Effects of perinatal di (2-ethylhexyl) phthalate exposure on thyroid function in rat offspring

Dong, Jing; Cong, Zhangzhao; You, Mingdan; Fu, Yuanyuan; Wang, Yi; Wang, Yuan; Fu, Hui; Wei, Lingling; Chen, Jie

doi:10.1016/j.etap.2019.01.012

Cited by 40 publications

(27 citation statements)

References 68 publications

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“…Similarly ADHD cases showed higher urinary MnBP levels among boys [44]. The study of prenatal exposure found that the sum of DEHP metabolites was associated with a monotonically increasing risk of ADHD [67]. From the case-control studies, an association between both prenatal and current exposure to DEHP and ADHD was suggested.…”

Section: Phthalates and Neurodevelopmentmentioning

confidence: 99%

“…Three case-control studies investigated associations with doctor-diagnosed ADHD and found that ADHD was associated with both prenatal and current phthalate exposure [44,[65][66][67]. Higher urinary concentrations of DEHP metabolites, including mono(2ethyl-5-hydroxyhexyl) phthalate (MEHHP), mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono-(2-ethyl)-hexyl phthalate (MEHP), were dose-dependently associated with ADHD [66].…”

Section: Phthalates and Neurodevelopmentmentioning

confidence: 99%

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A Review of Recent Studies on Bisphenol A and Phthalate Exposures and Child Neurodevelopment

Minatoya

Kishi

2021

IJERPH

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Purpose of Review: Bisphenol A and phthalate have been found in the environment, as well as in humans. In this narrative review pre- and postnatal bisphenol A and phthalate exposures, their relationship to neurodevelopment, and the behavioral outcomes of children are elucidated, focusing in particular on the recent case-control, cross-sectional, and longitudinal studies. This review also introduces some of the possible mechanisms behind the observed associations between exposures and outcomes. Recent Findings: Although bisphenol A and phthalate exposure have been reported to influence neurobehavioral development in children, there are various kinds of test batteries for child neurodevelopmental assessment at different ages whose findings have been inconsistent among studies. In addition, the timing and number of exposure assessments have varied. Summary: Overall, this review suggests that prenatal exposure to bisphenol A and phthalates may contribute to neurobehavioral outcomes in children. The evidence is still limited; however, Attention Deficit Hyperactivity Disorder (ADHD) symptoms, especially among boys, constantly suggested association with both prenatal and concurrent exposure to bisphenol A. Although there is limited evidence on the adverse effects of prenatal and postnatal bisphenol A and phthalate exposures provided, pregnant women and young children should be protected from exposure based on a precautionary approach.

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Section: Phthalates and Neurodevelopmentmentioning

confidence: 99%

Section: Phthalates and Neurodevelopmentmentioning

confidence: 99%

A Review of Recent Studies on Bisphenol A and Phthalate Exposures and Child Neurodevelopment

Minatoya

Kishi

2021

IJERPH

View full text Add to dashboard Cite

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“…In contrast to rodents, attributable risk of effects related to PPARα activation is considered to be low in human. Additionally, it is reported that DEHP has a potential to cause the fluctuation of mRNA expressions of Type 1, 2 and 3 iodothyronine deiodinase (D1, D2 and D3) in liver, and the reduction of gene/protein levels of transthyretin (TTR) and thyroperoxidase (TPO), sodium iodide symporter (NIS) in serum (Liu et al, 2015;Dong et al, 2019). Therefore, thyroid effects by DEHP exposure may originate in the combined effects on metabolism, biosynthesis, biotransformation and biotransport of thyroid hormones.…”

Section: A B C D E Fmentioning

confidence: 99%

The effects on the endocrine system under hepatotoxicity induction by phenobarbital and di(2-ethylhexyl)phthalate in intact juvenile male rats

