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1.
Chemosphere ; 238: 124602, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31545211

RESUMO

Polybrominated diphenyl ethers (PBDEs) have been known to exhibit neurotoxicity in rats; however, the underlying mechanism remains unknown and there is no available intervention. In this study, we aimed to investigate the role of oxidative and nitrosative stress in the neurotoxicity in the cerebral cortex and primary neurons in rats following the BDE-153 treatment. Compared to the untreated group, BDE-153 treatment significantly induced the neurotoxic effects in rats, as manifested by the increased lactate dehydrogenase (LDH) activities and cell apoptosis rates, and the decreased neurotrophic factor contents and cholinergic enzyme activities in rats' cerebral cortices and primary neurons. When compared to the untreated group, the oxidative and nitrosative stress had occurred in the cerebral cortex or primary neurons in rats following the BDE-153 treatment, as manifested by the increments in levels of reactive oxygenspecies (ROS), malondialdehyde (MDA), nitric oxide (NO), and neuronal nitric oxide synthase (nNOS) mRNA and protein expressions, along with the decline in levels of superoxide dismutase (SOD) activity, glutathione (GSH) content, and peroxiredoxin I (Prx I) and Prx II mRNA and protein expressions. In addition, the ROS scavenger N-acetyl-l-cysteine (NAC) or NO scavenger NG-Nitro-l-arginine (L-NNA) significantly rescued the LDH leakage and cell survival, reversed the neurotrophin contents and cholinergic enzymes, mainly via regaining balance between oxidation/nitrosation and antioxidation. Overall, our findings suggested that oxidative and nitrosative stresses are involved in the neurotoxicity induced by BDE-153, and that the antioxidation is a potential targeted intervention.


Assuntos
Córtex Cerebral/patologia , Éteres Difenil Halogenados/toxicidade , Síndromes Neurotóxicas/patologia , Estresse Nitrosativo/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Bifenil Polibromatos/toxicidade , Acetilcisteína/farmacologia , Animais , Antioxidantes/metabolismo , Apoptose/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Córtex Cerebral/efeitos dos fármacos , Glutationa/metabolismo , Éteres Difenil Halogenados/metabolismo , Masculino , Malondialdeído/metabolismo , Fatores de Crescimento Neural/metabolismo , Neurônios/efeitos dos fármacos , Neurotrofina 3/metabolismo , Óxido Nítrico/metabolismo , Óxido Nítrico Sintase Tipo I/metabolismo , Estresse Nitrosativo/fisiologia , Estresse Oxidativo/fisiologia , Ratos , Ratos Sprague-Dawley , Transdução de Sinais/efeitos dos fármacos
2.
Chemosphere ; 240: 124865, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31541897

RESUMO

Biologists have extensively investigated the toxicity of polybrominated diphenyl ethers (PBDEs) on plants in ecosystems, where experiments revealed that PBDEs can promote, inhibit, or have no significant effects on the physiological and biochemical functionality of plants. These studies have stimulated many theoretical works that aimed to elucidate the differences in the toxicity of PBDEs on various plants. However, there has been no quantitative attempt to reconcile theory with the results of empirical experiments. To close this gap between theory and experiments, we conducted a hierarchical meta-analysis to examine the toxicity of PBDEs on plants and confirmed potential sources of variation across numerous studies. Through the analysis of 1299 observations garnered from 41 studies, we revealed the significant toxicity of PBDEs on plants. This result was verified to be robust and showed no signs of bias. Our study affirmed that functional indexes can contribute to variations that lead to the toxicity of PBDEs on various plants. Furthermore, we found that lower congeners PBDEs were more toxic to plants than higher congeners PBDEs, and higher plants were more resistant to PBDEs induced phytotoxicity than lower plants. For interactive effects, only specific PBDEs concentrations had significant effects on glutathione S-transferase activities, and experimental durations had no significant impacts on any functional indexes. These results reconciled empirical studies and assisted us with elucidating the ecotoxicology of PBDEs induced phytotoxicity.


Assuntos
Éteres Difenil Halogenados/toxicidade , Plantas/efeitos dos fármacos , Éteres Difenil Halogenados/química , Relação Estrutura-Atividade
3.
Ecotoxicol Environ Saf ; 188: 109882, 2020 Jan 30.
Artigo em Inglês | MEDLINE | ID: mdl-31698175

RESUMO

Microplastics attract widespread attention, including for their potential to transport toxic chemicals in the form of plasticisers and associated hydrophobic organic chemicals, such as polybrominated diphenyl ethers (PBDEs). The aims of this study were to investigate how nylon (polyamide) microplastics may affect PBDE accumulation in snails, and the acute effects of nylon particles and PBDEs on survival, weight change and inherent microbiome diversity and community composition of the pond snail Lymnaea stagnalis. Snails were exposed for 96 h to BDEs-47, 99, 100 and 153 in the presence and absence of 1% w/w nylon microplastics in quartz sand sediment. No mortality was observed over the exposure period. Snails not exposed to microplastics lost significantly more weight compared to those exposed to microplastics. Increasing PBDE concentration in the sediment resulted in an increased PBDE body burden in the snails, however microplastics did not significantly influence total PBDE uptake. Based on individual congeners, uptake of BDE 47 by snails was significantly reduced in the presence of microplastics. The diversity and composition of the snail microbiome was not significantly altered by the presence of PBDEs nor by the microplastics, singly or combined. Significant effects on a few individual operational taxonomic units (OTUs) occurred when comparing the highest PBDE concentration with the control treatment, but in the absence of microplastics only. Overall within these acute experiments, only subtle effects on weight loss and slight microbiome alterations occurred. These results therefore highlight that L. stagnalis are resilient to acute exposures to microplastics and PBDEs, and that microplastics are unlikely to influence HOC accumulation or the microbiome of this species over short timescales.


