Perinatal exposure to 2,2′,4′4′ −Tetrabromodiphenyl ether induces testicular toxicity in adult rats

Khalil, Ahmed; Parker, Mikhail; Brown, Sarah E.; Cevik, Sebnem Eren; Guo, Lian W.; Jensen, Jake; Olmsted, Alexandra; Portman, Daneal; Wu, Haotian; Suvorov, Alexander

doi:10.1016/j.tox.2017.07.006

Cited by 43 publications

(37 citation statements)

References 91 publications

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“…This on-going persistence of PBDE exposure in humans can be attributed to many factors, including, the prevalence of PBDE in waste and recycling sites, indoor use of products containing PBDEs ( 10 ), global circulation of PBDE toward the Northern Hemisphere, biosynthesis of PBDE by microflora of the marine environment including γ-proteobacteria ( 11 ), and endosymbiotic microflora of benthic sponges ( 12 – 15 ) and high bioaccumulation and bioconcentration of PBDEs in food chains ( 16 ). Younger generations of Americans that were exposed in utero and during early postnatal life to the highest environmental doses of PBDE account for approximately one-fifth of the US population ( 17 , 18 ). The long-term consequences of developmental exposures to PBDE for this population are not well-understood.…”

Section: Introductionmentioning

confidence: 99%

Developmental Exposure to 2,2′,4,4′-Tetrabromodiphenyl Ether Permanently Alters Blood-Liver Balance of Lipids in Male Mice

et al. 2018

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Polybrominated diphenyl ethers (PBDEs) were used as flame-retardant additives starting 1965 and were recently withdrawn from commerce in North America and Europe. Approximately 1/5 of the total U.S. population were born when environmental concentrations of PBDE plateaued at their maximum. Accumulating evidence suggests that developmental exposures to PBDE may result in long-lasting programming of liver metabolism. In this study, CD-1 mice were exposed prenatally or neonatally to 1 mg/kg body weight of 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47), and changes in liver histology, transcriptome, and liver-blood balance of triglycerides were analyzed in 10 months old male offspring. In both exposure groups, long-term reprogramming of lipid metabolism was observed, including increased liver triglycerides and decreased blood triglycerides, and altered expression of metabolic genes in the liver. Significant upregulation of lipid influx transporter Cd36 2.3- and 5.7-fold in pre- and neonatal exposure groups, respectively was identified as a potential mechanism of blood/liver imbalance of triglycerides. Analysis of our and previously published all-genome gene expression data identified changes in expression of ribosomal protein genes as a transcriptomic signature of PBDE exposure. Further comparison of our new data and published data demonstrate that low doses (0.2 mg/kg body weight) of PBDE induce long-lasting up-regulation of ribosomal genes, suppression of Cd36 in liver and increase circulating triglycerides in blood, while moderated doses (≥1 mg/kg body weight) produce opposite long-lasting effects. To conclude, this study shows that an environmentally relevant developmental exposures to BDE-47 permanently alter lipid uptake and accumulation in the liver, with low and moderate doses having opposite effect on liver transcriptomics and triglyceride balance. Similar effects of pre- and neonatal exposures point at hepatocyte maturation as a sensitive window of the liver metabolism programming. These results suggest that PBDE exposure may be an important factor increasing risks of cardio-vascular disease and non-alcoholic fatty liver disease via modulation of liver/blood balance of lipids. The translational relevance of these findings for human remain to be studied.

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Section: Introductionmentioning

confidence: 99%

Developmental Exposure to 2,2′,4,4′-Tetrabromodiphenyl Ether Permanently Alters Blood-Liver Balance of Lipids in Male Mice

et al. 2018

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“…The commonly used ether solvents are diethyl ether, tetrahydrofuran, 1,4-dioxan etc. The ether solvents are toxic, many experimental models showed the toxicity of ether to the HepG2 cells [59], toxicity to blood lymphocytes [60], testicular toxicity [61], carcinogenicity [62]. The tetrahydrofuran (THF) shows CNS toxicity with dizziness, headache, loss of sense of smell and fatigue etc.…”

