effects on vaginal opening, fertility, and the estrus cycle. Exposure to BPA during prenatal or postnatal life resulted in advanced- (Honma et al 2002, Nikaido et al 2004, Nah et al 2011), delayed-(Nikaido et al 2005, or unaffected- (Howdeshell et al 1999, Tyl et al 2008 vaginal opening. Fertility was either reduced or unaltered in females exposed to BPA (Honma et al 2002, Tyl et al 2008, Cabaton et al 2011.…”

Section: Introductionmentioning

confidence: 99%

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Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Naulé¹,

Picot²,

Martini³

et al. 2014

Journal of Endocrinology

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Bisphenol A (BPA) is a widespread estrogenic compound. We investigated the effects of maternal exposure to BPA at reference doses on sexual behavior and neuroendocrine functions of female offspring in C57BL/6J mice. The dams were orally exposed to vehicle alone or vehicle-containing BPA at doses equivalent to the no observed adverse effect level (5 mg/kg body weight per day) and tolerable daily intake (TDI, 0.05 mg/kg body weight per day) level from gestational day 15 until weaning. Developmental exposure to BPA increased the lordosis quotient in naive females exposed to BPA at the TDI dose only. BPA exposure had no effect on olfactory preference, ability to express masculine behaviors or number of calbindin-positive cells, a sexually dimorphic population of the preoptic area. BPA at both doses selectively increased kisspeptin cell number in the preoptic periventricular nucleus of the rostral periventricular area of the third ventricle in adult females. It did not affect the number of GNRH-positive cells or percentage of kisspeptin appositions on GNRH neurons in the preoptic area. These changes were associated with higher levels of estradiol (E 2 ) at the TDI dose while levels of LH, estrus cyclicity, ovarian and uterine weights, and fertility remained unaffected. Delay in the time of vaginal opening was observed during the postnatal period at TDI dose, without any alteration in body growth. This shows that developmental exposure to BPA at reference doses did not masculinize and defeminize the neural circuitry underlying sexual behavior in female mice. The TDI dose specifically exacerbated responses normally induced by ovarian E 2 , through estrogen receptor a, during the postnatal/prepubertal period.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Naulé¹,

Picot²,

Martini³

et al. 2014

Journal of Endocrinology

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“…When treatment starts postnatally after 15 days, age at VO is not affected (Nikaido et al, 2005;Laws et al, 2000). During the age window comprised between birth and 15 days, age at VO is either not affected (Nagao et al, 1999;Adewale et al, 2009;Losa-Ward et al, 2012;Yu et al, 2010) or early (Adewale et al, 2009;Losa-Ward et al, 2012;Fernandez et al, 2009;Nah et al, 2011). A dose of 50 µg/kg causes advancement of puberty while 50 mg/kg has no effect, indicating a non-linear doseresponse relationship (Adewale et al, 2009;Losa-Ward et al, 2012).…”

Section: Female Rodentmentioning

confidence: 99%

Developmental variations in environmental influences including endocrine disruptors on pubertal timing and neuroendocrine control: Revision of human observations and mechanistic insight from rodents

Parent

Franssen

Fudvoye

et al. 2015

Frontiers in Neuroendocrinology

156

140

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Puberty presents remarkable individual differences in timing reaching over 5 years in humans. We put emphasis on the two edges of the age distribution of pubertal signs in humans and point to an extended distribution towards earliness for initial pubertal stages and towards lateness for final pubertal stages. Such distortion of distribution is a recent phenomenon. This suggests changing environmental influences including the possible role of nutrition, stress and endocrine disruptors. Our ability to assess neuroendocrine effects and mechanisms is very limited in humans. Using the rodent as a model, we examine the impact of environmental factors on the individual variations in pubertal timing and the possible underlying mechanisms. The capacity of environmental factors to shape functioning of the neuroendocrine system is thought to be maximal during fetal and early postnatal life and possibly less important when approaching the time of onset of puberty.

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“…The role of BPA in the canonical apoptotic pathways has been inadequately appraised and there is limited data associating its role in mitochondrial cell death of T cell lines [19] and germ cells after UV irradiation and hydroquinone treatment [20]. Moreover, epidemiological and genetic studies have shown that BPA is an environmental estrogenic compound that can exert proliferative responses and more specifically may induce hormonal--related effects [15, 20--26].…”

Section: Introductionmentioning

confidence: 99%

BPA qualtitative and quantitative assessment associated with orthodontic bonding in vivo

et al. 2015

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OBJECTIVE: To assess the in vivo amount of BPA released from a visible light-cured orthodontic adhesive, immediately after bracket bonding. METHODS: 20 orthodontic patients were recruited after obtaining informed consent. All patients received 24 orthodontic brackets in both dental arches. In Group A (11 patients), 25 ml of tap water were used for mouth rinsing, whereas in Group B (9 patients) a simulated mouth rinse formulation was used: a mixture of 20 ml de-ionized water plus 5 ml absolute ethanol. Rinsing solutions were collected before, immediately after placing the orthodontic appliances and after washing out the oral cavity and were then stored in glass tubes. Rinsing was performed in a single phase for 60s with the entire volume of each liquid. The BPA analysis was performed by gas chromatography-mass spectrometry. RESULTS: An increase in BPA concentration immediately after the 1st post-bonding rinse was observed, for both rinsing media, which was reduced after the 2nd postbonding rinse. Water exhibited higher levels of BPA concentration than water/ethanol after 1st and 2nd post-bonding rinses. Two-way mixed Repeated Measures ANOVA showed that the primary null hypothesis declaring mean BPA concentration to be equal across rinsing medium and rinsing status was rejected (p-value <0.001). The main effects of the rinsing medium and status, as well as their interaction were found to be statistically significant (p-values 0.048, <0.001 and 0.011 respectively). SIGNIFICANCE: A significant pattern of increase of BPA concentration, followed by a decrease that reached the initial values was observed. The amount of BPA was relatively low and far below the reference limits of tolerable daily intake. Methods: 20 volunteers were recruited after obtaining informed consent. All patients received 24 orthodontic brackets in both dental arches. In Group A (11 patients), 25 ml of tap water were used for mouth rinsing, whereas in Group B (9 patients) a simulated mouth rinse formulation was used: a mixture of 20 ml de--ionized water plus 5 ml absolute ethanol. Rinsing solutions were collected before, immediately after placing the orthodontic appliances and after washing out the oral cavity and were then stored in glass tubes. Rinsing was performed in a single phase for 60 seconds with the entire volume of each liquid. The BPA analysis was performed by gas chromatography--mass spectrometry.Results: An increase in BPA concentration immediately after the 1 st post--bonding rinse was observed, for both rinsing media, which was reduced after the 2 nd post--bonding rinse. Water exhibited higher levels of BPA concentration than water/ethanol after 1st and 2nd post--bonding rinses. Two--way mixed Repeated Measures ANOVA showed that the primary null hypothesis declaring mean BPA concentration to be equal across rinsing medium and rinsing status was rejected (p--value < 0.001). The main effects of the rinsing medium and status, as well as their interaction were found to be statistically significant (p--values 0.048, <0.001 an...

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Effects of early prepubertal exposure to bisphenol A on the onset of puberty, ovarian weights, and estrous cycle in female mice

Cited by 110 publications

References 54 publications

Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Neuroendocrine and behavioral effects of maternal exposure to oral bisphenol A in female mice

Developmental variations in environmental influences including endocrine disruptors on pubertal timing and neuroendocrine control: Revision of human observations and mechanistic insight from rodents

BPA qualtitative and quantitative assessment associated with orthodontic bonding in vivo

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