Assuntos
Éteres Difenil Halogenados/metabolismo , Lymnaea/efeitos dos fármacos , Microbiota/efeitos dos fármacos , Poluentes Químicos da Água/metabolismo , Animais , Carga Corporal (Radioterapia) , Exposição Ambiental/análise , Retardadores de Chama/análise , Retardadores de Chama/metabolismo , Retardadores de Chama/toxicidade , Éteres Difenil Halogenados/análise , Éteres Difenil Halogenados/toxicidade , Lymnaea/metabolismo , Lymnaea/microbiologia , Nylons/toxicidade , Poluentes Químicos da Água/análise , Poluentes Químicos da Água/toxicidade
4.
Wei Sheng Yan Jiu ; 48(4): 628-632, 2019 Jul.
Artigo em Chinês | MEDLINE | ID: mdl-31601347

RESUMO

OBJECTIVE: To investigate the effects of prenatal exposure to pentabromodiphenyl ether(BDE-99) on maternal serum thyroid hormone levels, as well as birth weight and anal-genital development in rat offspring. METHODS: Pregnant SD rats were randomly treated with BDE-99(0. 2, 2 and 20 mg/kg) or corn oil on gestational days 1-19. Maternal serum were collected from tail vein on the gestational day 11 and day 19, serum levels of TSH, TT4, FT4, TT3 and FT3 were measured. The weight of offspring was measured at postnatal day 3, 9, 15, 21 and 27, anorectal-genital spacing was measured at postnatal day 21. RESULTS: The levels of TT3 and FT3 in maternal serum of 2 mg/kg and 20 mg/kg groups were lower than those of control group at gestational day 11. At gestational day 19, TT4 levels in maternal serum were significantly lower than those in control group, and TSH levels of 20 mg/kg group were lower than those in control group. The body weight of female offspring in all dose groups was lower than that of control group on the postnatal day 27, and the anal-genital distance of male offspring in the 20 mg/kg dose group was significantly lower than that of the control group on the postnatal day 21. CONCLUSION: Prenatal exposure to BDE-99 may disrupt the maternal thyroid hormone levels, and cause the offspring's weight loss and shortened anal-genital spacing.


Assuntos
Poluentes Ambientais/toxicidade , Éteres Difenil Halogenados/toxicidade , Glândula Tireoide/metabolismo , Hormônios Tireóideos/metabolismo , Animais , Feminino , Masculino , Exposição Materna , Gravidez , Ratos , Ratos Sprague-Dawley
5.
Ecotoxicol Environ Saf ; 186: 109767, 2019 Dec 30.
Artigo em Inglês | MEDLINE | ID: mdl-31610358

RESUMO

Cadmium, a typical heavy metal, causes serious toxicities on many organs and tissues. As the last partially controlled class of polybrominated diphenyl ethers (PBDEs), BDE209 can also induce various health issues. Although apoptosis mediated by mitochondria has been known to be a key player in inducing toxicities by cadmium, the detailed mechanisms are incompletely understood. Moreover, co-existence of cadmium and PBDEs has been found in various environment context and human body. However, studies on the joint toxicity of cadmium and PBDEs are still limited with largely unknown mechanisms. In the present study, we investigated the adverse effects and mechanisms of single or combined treatment of CdCl2 and BDE209 on hepatocytes. We observed that apoptosis were significantly induced by CdCl2, and the combined treatment of CdCl2 and BDE209 greatly promoted the progression of apoptosis. BDE209 induced mild apoptosis. Mitochondria was the pivot of several mechanisms to induce apoptosis, including ROS production, decreased mitochondrial membrane potential (MMP), mtDNA damage and disordered calcium (Ca2+) homeostasis. However, we found that mtDNA damage and disordered Ca2+ homeostasis were the main mechanisms for CdCl2-induced apoptosis while ROS production played important roles in BDE209-induced apoptosis. Less mtDNA damage occurred in BDE209-treated cells. In the cells with combined treatment, CdCl2 and BDE209 exhibited a complementary pattern for the underlying mechanisms of apoptosis, leading to the joint toxicities, in which CdCl2 showed more contributions. In a conclusion, our results demonstrated that combined exposure to cadmium and BDE209 causes joint adverse effects on hepatocytes through diverse mechanisms as mediated by mitochondria.


