Thyroid disruption by technical decabromodiphenyl ether (DE-83R) at low concentrations in Xenopus laevis

Qin, Xuda; Xia, Xuewei; Yang, Zhongan; Yan, Shi-Shuai; Zhao, Yaxian; Wei, Rongguo; Li, Yan; Tian, Ming; Zhao, Xingru; Qin, Zhan-Fen; Xu, Xing

doi:10.1016/s1001-0742(09)60172-8

Cited by 17 publications

(7 citation statements)

References 36 publications

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“…In the amphibian Xenopus laevis , exposure of tadpoles to the technical decabromodiphenyl ether mixture DE-83R (containing 96 to 99% BDE-209, as well as other PBDEs) in water, from stage 46/47 (free swimming larvae) to stage 62, at the concentrations of 1 to 1000 ng/L, did not cause any malformation or abnormal behavior. However, histological alterations of follicular epithelial cells were found at 100 and 1000 ng/L, with a decrease in thyroid receptor (TR βA) mRNA levels observed at all DE-83R concentrations (Qin et al 2010). …”

Section: Evidence Of Developmental Neurotoxicity Of Bde-209mentioning

confidence: 99%

Is decabromodiphenyl ether (BDE-209) a developmental neurotoxicant?

2011

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Polybrominated diphenyl ether (PBDE) flame retardants have become ubiquitous environmental pollutants. The relatively higher body burden in toddlers and children has reaised concern for their potential developmental neurotoxicity, which has been suggested by animal studies, in vitro experiments, and recent human epidemiological evidence. While lower brominated PBDEs have been banned in several countries, the fully brominated decaBDE (BDE-209) is still utilized, though manufacturers will discontinue production in the U.S.A. in 2013. The recent decision by the U.S. Environmental Protection Agency to base the Reference Dose (RfD) for BDE-209 on a developmental neurotoxicity study has generated some controversy. Because of its bulky configuration, BDE-209 is poorly absorbed and does not easily penetrate the cell wall. Its acute and chronic toxicities are relatively low, with the liver and the thyroid as the primary targets, though there is some evidence of carcinogenicity. A few animal studies have indicated that BDE-209 may cause developmental neurotoxicity, affecting motor and cognitive domains, as seen for other PBDEs. Limited in vivo and in vitro studies have also evidenced effects of BDE-209 on thyroid hormone homeostasis and direct effects on nervous cells, again similar to what found with other lower brominated PBDEs. In contrast, a recent developmental neurotoxicity study, carried out according to international guidelines, has provided no evidence of adverse effects on neurodevelopment, and this should be considered in a future re-evaluation of BDE-209. While estimated exposure to BDE-209 in children is believed to be several orders of magnitude below the most conservative RfD proposed by the USEPA, questions remain on the extent and relevance of BDE-209 metabolism to lower brominated PBDEs in the environment and in humans.

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Section: Evidence Of Developmental Neurotoxicity Of Bde-209mentioning

confidence: 99%

Is decabromodiphenyl ether (BDE-209) a developmental neurotoxicant?

2011

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“…Exposure of tadpoles to chemicals Following the method described by Qin et al (2010), exposure experiment was conducted as follows. On the sixth day of the post-fertilization period, healthy tadpoles at NF stage 46/47 (system of Nieuwkoop and Faber 1956) were randomly selected from a pair of parental frogs' offspring for the exposure experiment.…”

Section: Breeding and Housingmentioning

confidence: 99%

“…The time to forelimb emergence (FLE), thyroid histology and mRNA expressions of HPT axis relevant genes were measured as endpoints (Qin et al 2010;Opitz et al 2006a, b), to assess thyroid disruption by PFOS.…”

Section: Introductionmentioning

confidence: 99%

Thyroid disruption effects of environmental level perfluorooctane sulfonates (PFOS) in Xenopus laevis

et al. 2011

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Perfluorooctane sulfonate (PFOS), one of the emerging persistent organic pollutants (POPs), has caused growing international concern especially related to the potential disruption in the development and function of thyroid system. Xenopus laevis is an amphibian species widely used as a suitable amphibian model for thyroid disruption research. To study the thyroid disruption effects related to PFOS exposure at environmental low levels, X. laevis tadpoles were exposed to 0.1, 1, 10 and 100 μg/l PFOS in water respectively from stage 46/47 to stage 62. The results showed that the time to metamorphosis (presented by forelimb emergence, FLE) did not significantly change with PFOS exposure, but exhibited an increasing trend (except for 10 μg/l exposure). Partial colloid depletion was observed for PFOS exposure, but no significant histological abnormality was observed in treatment groups. In addition, PFOS exposure resulted in up-regulation of thyroid hormone-regulated genes-thyroid receptor beta A (TRβA), basic transcription element-binding protein (BTEB) and type II deiodinase (DI2) mRNA expression, presented as an inverted U-shaped dose response pattern. However, the mRNA expression of type III deiodinase (DI3) remained unaffected compared with the control. These results demonstrated that PFOS might disrupt the thyroid system in X. laevis tadpoles regarding FLE changes and regulation alternation of thyroid hormone-regulated genes. Our study has raised new concerns for possible thyroid disruption of PFOS in amphibians at environmental relevant levels.

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“…[31] Histological structures of thyroid gland can be induced by various chemicals, such as acetochlor [32] and decabromodiphenyl ethre (De-83R). [33] Usually, pathologic changes in thyroid gland were characterised by reduced colloid, glandular hypertrophy and cellular hyperplasia and hypertrophy. [34] However, in the present study, there were no pathologic changes in thyroid gland in tadpoles exposed to copper.…”

Section: Discussionmentioning

confidence: 99%

Chronic exposure effects of copper on growth, metamorphosis and thyroid gland, liver health in Chinese toad,Bufo gargarizanstadpoles

Chai¹,

Wang²,

Deng³

et al. 2014

Chemistry and Ecology

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The impact of copper exposure on Chinese toad (Bufo gargarizans) tadpoles was investigated in this study. First, the 96h LC50 value of copper was 8.697 μM, by means of a 4 d acute toxicity test. Second, we studied the chronic effects of copper on B. gargarizans tadpoles at control, 0.025, 0.1 and 1.0 μM concentration. Survival, body length, body weight, developmental stage, incidence of metamorphic climax, and size at metamorphic climax were determined. In tadpoles developed to metamorphic climax (stage G42), liver and thyroid gland were assessed histologically. Copper at 0.1 and 1.0 μM could inhibit tadpole growth and prolong tadpole metamorphic progress relative to controls. Tadpole size (total length and weight) at stage G42 is also affected in the 0.1 and 1.0 μM treatments. In addition, histological examinations have revealed that 1.0 μM copper could cause significant pathological changes and hepatocytes degeneration in liver. Furthermore, histomorphological measurements indicated that copper at 0.1 and 1.0 μM reduced thyroid gland size, diameter and number of follicle. In conclusion, our study suggests that Cu could damage the liver and thyroid gland, so growth and metamorphosis of B. gargarizans tadpoles were inhibited resulted of disrupting liver metabolism and THs homeostasis.

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Thyroid disruption by technical decabromodiphenyl ether (DE-83R) at low concentrations in Xenopus laevis

Cited by 17 publications

References 36 publications

Is decabromodiphenyl ether (BDE-209) a developmental neurotoxicant?

Is decabromodiphenyl ether (BDE-209) a developmental neurotoxicant?

Thyroid disruption effects of environmental level perfluorooctane sulfonates (PFOS) in Xenopus laevis

Chronic exposure effects of copper on growth, metamorphosis and thyroid gland, liver health in Chinese toad,Bufo gargarizanstadpoles

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