et al. 2019

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Phenobarbital (PB) and Di (2-ethylhexyl) phthalate (DEHP), an anti-epileptic drug and a plasticizer used in flexible polyvinylchloride formulations, respectively, are well-known typical hepatotoxicants. This study investigated the effects of PB (100 mg/kg/day) or DEHP (500 mg/kg/day) on the endocrine system in intact juvenile/peripubertal male rats exposed for 31 days beginning on postnatal day 23. Slight hormone level changes, histopathological changes in thyroid gland or induction of UDPglucuronosyltransferase in liver were observed in both the PB and DEHP groups. One of the assumed mechanisms inducing thyroid effects is predictable to be secondary changes based on the enhancement in thyroid hormone metabolism via the induction of hepatic microsomal enzymes. No reproductive systemrelated changes in organ weights, histopathology, and sexual maturation were observed in both groups. Lower testosterone level was observed in the PB group. CYP2B and CYP3A, which are involved in testosterone metabolism, were induced in liver of the PB group. There was no change of 17β-hydroxysteroid dehydrogenase activity in testis of both groups. Lower testosterone level in the PB-treated male rats was attributed to an indirect, hepatotoxicity-associated effect on the reproductive system and not to direct effects on testis such as the antiandrogenic activity and the inhibition of steroidogenesis. These results did not indicate that PB or DEHP exposure affects the endocrine system directly.

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“…Type 2 diabetes mellitus (T2DM) and obesity arise at the interface of genetics and environmental factors, including physical inactivity, smoking and nutrition intake. Interestingly, a large number of human studies and experimental animal models demonstrated that adverse environmental exposures experienced by their parents during intrauterine or early postnatal life significantly influenced health of the next generations (Dong et al, 2019; Lund et al, 2019; Zhang et al, 2019). More specifically, poor early-life exposures robustly increased the risks of developing chronic metabolic diseases in adult life, including glucose intolerance, T2DM and obesity (Csongova et al, 2018; Kearney et al, 2018; Wen et al, 2018; Yu et al, 2018; Chang et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Maternal Genistein Intake Mitigates the Deleterious Effects of High-Fat Diet on Glucose and Lipid Metabolism and Modulates Gut Microbiota in Adult Life of Male Mice

et al. 2019

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Adverse early-life exposures program increased risk of chronic metabolic diseases in adulthood. However, the effects of genistein supplementation in early life on metabolic health in later life are largely unclear. Our objective was to investigate whether maternal genistein intake could mitigate the deleterious influence of a maternal high-fat diet on glucose and lipid metabolism in offspring and to explore the role of gut microbiota in mediating the transgenerational effects. C57BL/6 female mice were fed either a high-fat diet (HF), high-fat diet with genistein (0.6 g /kg diet) (HFG) or normal control diet (C) for 3 weeks before pregnancy and throughout pregnancy and lactation. The male offspring had ad libitum access to normal chow diet from weaning to 24 weeks of age. Then the content of inguinal subcutaneous adipose tissue (SAT) and epididymal visceral adipose tissue (VAT) were weighed. Glucose tolerance test (GTT), the level of serum insulin and lipid profiles were analyzed. The caecal contents were collected for 16S rDNA sequencing. The results showed that maternal genistein intake could significantly reduce blood glucose levels during GTT, fasting insulin levels, VAT mass and serum triglyceride levels as well as increase high-density lipoprotein cholesterol in adult male offspring. Significant decrease of germs from the Tenericutes phylum and enrichment of Rikenella as well as SCFA (short-chain fatty acid)-producing bacteria, including Alloprevotella, Odoribacter , and Clostridium XlVa , in offspring of genistein fed dams might play crucial roles in the improvement of glucose and lipid metabolism. Overall, early-life genistein intake attenuated the harmful effects of maternal HF on metabolism in adult offspring and the protective effects were associated with the alterations in gut microbiota, which provides new evidence and targets for mitigate the poor effects of adverse early-life exposures on metabolic health in later life.

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Effects of perinatal di (2-ethylhexyl) phthalate exposure on thyroid function in rat offspring

Cited by 40 publications

References 68 publications

A Review of Recent Studies on Bisphenol A and Phthalate Exposures and Child Neurodevelopment

A Review of Recent Studies on Bisphenol A and Phthalate Exposures and Child Neurodevelopment

The effects on the endocrine system under hepatotoxicity induction by phenobarbital and di(2-ethylhexyl)phthalate in intact juvenile male rats

Maternal Genistein Intake Mitigates the Deleterious Effects of High-Fat Diet on Glucose and Lipid Metabolism and Modulates Gut Microbiota in Adult Life of Male Mice

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