Assuntos
Cádmio/toxicidade , Dano ao DNA , DNA Mitocondrial , Éteres Difenil Halogenados/toxicidade , Homeostase/efeitos dos fármacos , Apoptose/efeitos dos fármacos , Apoptose/genética , Sinergismo Farmacológico , Hepatócitos/efeitos dos fármacos , Hepatócitos/patologia , Homeostase/genética , Humanos , Potencial da Membrana Mitocondrial/efeitos dos fármacos
6.
Environ Pollut ; 255(Pt 1): 113097, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31520908

RESUMO

Decabromodiphenyl ether (BDE-209) is commonly used as a flame retardant, usually in products that were utilized in electronic equipment, plastics, furniture and textiles. To identify the impacts of BDE-209 on the male reproductive system and the underlying toxicological mechanisms, 40 male ICR mice were randomly divided into four groups, which were then exposed to BDE-209 at 0, 7.5, 25 and 75 mg kg-1 d-1 for four weeks, respectively. With regard to the in vitro study, GC-2spd cells were treated with BDE-209 at 0, 2, 8 and 32 µg mL-1 for 24 h, respectively. The results from the in vivo experiments showed that BDE-209 resulted in damage to the testis structure, led to cell apoptosis in testis and decreased sperm number and motility, while sperm malformation rates were significantly increased. Moreover, BDE-209 could induce oxidative stress with decreased testosterone levels, result in DNA damage and activate DNA damage response signaling pathways (ATM/Chk2, ATR/Chk1 and DNA-PKcs/XRCC4/DNA ligase Ⅳ). The data from the in vitro experiments showed that BDE-209 led to cytotoxicity by reducing cell viability and increasing LDH release as well. BDE-209 also induced DNA strand breaks, cell cycle arrest at G1 phase and elevated reactive oxygen species (ROS) level in GC-2 cells. These results suggested that BDE-209 could lead to male reproductive toxicity by inducing DNA damage and failure of DNA damage repair which resulted in cell cycle arrest and apoptosis of spermatogenic cell. The present study provided new evidence to elucidate the potential mechanism of male reproductive toxicity induced by BDE-209.


Assuntos
Apoptose/efeitos dos fármacos , Dano ao DNA/efeitos dos fármacos , Retardadores de Chama/toxicidade , Pontos de Checagem da Fase G1 do Ciclo Celular/efeitos dos fármacos , Éteres Difenil Halogenados/toxicidade , Espermatozoides/patologia , Animais , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Reparo do DNA/genética , Masculino , Camundongos , Camundongos Endogâmicos ICR , Estresse Oxidativo/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo , Transdução de Sinais/efeitos dos fármacos , Contagem de Espermatozoides , Motilidade Espermática/efeitos dos fármacos , Espermatozoides/citologia , Testículo/citologia , Testículo/patologia , Testosterona/sangue
7.
Chemosphere ; 236: 124406, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31545203

RESUMO

Pot experiments were conducted under abiotic conditions to investigate the interactive influence of decabromodiphenyl ether (BDE-209) and lead (Pb) on the seed germination, germ length, root exudation and physiological characteristics of tall fescue (Festuca arundinaceae), and the uptake, accumulation of Pb and BDE-209 in the plant tissues. Results show that seed germination and germ length were impacted by Pb but less influenced by BDE-209. BDE-209 spiking (10 and 50 mg/L) could alleviate the toxicity of high Pb concentration on seed germination and growth. The chlorophyll content was significantly increased at 500 mg/kg Pb but declined at 2000 mg/kg Pb. Low-level Pb contamination (500 mg/kg) activated antioxidase activity; however, 2000 mg/kg Pb significantly reduced the antioxidase activity. Plant biomass slightly decreased at 500 mg/kg Pb but significantly declined at 2000 mg/kg Pb. The addition of a moderate dosage of BDE-209 (10-50 mg/kg) lessened Pb phytotoxicity, leading to improved plant growth relative to the case of Pb spiking alone. The exudate secretion was significantly enhanced by Pb addition, but BDE-209 spiking only caused slightly increased secretion. Pb could interfere with BDE-209 adsorption and translocation of tall fescue by affecting physiological behavior of the plant, but BDE-209 exhibited little influence on the Pb fate in the plant. Overall, BDE-209 had slight interference on the impact of Pb towards tall fescue. The results demonstrate the complex interactive effects of organic pollutants and heavy metals in the soil-plant system.


Assuntos
Festuca/efeitos dos fármacos , Éteres Difenil Halogenados/toxicidade , Chumbo/toxicidade , Poluentes do Solo/toxicidade , Biomassa , Clorofila/metabolismo , Ecotoxicologia/métodos , Festuca/crescimento & desenvolvimento , Festuca/metabolismo , Germinação/efeitos dos fármacos , Éteres Difenil Halogenados/farmacocinética , Chumbo/farmacocinética , Exsudatos de Plantas/análise , Exsudatos de Plantas/metabolismo , Raízes de Plantas/efeitos dos fármacos , Raízes de Plantas/crescimento & desenvolvimento , Raízes de Plantas/metabolismo , Poluentes do Solo/farmacocinética
8.
Ecotoxicol Environ Saf ; 184: 109606, 2019 Nov 30.
Artigo em Inglês | MEDLINE | ID: mdl-31472382