Section: Ethersmentioning

confidence: 99%

An Overview on Common Organic Solvents and Their Toxicity

Joshi

Adhikari

2019

JPRI

384

156

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Organic solvents are known as carbon-based solvents and their general property is primarily based on their volatility, boiling point, the molecular weight and color. Having enormous hazards associated with the organic solvents, they are used for millions of purposes which alert us to think more on its toxicity points. Almost all of the solvents are hazardous to health, if swallowed or inhaled more than the limit quantity and on contact to the skin most of them cause irritation. Some of the common solvents are acetone, ethyl acetate, hexane, heptane, dichloromethane, methanol, ethanol, tetrahydrofuran, acetonitrile, dimethylformamide, toluene, dimethylsulfoxide etc. Researchers, scientists, workers in the chemical industry and research institutes use these solvents on regular basis leading them to be affected in major aspects. But also, the nearby persons are affected by the contamination to the soil, water, air etc. If constantly exposed with solvents, it will badly affect the function of CNS and other body parts. The level of impact, sign and symptoms will depend on concentration, time, duration, frequency and nature of solvents, leading to common effects like headache, dizziness, tiredness, blurred vision, behavioral changes, unconsciousness, and even(Zimmermann, Mayer et al. 1985) death. To overcome it, the green chemistry concept is growing rapidly, and the solvent selection guide is in practice in many big company and research institute. A researcher or chemical worker is the primary person who works with solvents and they need to consider throughout these things while performing their activities for their own good health and for the sake of the world. The purpose of this review is to provide needed basic knowledge about common organic solvents and their potential toxicities which will alert researchers to think twice and always think for their health as well as for the environment via safe and green practice.

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“…For example, Pb exposure altered DNA methylation in both the present generation [36] and the offspring [37]. The PBDE exposure formed DNA adducts [38] and disturbed the microRNA profiling [39] in the present generation and altered the DNA methylation and histone-protamine exchange in offspring adults [15,16]. The epigenetic changes underlying the transgenerational effects might also contribute to the interactions.…”

Section: Transgenerational Effects Between Individual and Sequential mentioning

confidence: 99%

“…Regarding the persistence, PBDE and Pb showed long-term influences over generations. Perinatal exposure to 2,2′,4,4′-tetra-brominated diphenyl ether (BDE47) significantly damaged the normal spermatogenesis of adult rats [15,16]. Lead (Pb) inhibited the growth of daughters (F1) of Caenorhabditis elegans more than that of parents (F0) [17].…”

mentioning

confidence: 99%

Transgenerational effects of different sequential exposure to 2,2′,4,4′-tetra-brominated diphenyl ether (BDE47) and lead (Pb) on Caenorhabditis elegans

Zhang

2020

Environ Sci Eur

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Background: Poly-brominated diphenyl ethers (PBDEs) and heavy metals are persistent pollutants in Yangtze River basin, China and also around the globe. In the exposure reality, they may have sequential exposures and long-term outcomes. Yet, the effects combining these two aspects remained largely unexplored. At present, the effects of 2,2′,4,4′-tetra-brominated diphenyl ether (BDE47) and lead (Pb) on Caenorhabditis elegans were studied with two sequential arrangements. One was first exposure to BDE47 and then to Pb (or vice versa) in one generation, and the other one was an early exposure to BDE47 in the parent generation (F0) and then a later exposure to Pb in the offspring (F1) (or vice versa). Results: On growth, sequential Pb-BDE47 exposure caused inhibition in exposure but stimulation in recovery, showing similarity to individual Pb results. Meanwhile, the opposite sequential BDE47-Pb exposure showed inhibition in both exposure and recovery, similar to those of individual BDE47 results. On behavior, the effects of sequential exposure were significantly different from individual results without any similarity. In transgenerational effects, F0 Pb exposure with F1 BDE47 exposure (Pb-F1-BDE47) inhibited growth, similar to the transgenerational results of individual Pb exposure. Meanwhile, the recovery effects were similar to the transgenerational results of individual BDE47. At the same time, Pb-F1-BDE47 exposure significantly hindered the recovery of behavior while the opposite BDE47-F1-Pb exposure resulted in different results. The behavioral effects in F1 showed negative correlation with the contents of γ-aminobutyric acid (GABA), while those in F1 were positively correlated with the activities of acetylcholine esterase (AChE). Conclusions: Sequential exposure to BDE47 and Pb within one generation or over generations showed significant different effects from individual results. Further studies are still needed to investigate the toxicity patterns and underlying mechanisms.

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Perinatal exposure to 2,2′,4′4′ −Tetrabromodiphenyl ether induces testicular toxicity in adult rats

Cited by 43 publications

References 91 publications

Developmental Exposure to 2,2′,4,4′-Tetrabromodiphenyl Ether Permanently Alters Blood-Liver Balance of Lipids in Male Mice

Developmental Exposure to 2,2′,4,4′-Tetrabromodiphenyl Ether Permanently Alters Blood-Liver Balance of Lipids in Male Mice

An Overview on Common Organic Solvents and Their Toxicity

Transgenerational effects of different sequential exposure to 2,2′,4,4′-tetra-brominated diphenyl ether (BDE47) and lead (Pb) on Caenorhabditis elegans

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