Effects of in Utero and Lactational Exposure to Bisphenol A on Thyroid Status in F1 Rat Offspring

Kobayashi, Kenichi; Miyagawa, Munéyuki; Wang, Rui-Sheng; Suda, Megumi; Sekiguchi, Soichiro; Honma, Takeshi

doi:10.2486/indhealth.43.685

Cited by 25 publications

(17 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This paper deals with a portion of a comprehensive study of PCB153 effects including neurochemistry, laboratory animal ethology, and endocrinology. Similar experiments were performed previously using bisphenol A in our laboratory, and those experiments have been published in part 13,14) .…”

supporting

confidence: 62%

Alteration of Brain Neurotransmitters in Female Rat Offspring Induced by Prenatal Administration of 16 and 64 mg/kg of 2,2',4,4',5,5'-hexachlorobiphenyl (PCB153)

et al. 2009

Self Cite

View full text Add to dashboard Cite

supporting

confidence: 62%

Alteration of Brain Neurotransmitters in Female Rat Offspring Induced by Prenatal Administration of 16 and 64 mg/kg of 2,2',4,4',5,5'-hexachlorobiphenyl (PCB153)

et al. 2009

Self Cite

View full text Add to dashboard Cite

“…The findings indicated that BPA antagonized TRβ, which mediates the negativefeedback effect of TH on the pituitary gland, but is less effective at blocking TRα, allowing TRα-mediated events to respond to elevated levels of thyroxine. However, Kobayashi et al (2005) observed that BPA did not affect thyroid functions in the first filial generation of male and female rats after in utero and lactational exposure to BPA (at 4-40 mg/kg/d).…”

Section: Effects On Thyroid Hormone (Th)smentioning

confidence: 79%

Neurotoxicity of Endocrine Disruptors: Possible Involvement in Brain Development and Neurodegeneration

Masuo

Ishido

2011

Journal of Toxicology and Environmental Health, Part B

107

View full text Add to dashboard Cite

Environmental chemicals that act as endocrine disruptors do not appear to pose a risk to human reproduction; however, their effects on the central nervous systems are less well understood. Animal studies suggested that maternal exposure to endocrine-disrupting chemicals (EDC) produced changes in rearing behavior, locomotion, anxiety, and learning/memory in offspring, as well as neuronal abnormalities. Some investigations suggested that EDC exert effects on central monoaminergic neurons, especially dopaminergic neurons. Our data demonstrated that EDC attenuate the development of dopaminergic neurons, which might be involved in developmental disorders. Perinatal exposure to EDC might affect neuronal plasticity in the hippocampus, thereby potentially modulating neuronal development, leading to impaired cognitive and memory functions. Endocrine disruptors also attenuate gender differences in brain development. For example, the locus ceruleus is larger in female rats than in males, but treatments with bisphenol-A (BPA) enlarge this region in males. Some reports indicated that EDC induce hypothyroidism, which might be evidenced as abnormal brain development. Endocrine disruptors might also affect mature neurons, resulting in neurodegenerative disorders such as Parkinson's disease. The current review focused on alterations in the brain induced by EDC, specifically on the possible involvement of EDC in brain development and neurodegeneration.

show abstract

“…We speculate that such differences, if further elucidated, may extend to the female fetal thyroid and account for sexually dimorphic sensitivity of the thyroid to environmental chemicals. However, rodent studies specifically assessing the effect of prenatal BPA exposure on thyroid hormones have been inconsistent, with one study suggesting that BPA affects thyroid hormones among male pups only (Xu et al, 2007), another reporting similar thyroid hormone responses to BPA in both male and female pups (Zoeller et al, 2005), and another observing no effect of BPA on thyroid function for male or female pups (Kobayashi et al, 2005). …”

Section: Discussionmentioning

confidence: 99%

Gestational urinary bisphenol A and maternal and newborn thyroid hormone concentrations: The HOME Study

Romano

Webster

Vuong

et al. 2015

Environmental Research

111

View full text Add to dashboard Cite

Bisphenol A (BPA), an endocrine disruptor used in consumer products, may perturb thyroid function. Prenatal BPA exposure may have sex-specific effects on thyroid hormones (THs). Our objectives were to investigate whether maternal urinary BPA concentrations during pregnancy were associated with THs in maternal or cord serum, and whether these associations differed by newborn sex or maternal iodine status. We measured urinary BPA concentrations at 16 and 26 weeks gestation among pregnant women in the HOME Study (2003–2006, Cincinnati, Ohio). Thyroid stimulating hormone (TSH) and free and total thyroxine (T4) and triiodothyronine (T3) were measured in maternal serum at 16 weeks (n=181) and cord serum at delivery (n=249). Associations between BPA concentrations and maternal or cord serum TH levels were estimated by multivariable linear regression. Mean maternal urinary BPA was not associated with cord THs in all newborns, but a 10-fold increase in mean BPA was associated with lower cord TSH in girls (percent change= −36.0%; 95% confidence interval (CI): −58.4, −1.7%), but not boys (7.8%; 95% CI: −28.5, 62.7%; p-for-effect modification=0.09). We observed no significant associations between 16-week BPA and THs in maternal or cord serum, but 26-week maternal BPA was inversely associated with TSH in girls (−42.9%; 95% CI: −59.9, −18.5%), but not boys (7.6%; 95% CI: −17.3, 40.2%; p-for-effect modification=0.005) at birth. The inverse BPA-TSH relation among girls was stronger, but less precise, among iodine deficient versus sufficient mothers. Prenatal BPA exposure may reduce TSH among newborn girls, particularly when exposure occurs later in gestation.

show abstract

Effects of in Utero and Lactational Exposure to Bisphenol A on Thyroid Status in F1 Rat Offspring

Cited by 25 publications

References 27 publications

Alteration of Brain Neurotransmitters in Female Rat Offspring Induced by Prenatal Administration of 16 and 64 mg/kg of 2,2',4,4',5,5'-hexachlorobiphenyl (PCB153)

Alteration of Brain Neurotransmitters in Female Rat Offspring Induced by Prenatal Administration of 16 and 64 mg/kg of 2,2',4,4',5,5'-hexachlorobiphenyl (PCB153)

Neurotoxicity of Endocrine Disruptors: Possible Involvement in Brain Development and Neurodegeneration

Gestational urinary bisphenol A and maternal and newborn thyroid hormone concentrations: The HOME Study

Contact Info

Product

Resources

About