RESUMO

Epidemiological and animal studies have revealed a possible linkage between 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) exposure and neurodegenerative disease such as Parkinson's disease (PD). However, whether or how BDE-47 would affect the PD progression remains unclear. Here, we carried out a metabolomics study based on liquid chromatography-mass spectrometry (LC-MS) and gas chromatography-mass spectrometry (GC-MS) to investigate the possible contribution of BDE-47 exposure to PD progression in Drosophila (fly) model. Transgenic PD flies were exposed to BDE-47 through diet for 30 days. Global metabolomic analysis identified 48 altered metabolites after the exposure. These metabolites were mainly involved in tryptophan metabolism, phenylalanine metabolism, purine metabolism, and alanine, aspartate and glutamate metabolism. Further, by quantifying metabolites of interest using LC-MS/MS, we confirmed that the formation of neuro-protector kynurenic acid was slowed down while the formation of neurotoxin 3-hydroxy-kynurenine was speeded up on the 20th exposure day. Moreover, the levels of SAM/SAH (an index of methylation potential) and GSH/GSSG (an indicator of oxidative stress) were found to decrease on the 30th exposure day. Our results suggest that BDE-47 could induce imbalance of kynurenine metabolism and methylation potential, and oxidative stress, which might further accelerate PD progression.


Assuntos
Exposição Dietética , Drosophila/efeitos dos fármacos , Éteres Difenil Halogenados/toxicidade , Animais , Modelos Animais de Doenças , Drosophila/metabolismo , Doenças Metabólicas/etiologia , Doenças Metabólicas/metabolismo , Redes e Vias Metabólicas/efeitos dos fármacos , Metabolômica , Metilação/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos
9.
Aquat Toxicol ; 215: 105266, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31401474

RESUMO

The persistent pollutants polybrominated diphenyl ethers (PBDEs) have been demonstrated to produce several negative effects on marine organisms. Although Mytilus galloprovincialis was extensively studied as model system, the effects of PBDEs on the innate immune system of mussels remains unclear. In this study, except for the control treatment, specimens of M. galloprovincialis were fed with microalgae treated with increasing concentrations of PBDEs (maximum level 100 ng L-1 of BDE-47 per day). BDE-47 treatment was maintained for 15 days and then the animals were fed with the same control diet, without contaminants, for 15 days. Samples of haemolymph (HL) were obtained at T0, T15 and T30 days of the experiment to evaluate different parameters related to immunity, such as neutral red retention time, and peroxidase, protease, antiprotease, lysozyme and bactericidal activities. BDE-47 exposure for 15 days affected both the stability of haemocytes and humoral parameters. In addition, the obtained results indicated that, at 30 days, after 15 days of culture without contaminant, the immune parameters were still affected, as some of them did not return to the basal levels, and others remained stimulated. Overall the results indicate that BDE-47 exposures at environmentally realistic levels may affect various aspects of immune function in M. galloprovincialis, acting as stressor that can compromise the general welfare.


Assuntos
Exposição Ambiental , Éteres Difenil Halogenados/toxicidade , Mytilus/imunologia , Animais , Antibacterianos/farmacologia , Comportamento Alimentar/efeitos dos fármacos , Hemócitos/efeitos dos fármacos , Hemócitos/metabolismo , Hemolinfa/efeitos dos fármacos , Hemolinfa/metabolismo , Hemolinfa/microbiologia , Membranas Intracelulares/efeitos dos fármacos , Membranas Intracelulares/metabolismo , Lisossomos/efeitos dos fármacos , Lisossomos/metabolismo , Microalgas/fisiologia , Mytilus/efeitos dos fármacos , Mytilus/microbiologia , Peptídeo Hidrolases/metabolismo , Análise de Sobrevida , Poluentes Químicos da Água/toxicidade
10.
Ecotoxicol Environ Saf ; 183: 109566, 2019 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-31437728

RESUMO

Polybrominated diphenyl ethers (PBDEs) are brominated flame retardants. Biomonitoring studies have shown widespread presence of PBDEs in humans and their accumulation in food chain cause concern to human health, especially for foetus and infant development. The early-life stages are generally considered more sensitive to exposure to toxic compounds than juvenile or adults. For this reason the aim of this study was to evaluate the effects of the three most environmentally relevant BDE (BDE- 47, 99 and 209) on zebrafish embryos. The fish embryo toxicity (FET) OECD tests on zebrafish were performed followed by histopathogical examination to assess morphological changes. The gene expression of the thyroid stimulating hormone ß (Tshß), the transport proteins transthyretin (Ttr) and thyroxine-binding globulin (Tbg) as well as the enzyme iodothyronine deiodinase 1 (Dio1) was also assessed by Real-time PCR. BDE-47 and BDE-99 showed an increase of the severity of the effects at the lower concentrations while for the BDE-209 the effects were higher to the high concentrations. Although all compounds did not show any acute toxicity for none of the concentrations tested, they reported interesting sub-acute lesions, including yolk and pericardial edema, tail and head malformation, reduced and extremely reduced heart beat rate, blood stasis and spinal curvature, with the highest percentage recorded for BDE-209. Cardiac edema, damage of eye structure and hydrocephaly were confirmed also by histophatological examination. Furthermore, a toxic and dose-dependent liver vacuolization in BDE-209 was observed in all experimental groups. Although no statistically significant difference in gene expression was observed, BDE-209 up-regulated only Dio1 while the other congeners induced Tshß, Ttr, Tbg and Dio1. Overall, this research highlighted that exposure to BDE-47, BDE-99 and BDE-209 at realistic concentrations caused lethal and sub-lethal alterations and impaired genes involved in thyroid hormones homeostasis leading to abnormal development of zebrafish embryos.


