Developmental neurotoxicity of polybrominated diphenyl ethers mixture de71 in Sprague-Dawley rats

Gill, Santokh; Hou, Yang-Xun; Li, Nanqin; Pulido, Olga; Bowers, Wayne J.

doi:10.1080/15287394.2016.1182001

Cited by 17 publications

(15 citation statements)

References 68 publications

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“…However, BDE congeners are still widely used as flame retardant in many household materials in countries where no apparent legislation exists . There have been a growing number of investigations regarding the neurotoxic potential of these congeners (Chen et al 2010;Giordano 2007, 2011;Goodman 2009;Gill et al 2016); these compounds are also known to produce liver damage (Cowens et al 2015;Nash et al 2013;Souza et al 2013;Zhang et al 2008a). Recently, PBDE were found to produce mitochondrial damage, which interfered in cell homeostasis (Hu et al 2007(Hu et al , 2009Pazin et al 2015;Pereira et al 2013Pereira et al , 2014Souza et al 2013).…”

Section: Discussionmentioning

confidence: 99%

“…However, increasing PBDE levels in the environment and human tissue samples in the order of ng/g samples (Eskenazi et al 2013;Hites 2004;Lee et al 2013;Meironyte et al 1999) are a cause for concern. Indeed, these substances produced adverse effects including neurotoxicity, hepatotoxicity, cancer in vivo in the order of μg/g as well as following a high, single exposure dose of 10 mg/kg (Alves et al 2007;Bellinger 2013;Chen et al 2010;Costa and Giordano 2007;Cowens et al 2015;Darnerud 2003;Gill et al 2016;Nash et al 2013;Zhang et al 2008b), and in vitro cytotoxicity including the death of hepatic-derived cells in the order of micromoles (Hu et al 2009;Madia et al 2004;Souza et al 2013;Yan et al 2011).…”

Section: Introductionmentioning

confidence: 99%

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Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death

Pereira

Souza

Tasso

et al. 2017

Journal of Toxicology and Environmental Health, Part A

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Polybrominated diphenyl ethers (PBDE) are ubiquitous environmental pollutants. Exposure to these chemicals has been associated with developmental neurotoxicity, endocrine dysfunctions, reproductive disorders, and hepatotoxicity. The widespread use of PBDE as flame retardants has culminated in daily exposure of humans and wildlife to these contaminants and resulted in their banned use. Thus assessment of the potential effects of each PBDE congener on living organisms has become cause for concern. The aim of this study was to (1) examine the effects of decabromodiphenyl ether (BDE)-209 on different functions of HepG2 cells and (2) investigate whether this congener is involved in mitochondrial toxicity. The use of multiple methods was employed to (i) study the influence of BDE-209 on mitochondrial permeability transition (MPT) process in mitochondria isolated from rat liver and (ii) determine the consequential cellular damage. Our results showed that BDE-209 induced matrix swelling related to MPT with 10 µM and ATP depletion with 0.1 µM. In addition, 0.5 μM BDE-209 reduced HepG2 cell viability, produced collapse of membrane potential, but increased levels of reactive oxygen species (ROS) after 48 h incubation. After 24 h with 5 μM treatment elevated levels of ROS, DNA fragmentation and cytochrome c release, accompanied by caspase 9 and caspase 3 activation was noted. Taken together, these results suggest that short-duration exposure (24 or 48 h) to 0.5 μM or 5 μM BDE-209 concentrations diminished HepG2 cell viability due to apoptosis associated with mitochondrial dysfunction.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death

Pereira

Souza

Tasso

et al. 2017

Journal of Toxicology and Environmental Health, Part A

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“…In experimental studies, PBDEs exert effects on the liver, the nervous system, and other organs; PBDEs and OH-BDEs have been associated with possible endocrine-disrupting effects (Cowens et al 2015; EFSA 2011; Gill et al 2016; Linares, Bellés, and Domingo 2015). The OH-BDE exhibit greater endocrine activity than their parent PBDE (Ptak et al 2006, 2005).…”

Section: Introductionmentioning

confidence: 99%

Polybrominated diphenyl ether (PBDE) neurotoxicity: a systematic review and meta-analysis of animal evidence

