Effects of bisphenol-A (BPA), dibutylphtalate (DBP), benzophenone-2 (BP2), procymidone (Proc), and linurone (Lin) on fat tissue, a variety of hormones and metabolic parameters: A 3 months comparison with effects of estradiol (E2) in ovariectomized (ovx) rats

Seidlová-Wuttke, Dana; Jarry, Hubertus; Christoffel, Julie; Rimoldi, Guillermo; Wuttke, W.

doi:10.1016/j.tox.2005.05.001

Cited by 82 publications

(49 citation statements)

References 53 publications

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“…Dodge et al 29) reported that the 4-day oral administration of BPA (0.1, 1.0 or 10 mg/ kg body weight/day) to ovariectomized rats (6 months old) did not change the serum TC level, but BPA at the highest dose (30 mg/kg body weight/day) decreased it. Seidlová-Wuttke et al 14) reported that the 3-month administration of pellet food containing BPA (0.033 or 0.333 mg/kg body weight/day) to ovariectomized rats (3 months old) did not change serum TC and TG levels. We recently observed that the 30-day administration of a 30% fat diet containing BPA (approximately 0.19 or 18.9 mg/kg body weight/day) to male ICR mice (4 weeks old) did not cause any changes in serum TC and TG levels (H Masuno -unpublished data).…”

Section: Discussionmentioning

confidence: 99%

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Perinatal and Postnatal Exposure to Bisphenol A Increases Adipose Tissue Mass and Serum Cholesterol Level in Mice

Miyawaki

Sakayama

Kobayashi

et al. 2007

JAT

248

158

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Aim: To investigate whether the perinatal and postnatal exposure of mice to bisphenol A (BPA) caused the development of obesity and/or hyperlipidemia. Methods: Pregnant mice were exposed to BPA in drinking water at concentrations of either 1 g/mL (LD group) or 10 g/mL (HD group) from gestation day 10 and throughout the lactating period. After weaning, the pups were allowed free access to drinking water containing the appropriate concentrations of BPA. The body weight, adipose tissue weight, and serum lipid levels were measured in the offspring at postnatal day 31.

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Section: Discussionmentioning

confidence: 99%

“…To date, however, whether this increase in body weight resulted from an increase in the adipose tissue mass remains unclear. Seidlová-Wuttke et al 14) reported that the exposure of ovariectomized rats to BPA did not cause an increase in paratibial fat storage.…”

Section: Introductionmentioning

confidence: 99%

Perinatal and Postnatal Exposure to Bisphenol A Increases Adipose Tissue Mass and Serum Cholesterol Level in Mice

Miyawaki

Sakayama

Kobayashi

et al. 2007

JAT

248

158

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show abstract

“…Cyr et al 1988, Mercure et al 2001, Qu et al 2001, McCormick et al 2005, although responses were highly variable between studies. In rat, E 2 also decreased serum T 3 (but not T 4 ) levels (probably through an inhibitory effect of E 2 on deiodinase conversion of bioinactive T 4 to bioactive T 3 ), and may influence the hypothalamic/pituitary setpoint for the negative feedback effect of thyroid hormone on thyroid stimulating hormone secretion (Schmutzler et al 2004, Seidlova-Wuttke et al 2005. There is also evidence from salmonids that, through contrasting effects at multiple sites on the hypothalamus-pituitary-interrenal axis, E 2 regulates F production from the fish interrenal.…”