Assuntos
Embrião não Mamífero/efeitos dos fármacos , Monitoramento Ambiental/métodos , Retardadores de Chama/toxicidade , Expressão Gênica/efeitos dos fármacos , Éteres Difenil Halogenados/toxicidade , Peixe-Zebra , Adulto , Animais , Relação Dose-Resposta a Droga , Embrião não Mamífero/patologia , Retardadores de Chama/análise , Éteres Difenil Halogenados/análise , Humanos , Hormônios Tireóideos/metabolismo , Peixe-Zebra/genética , Peixe-Zebra/metabolismo
11.
Artigo em Inglês | MEDLINE | ID: mdl-31362383

RESUMO

Disruption of epigenetic regulation by environmental toxins is an emerging area of focus for understanding the latter's impact on human health. Polybrominated diphenyl ethers (PBDEs), one such group of toxins, are an environmentally pervasive class of brominated flame retardants that have been extensively used as coatings on a wide range of consumer products. Their environmental stability, propensity for bioaccumulation, and known links to adverse health effects have evoked extensive research to characterize underlying biological mechanisms of toxicity. Of particular concern is the growing body of evidence correlating human exposure levels to behavioral deficits related to neurodevelopmental disorders. The developing nervous system is particularly sensitive to influence by environmental signals, including dysregulation by toxins. Several major modes of actions have been identified, but a clear understanding of how observed effects relate to negative impacts on human health has not been established. Here, we review the current body of evidence for PBDE-induced epigenetic disruptions, including DNA methylation, chromatin dynamics, and non-coding RNA expression while discussing the potential relationship between PBDEs and neurodevelopmental disorders.


Assuntos
Poluentes Ambientais/toxicidade , Epigênese Genética/efeitos dos fármacos , Retardadores de Chama/toxicidade , Éteres Difenil Halogenados/toxicidade , Metilação de DNA , Humanos
12.
Obstet Gynecol Clin North Am ; 46(3): 455-468, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31378288

RESUMO

Our genetic makeup and environment interact. Evidence has emerged demonstrating preconception and prenatal exposure to toxic agents have a profound effect on reproductive health. We cannot change our genetics, but we can change our environment. Health providers can protect pregnancies from harmful exposures. Pregnancy is the most critical time-window for human development, when any toxic exposure can cause lasting damage to brain development. Reproductive care professionals can provide useful information to patients and refer patients to appropriate specialists when hazardous exposure is identified. Clinical experience and expertise in communicating risks of treatment are transferable to environmental health.


Assuntos
Exposição Ambiental/efeitos adversos , Desenvolvimento Fetal/efeitos dos fármacos , Troca Materno-Fetal , Saúde Reprodutiva , Aconselhamento , Feminino , Éteres Difenil Halogenados/toxicidade , Humanos , Chumbo/toxicidade , Mercúrio/toxicidade , Transtornos do Neurodesenvolvimento/induzido quimicamente , Organofosfatos/toxicidade , Bifenilos Policlorados/toxicidade , Gravidez , Saúde da Mulher
13.
Arch Environ Contam Toxicol ; 77(4): 594-604, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31388704

RESUMO

A total of 39 lower brominated PBDE congeners in surface soils from the Yellow River Delta Natural Reserve (YRDNR) were analyzed in the present study. The total concentrations of PBDEs (ΣPBDEs) ranged from "not detected" to 0.732 ng g-1, with a mean concentration of 0.142 ng g-1. The concentrations of the ΣPBDEs displayed no correlation with the content of the total organic carbon in the YRDNR. The ΣPBDEs concentrations in the Experimental Area were significantly higher than that of the Buffer Area and Core Area, and ΣPBDEs in soils in the North were lower than that of the South. PentaBDEs and HexaBDEs were the most abundant homologues, and the occurrence of PBDEs in the YRDNR may be attributed to the debromination and long range transport of DecaBDEs. Even though the cancer risk and mass inventory of PBDEs in the present study area were estimated to be very low, due to the widespread presence of PBDEs and the particularity of the natural reserve, vigilance should not be let up on the issue of environmental contamination caused by these compounds despite the gradual phase out of their commercial products in the world.