Dorman

Chiu

Hales

et al. 2018

Journal of Toxicology and Environmental Health, Part B

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A recent systematic review (SR) and meta-analysis of human studies found an association between prenatal serum polybrominated diphenyl ethers (PBDE) concentrations and a decrease in the IQ of children. A SR of experimental developmental animal PBDE-mediated neurotoxicity studies was performed in the present study. Outcomes assessed included measures related to learning, memory, and attention, which parallel the intelli9ence-related outcomes evaluated in the human studies SR. PubMed, Embase, and Toxline were searched for relevant experimental nonhuman mammalian studies. Evaluation of risk of bias (RoB) and overall body of evidence followed guidance developed by the National Toxicology Program. Animal studies using varying designs and outcomes were available for BDEs 47, 99, 153, 203, 206, and 209 and the technical mixture DE-71. Study reporting of methods and results was often incomplete leading to concerns regarding RoB. A meta-analysis of 6 Morris water maze studies showed evidence of a significant increase in last trial latency (effect size of 25.8 [CI, 20.3 to 31.2]) in PBDE-exposed animals with low heterogeneity. For most endpoints, there were unexplained inconsistencies across studies and no consistent evidence of a dose-response relationship. There is a “moderate” level of evidence that exposure to BDEs 47, 99, and 209 affects learning. For other PBDEs and other endpoints, the level of evidence was “low” or “very low”. The meta-analysis led to stronger conclusions than that based upon a qualitative review of the evidence. The SR also identified RoB concerns that might be remedied by better study reporting.

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“…The health risk of PBDEs has recently raised global concern. PBDEs may disrupt the endocrine system, have neurodevelopment toxicity, teratogenicity and potential carcinogenicity 8 , 9 . PBDEs could affect the male reproductive function, exposure level of PBDEs in human serum is negatively associated with sperm mobility and concentration 10 , 11 .…”

Section: Introductionmentioning

confidence: 99%

“…Exposure to 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) decreased the rate of sperm capacitation, altered sperm motility parameters and increased germ cell loss and apoptosis in both mice and rat 12 , 13 . Previous studies have shown that PBDEs with fewer bromines are more volatile and bioaccumulative 8 , 9 and hence may be more harmful to human health 14 . Mono-BDE may induce genetic recombination in mammalian cells 15 .…”

Section: Introductionmentioning

confidence: 99%

Metabolomics coupled with pathway analysis characterizes metabolic changes in response to BDE-3 induced reproductive toxicity in mice

Wei

Jin

Gao

et al. 2018

Sci Rep

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Polybrominated diphenyl ethers (PBDEs) may affect male reproductive function. 4-bromodiphenyl ether (BDE-3), the photodegradation products of higher brominated PBDEs, is the most fundamental mono-BDE in environment but is less studied. The purpose of this study was to investigate the reproductive toxicity induced by BDE-3 and explore the mechanism by metabolomics approach. In this study, mice were treated intragastrically with BDE-3 for consecutive six weeks at the dosages of 0.0015, 1.5, 10 and 30 mg/kg. The reproductive toxicity was evaluated by sperm analysis and histopathology examinations. UPLC-Q-TOF/MS was applied to profile the metabolites of testis tissue, urine and serum samples in the control and BDE-3 treated mice. Results showed the sperm count was dose-dependently decreased and percentage of abnormal sperms increased by the treatment of BDE-3. Histopathology examination also revealed changes in seminiferous tubules and epididymides in BDE-3 treated mice. Metabolomics analysis revealed that different BDE-3 groups showed metabolic disturbances to varying degrees. We identified 76, 38 and 31 differential metabolites in testis tissue, urine and serum respectively. Pathway analysis revealed several pathways including Tyrosine metabolism, Purine metabolism and Riboflavin metabolism, which may give a possible explanation for the toxic mechanism of BDE-3. This study indicates that UHPLC-Q-TOFMS-based metabolomics approach provided a better understanding of PBDEs-induced toxicity dynamically.

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Developmental neurotoxicity of polybrominated diphenyl ethers mixture de71 in Sprague-Dawley rats

Cited by 17 publications

References 68 publications

Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death

Exposure to decabromodiphenyl ether (BDE-209) produces mitochondrial dysfunction in rat liver and cell death

Polybrominated diphenyl ether (PBDE) neurotoxicity: a systematic review and meta-analysis of animal evidence

Metabolomics coupled with pathway analysis characterizes metabolic changes in response to BDE-3 induced reproductive toxicity in mice

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