Low dose effect of in utero exposure to bisphenol A and diethylstilbestrol on female mouse reproduction

Honma, Shizuka; Suzuki, Atsushi; Buchanan, David L.; Katsu, Yoshinao; Watanabe, Hidenobu; Iguchi, Taisen

doi:10.1016/s0890-6238(02)00006-0

Cited by 267 publications

(170 citation statements)

References 29 publications

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“…It was also demonstrated that low-dose BPA increased AGD after birth in CD-1 mice 16) and ICR mice 17) . The discrepancy between their studies and ours could be due to differences in the route and doses of chemicals, and animal species.…”

mentioning

confidence: 87%

Effects of in Utero and Lactational Exposure to Bisphenol A on Somatic Growth and Anogenital Distance in F1 Rat Offspring.

Kobayashi¹,

Miyagawa²,

Wang³

et al. 2002

INDUSTRIAL HEALTH

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Bisphenol A (BPA), a xenoestrogen, has been reported to mimic the actions of estrogen or to affect the endocrine glands in vivo and in vitro. In this study, we examined whether in utero and lactational exposure to BPA altered the somatic growth and anogenital distance (AGD) of F 1 offspring (1, 3, and 9 weeks of age) in vivo in rats. Dams were orally administered with various doses of BPA (0, 4, or 40 mg/kg body weight (BW)/day) from gestation day (GD) 6 through postnatal day (PND) 20. There were no significant changes in body weight, liver weight, kidneys weight, testes weight, AGD, the ratio of AGD to BW, or the ratio of AGD to the cube root of BW in BPA exposed pups compared to the vehicle-exposed control. This suggests that prenatal and postnatal exposure (indirect exposure) to BPA (4-40 mg/kg/day, GD 6-PND 20) does not affect on somatic growth or AGD of F 1 generation of male and female rats.

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mentioning

confidence: 87%

Effects of in Utero and Lactational Exposure to Bisphenol A on Somatic Growth and Anogenital Distance in F1 Rat Offspring.

Kobayashi¹,

Miyagawa²,

Wang³

et al. 2002

INDUSTRIAL HEALTH

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“…When the animals are exposed to BPA during pregnancy only, age at VO is either not affected (Tinwell et al, 2002;Murray et al, 2007;Howdeshell et al, 1999) or early (Honma et al, 2002;Nikaido et al, 2004), the latter authors restricting treatment to late gestation only. When treatment starts postnatally after 15 days, age at VO is not affected (Nikaido et al, 2005;Laws et al, 2000).…”

Section: Female Rodentmentioning

confidence: 99%

“…In the vast majority of studies, prenatal or early postnatal exposure to DES is followed by early VO (Honma et al, 2002;Nikaido et al, 2004;Maranghi et al, 2008;Rothschild et al, 1988;Burroughs et al, 1985;Willoughby et al, 2005). This possibly results from premature hypothalamic-pituitary maturation because DES is not present at the time of VO anymore.…”

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

157

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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“…Honma et al (2002), supported by the Japanese Ministry of Education, Culture, Sports, Sciences, and Table 79. There were no effects on gestation duration, number of pups/litter, or sex ratio.…”

Section: [No Additional Information Was Provided For Statistical Analmentioning

confidence: 99%

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

402

304

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Low dose effect of in utero exposure to bisphenol A and diethylstilbestrol on female mouse reproduction

Cited by 267 publications

References 29 publications

Effects of in Utero and Lactational Exposure to Bisphenol A on Somatic Growth and Anogenital Distance in F1 Rat Offspring.

Effects of in Utero and Lactational Exposure to Bisphenol A on Somatic Growth and Anogenital Distance in F1 Rat Offspring.

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

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

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