Assuntos
Éteres Difenil Halogenados/análise , Poluentes do Solo/análise , Carcinógenos Ambientais/análise , Carcinógenos Ambientais/toxicidade , China , Conservação dos Recursos Naturais , Monitoramento Ambiental , Retardadores de Chama/análise , Éteres Difenil Halogenados/toxicidade , Humanos , Medição de Risco , Poluentes do Solo/toxicidade
14.
Aquat Toxicol ; 214: 105253, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31352076

RESUMO

Diclofop-methyl (DM) is widely used in agriculture and may lead to serious toxicity. However, a limited number of studies have been performed to evaluate the toxicity of DM in the immune and nervous systems of animals. Here, we utilized a good vertebrate model, zebrafish, to evaluate the toxicity of DM during the developmental process. Exposure of zebrafish embryos to 0.1, 0.3 and 0.5 mg/l DM from 6 h post fertilization (hpf) to 72 hpf induced developmental abnormalities, such as shorter body lengths and yolk sac edemas. The number of immune cells in zebrafish larvae was significantly reduced, but the inflammatory response was not influenced by DM treatment. The expression of immune-related genes were downregulated and the levels of oxidative stress were upregulated by DM exposure. Moreover, locomotor behaviors were inhibited by DM exposure. Therefore, our results suggest that DM has the potential to induce immunotoxicity and cause behavioral changes in zebrafish larvae. This study provides new evidence of the influence of DM exposure on aquatic ecosystems.


Assuntos
Comportamento Animal/efeitos dos fármacos , Embrião não Mamífero/imunologia , Exposição Ambiental , Éteres Difenil Halogenados/toxicidade , Peixe-Zebra/embriologia , Animais , Encéfalo/efeitos dos fármacos , Regulação para Baixo/efeitos dos fármacos , Embrião não Mamífero/efeitos dos fármacos , Embrião não Mamífero/metabolismo , Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos , Larva/efeitos dos fármacos , Larva/metabolismo , Neutrófilos/efeitos dos fármacos , Neutrófilos/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Timócitos/efeitos dos fármacos , Timócitos/metabolismo , Regulação para Cima/efeitos dos fármacos , Regulação para Cima/genética , Poluentes Químicos da Água/toxicidade , Peixe-Zebra/genética
15.
Environ Pollut ; 253: 429-438, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31325888

RESUMO

Recently, the essentiality and fatalness of cardiovascular diseases is attracting much attention. Polybrominated diphenyl ethers (PBDEs) are persistent environmental pollutants, which could induce the toxic effect and have been implicated in the occurrence and development of cardiovascular diseases. However, it is unclear how autophagy and apoptosis induced by BDE-209 in endothelial cells are regulated. The aim of the present study was to investigate the effects of BDE-209 on human umbilical vein endothelial cells (HUVECs) and elucidate the mechanisms involved. HUVECs were treated with a wide range concentration of BDE-209 for 24 h. The appearance of autophagy was tested by the testing index such as outcomes of monodansylcadaverine (MDC) staining and lysotracker staining, observation of autophagosomes and conversion between autophagy marker light chain 3 (LC3)-I and LC3-II. Besides, the apoptotic cell rate was detected with flow cytometry. In addition, BDE-209 induced endoplasmic reticulum (ER) stress was detected by transmission electron microscopy (TEM). Our data suggest that the exposure of BDE-209 could induce autophagy, which was confirmed by MDC staining, transmission electron microscopy observation, lysotracker staining and LC3-I/LC3-II conversion. Besides, the ER stress-related inositol-requiring enzyme 1α (IRE1α)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway could be activated by reactive oxygen species (ROS) to regulate autophagy. Moreover, the apoptosis of endothelial cells was alleviated when autophagy was blocked by 3-Methyladenine (3-MA). The results demonstrated that BDE-209 could induce the production of ROS and ER stress, activate autophagy through IRE1α/AKT/mTOR signaling pathway and ultimately induce apoptosis of vascular endothelial cells. These findings indicate that exposure to PBDE is possible to be a potential risk factor for cardiovascular diseases.


Assuntos
Poluentes Ambientais/toxicidade , Éteres Difenil Halogenados/toxicidade , Apoptose/efeitos dos fármacos , Autofagia/efeitos dos fármacos , Estresse do Retículo Endoplasmático/efeitos dos fármacos , Endorribonucleases , Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Humanos , Inositol , Proteínas Proto-Oncogênicas c-akt/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Transdução de Sinais/efeitos dos fármacos , Serina-Treonina Quinases TOR/metabolismo , Testes de Toxicidade , Veias Umbilicais
16.
Aquat Toxicol ; 214: 105224, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31255847

RESUMO

Polybrominated diphenyl ethers (PBDEs) are distributed throughout the environment. Despite a moratorium on their use, concentrations of PBDEs in the atmosphere and in residential environments remain high due to their persistence. The environmental health risks remain concerning and one of the major adverse effects is neurodevelopmental toxicity. However, the early response and effects of PBDEs exposure on the developing brain remain unknown. In the present study, we investigated the impacts of 2,2',4,4',5-pentabrominated diphenyl ether (BDE-99) on vascular growth and vascular barrier function with an emphasis on cerebral blood vessels, in the early life stages, using a zebrafish model. No general toxicity was observed in exposing zebrafish larvae to 0-0.5 µM BDE-99 at 72 hpf. BDE-99 exposure resulted in neither general toxicity nor pronounced developmental impairment in somatic blood vessels, including intersegmental vessels (ISV) and common cardinal veins (CCV). Meanwhile, both 0.05 µM and 0.5 µM of BDE-99 reduced cerebrovascular density as well as down-regulation of VEGFA and VEGFR2 in the head. In addition, BDE-99 exposure increased vascular leakage, both in cerebral and truncal vasculature at 72 hpf. The accentuated vascular permeability was observed in the head. The mRNA levels of genes encoding tight junction molecules decreased in the BDE-99-exposed larvae, and more robust reductions in Cldn5, Zo1 and Jam were detected in the head than in the trunk. Moreover, proinflammatory factors including TNF-α, IL-1ß and ICAM-1 were induced, and the expression of neurodevelopment-related genes was suppressed in the head following BDE-99 exposure. Taken together, these results reveal that developmental exposure to BDE-99 impedes cerebrovascular growth and disturbs vascular barrier formation. The cerebral vasculature in developing zebrafish, a more sensitive target for BDE-99, may be a promising tool for the assessment of the early neurodevelopmental effects due to PBDEs exposure.