Section: Discussionmentioning

confidence: 99%

Multiple molecular effect pathways of an environmental oestrogen in fish

Filby¹,

Thorpe²,

Tyler³

2006

Journal of Molecular Endocrinology

130

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Complex interrelationships in the signalling of oestrogenic effects mean that environmental oestrogens present in the aquatic environment have the potential to disrupt physiological function in fish in a more complex manner than portrayed in the present literature. Taking a broader approach to investigate the possible effect pathways and the likely consequences of environmental oestrogen exposure in fish, the effects of 17b-oestradiol (E 2 ) were studied on the expression of a suite of genes which interact to mediate growth, development and thyroid and interrenal function (growth hormone GH (gh), GH receptor (ghr ), insulin-like growth factor (IGF-I) (igf1), IGF-I receptor (igf1r ), thyroid hormone receptors-a (thra) and -b (thrb) and glucocorticoid receptor (gr )) together with the expression analyses of sex-steroid receptors and ten other genes centrally involved in sexual development and reproduction in fathead minnow (fhm; Pimephales promelas). Exposure of adult fhm to 35 ng E 2 /l for 14 days induced classic oestrogen biomarker responses (hepatic oestrogen receptor 1 and plasma vitellogenin), and impacted on the reproductive axis, feminising 'male' steroidogenic enzyme expression profiles and suppressing genes involved in testis differentiation. However, E 2 also triggered a cascade of responses for gh, ghr, igf1, igf1r, thra, thrb and gr in the pituitary, brain, liver, gonad and gill, with potential consequences for the functioning of many physiological processes, not just reproduction. Molecular responses to E 2 were complex, with most genes showing differential responses between tissues and sexes. For example, igf1 expression increased in brain but decreased in gill on exposure to E 2 , and responded in an opposite way in males compared with females in liver, gonad and pituitary. These findings demonstrate the importance of developing a deeper understanding of the endocrine interactions for unravelling the mechanisms of environmental oestrogen action and predicting the likely health consequences.

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“…These results suggest that TBBPA may not bind or limitation of bind to ERα. BBP and BPA were well known as ERα bounded weak agonists (Soto et al, 1995;Miller et al, 2001) while DBP was known that it did not bind to recombinant human ERα protein (Seidlová -Wuttke et al, 2005;Kolle et al, 2010). Additionally, the difference of ranking order for BPA and NP was resulted in the assay principle between transcriptional assay and binding affinity.…”

Section: Estrogenic Activities Of Phthalates and Alkylphenolsmentioning

confidence: 99%

Evaluation of <i>in vitro</i> screening system for estrogenicity: comparison of stably transfected human estrogen receptor-α transcriptional activation (OECD TG455) assay and estrogen receptor (ER) binding assay

Lee

Kim

et al. 2012

J. Toxicol. Sci.

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-The estrogenic activity of industrial chemicals, di(2-ethylhexyl) phthalate (DEHP), di(n-butyl) phthalate (DBP), benzylbutyl phthalate (BBP), diethyl phthalate (DEP), tetrabromobisphenol A (TBBPA), bisphenol A (BPA), and nonylphenol (NP), was compared using OECD test guideline 455(TG455), stably transfected transcriptional activation (STTA) and estrogen receptor (ER) binding assays. The estrogenic activity of BBP, BPA and NP were approximately 180,000-fold (PC 50 , 4.32 x 10 -6 M), 5,000-fold (PC 50 , 1.26 x 10 -7 M) and 120,000-fold (PC 50 , 2.92 x 10 -6 M) less than 17β-estradiol (PC 50 , 2.43 x 10 -11 M), whereas DEHP, DBP and DEP did not show any estrogenicity activity in the STTA assay. Moreover, binding affinities to human ERα of BBP, BPA, and NP were approximately 200,000-fold (IC 50 , 4.91 x 10 -4 M), 8000-fold (IC 50 , 1.92 x 10 -5 M) and 1400-fold (IC 50 , 3.34 x 10 -6 M) less than 17β-estradiol (IC 50 , 2.45 x 10 -9 M) in competitive human ERα binding assay. The relative potencies of STTA assay were very similar to ER binding, E-screen, and Yeast screening assays. Therefore, our results suggested that OECD test guideline TG455 may be useful as a screening test for potential endocrine disruptors.

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Effects of bisphenol-A (BPA), dibutylphtalate (DBP), benzophenone-2 (BP2), procymidone (Proc), and linurone (Lin) on fat tissue, a variety of hormones and metabolic parameters: A 3 months comparison with effects of estradiol (E2) in ovariectomized (ovx) rats

Cited by 82 publications

References 53 publications

Perinatal and Postnatal Exposure to Bisphenol A Increases Adipose Tissue Mass and Serum Cholesterol Level in Mice

Perinatal and Postnatal Exposure to Bisphenol A Increases Adipose Tissue Mass and Serum Cholesterol Level in Mice

Multiple molecular effect pathways of an environmental oestrogen in fish

Evaluation of <i>in vitro</i> screening system for estrogenicity: comparison of stably transfected human estrogen receptor-α transcriptional activation (OECD TG455) assay and estrogen receptor (ER) binding assay

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