Assuntos
Vasos Sanguíneos/efeitos dos fármacos , Exposição Ambiental , Éteres Difenil Halogenados/toxicidade , Peixe-Zebra/crescimento & desenvolvimento , Animais , Encéfalo/irrigação sanguínea , Encéfalo/crescimento & desenvolvimento , Permeabilidade Capilar/efeitos dos fármacos , Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos , Inflamação/genética , Inflamação/patologia , Larva/efeitos dos fármacos , Neovascularização Fisiológica/efeitos dos fármacos , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Junções Íntimas/efeitos dos fármacos , Junções Íntimas/metabolismo , Fator A de Crescimento do Endotélio Vascular/genética , Fator A de Crescimento do Endotélio Vascular/metabolismo , Receptor 2 de Fatores de Crescimento do Endotélio Vascular/genética , Receptor 2 de Fatores de Crescimento do Endotélio Vascular/metabolismo , Poluentes Químicos da Água/toxicidade , Peixe-Zebra/genética
17.
Ecotoxicol Environ Saf ; 182: 109427, 2019 Oct 30.
Artigo em Inglês | MEDLINE | ID: mdl-31302334

RESUMO

Polybrominated diphenyl ethers (PBDEs) as potential neurotoxicants in environment may possess hazards to human health. Previous studies have reported that PBDEs exposure could induce oxidative stress and disturb mitochondrial functions in mammalian cells. However, the toxicological mechanism remains to be clarified. In this work, the neurotoxic effect and underlying mechanism of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) was investigated by using human neuroblastoma SK-N-SH cells as an effective model. A liquid chromatography-mass spectrometry (LC-MS)-based metabolomics approach combined with cell viability assay was applied to elucidate the metabolic perturbations and relevant toxicological pathways upon BDE-47 exposure. Our results shown that the SK-N-SH cell viability decreased in a dose-dependent manner after exposure to BDE-47 at 24 h within the concentration range of 5-250 µM, and an IC50 value of 88.8 µM was obtained. Based on the dose-response curve and cell morphological observation, the 5 and 10 µM BDE-47 doses (equal to IC5 and IC10, respectively) were used for metabolomics study to capture the sensitive metabolic response following BDE-47 exposure. After BDE-47 treatment, nine metabolites were identified as potential biomarkers, and the most disturbed metabolic pathways were mainly involved in alanine, aspartate and glutamate metabolism, glutathione metabolism, tyrosine and phenylalanine metabolism, and pyrimidine metabolism, which imply that metabolic changes related to neurotransmitters, oxidative stress, and nucleotide-mediated signal transduction systems were the sensitive pathways mostly influenced. Our findings reported here may provide potential neurotoxic effect biomarkers and prompt deep understanding of the molecular and metabolic mechanisms triggered by BDE-47 exposure.


Assuntos
Ácido Glutâmico/metabolismo , Éteres Difenil Halogenados/toxicidade , Pirimidinas/metabolismo , Biomarcadores/metabolismo , Linhagem Celular Tumoral , Sobrevivência Celular , Humanos , Metabolômica/métodos , Mitocôndrias/metabolismo , Neuroblastoma , Síndromes Neurotóxicas/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Testes de Toxicidade
18.
Toxicol Mech Methods ; 29(8): 569-579, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31161897

RESUMO

The present study investigated the alterations in nerve function and its potential mechanism of offspring result from the decabromodiphenyl ether (BDE209) orally gavage (0, 1.5, and 225 mg/kg.d body weight) in pregnant and lactating mice. Weight gain and litter size of maternal mice and body weight of offspring were examined. Learning and memory abilities of offspring were tested by the Morris water maze experiment. Thyroid hormones (THs) concentrations in peripheral blood of offspring were detected by the chemiluminescence enzyme immunoassay. Relative mRNA expression of type 1 iodothyronine deiodinase (dio1), type 2 iodothyronine deiodinase (dio2), and type 3 iodothyronine deiodinase (dio3) in the livers and brains of offspring were measured by QRT-PCR (quantitative real-time polymerase chain reaction). Protein expression of dio3 in the livers and brains of offspring was measured by Western blot. All indexes of offspring were tested at postnatal day (PND) 21 and PND 60, respectively. As a result, administration of BDE209 decreased weight gain and litter size of maternal mice, and reduced body weight of offspring mice, prolonged escape latency and declined guardant time of offspring in the Morris water maze experiment. Moreover, BDE209 elevated serum levels of total thyroxine (T4), total triiodothyronine (T3), free T4, and free T3 in offspring. In addition, maternal exposure to BDE209 inhibited dio1, dio2, dio3 mRNA expression in the livers of offspring, while elevated dio1 mRNA expression and reduced dio3 mRNA expression in the brains of offspring. BDE209 also inhibited the protein expression of dio3 in the livers and brains of offspring. These results indicate that BDE209 exposure to pregnant and lactating mice can cause disruption in serum THs of offspring by altering mRNA and protein expression of iodothyronine deiodinases, which might consequently result in neurologic impairment of offspring mice.


Assuntos
Poluentes Ambientais/toxicidade , Éteres Difenil Halogenados/toxicidade , Iodeto Peroxidase/genética , Exposição Materna/efeitos adversos , Neurônios/efeitos dos fármacos , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Transcrição Genética/efeitos dos fármacos , Animais , Animais Recém-Nascidos , Feminino , Lactação , Masculino , Aprendizagem em Labirinto/efeitos dos fármacos , Camundongos Endogâmicos ICR , Gravidez , Natação , Hormônios Tireóideos/sangue
19.
Ecotoxicol Environ Saf ; 180: 705-714, 2019 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-31151067

RESUMO

Heavy metals and polybrominated diphenyl ethers (PBDEs) are ubiquitous pollutants at electronic waste (e-waste) contaminated sites, their individual impacts on soil microbial community has attracted wide attention, however, limited research is available on the combined effects of heavy metals and PBDEs on microbial community of e-waste contaminated. Therefore, combined effects of heavy metals and PBDEs on the microbial community in the e-waste contaminated soil were investigated in this study. Samples were collected from Ziya e-waste recycling area in Tianjin, northern China, and the soil microbial communities were then analyzed by the high-throughput MiSeq 16S rRNA sequencing to assess the effects of soil properties, heavy metals, and PBDEs on the soil microbial community. Candidatus Nitrososphaera, Steroidobacter and Kaistobacter were the dominant microbial species in the soils. Similar microbial metabolic functions, including amino acid metabolism, carbohydrate metabolism and membrane transport, were found in all soil samples. Redundancy analysis and variation partition analysis revealed that the microbial community was mainly influenced by PBDEs (including BDE 183, BDE 99, BDE 100 and BDE 154) in horizontal soil samples. However, TN, biomass, BDE 100, BDE 99 and BDE 66 were the major drivers shaping the microbial community in vertical soil samples.


Assuntos
Resíduo Eletrônico , Éteres Difenil Halogenados/toxicidade , Metais Pesados/toxicidade , Microbiota/efeitos dos fármacos , Microbiologia do Solo , China , Resíduo Eletrônico/análise , Monitoramento Ambiental , Éteres Difenil Halogenados/análise , Metais Pesados/análise , Microbiota/genética , Microbiota/fisiologia , RNA Ribossômico 16S/genética , Solo/química , Poluentes do Solo/análise , Poluentes do Solo/toxicidade
20.
Chemosphere ; 233: 174-182, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31173955

RESUMO

Emerging evidence suggests environmental contaminant exposures during critical windows of development may contribute to the increasing prevalence of obesity. It has been shown that early life polybrominated diphenyl ethers exposures have critical impacts on child weight trajectories, however, little is known about their maternal mechanisms responsible for offspring obesity development. In this study, we investigated the effects of perigestational low-dose 2, 2', 4, 4'-tetrabromodiphenyl ether (BDE-47) exposure on maternal metabolome, and its possible link to adult offspring bodyweight changes. Female Sprague-Dawley rats were exposed to daily doses of 0.1, or 1 mg/kg BDE-47 from 10 days prior to conception until offspring were weaned on postnatal day 21, and then a gas chromatography-mass spectrometry based metabolomics analysis was used to uncover the global metabolic response in dams. The pups continued to grow into adulthood for measurements of bodyweight. Perigestational BDE-47 exposure caused increased adult bodyweight in male but not in female offspring and dams. Metabolomics revealed significant changes in maternal serum metabolites that clearly distinguish BDE-47 from control rats. These differentially expressed metabolites were primarily implicated in amino acid, lipid, carbohydrate, and energy metabolisms, which was confirmed by pathway analysis. Importantly, most of these identified metabolites were decreased, a state similar to maternal malnutrition that can predispose adult male offspring to weight increase and adiposity in a postnatal environment with abundant calories. Collectively, our data suggest that perigestational exposure to low-dose BDE-47 produces altered maternal serum metabolome, which may be an additional contributing factor to weight gain in adult male offspring.


Assuntos
Peso Corporal/efeitos dos fármacos , Éteres Difenil Halogenados/toxicidade , Exposição Materna/efeitos adversos , Metaboloma/efeitos dos fármacos , Animais , Relação Dose-Resposta a Droga , Poluentes Ambientais/administração & dosagem , Poluentes Ambientais/toxicidade , Feminino , Cromatografia Gasosa-Espectrometria de Massas , Éteres Difenil Halogenados/administração & dosagem , Lactação , Masculino , Gravidez , Efeitos Tardios da Exposição Pré-Natal , Ratos Sprague-Dawley , Ganho de Peso/efeitos dos fármacos
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