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1.
Environ Pollut ; 274: 116605, 2021 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-33545521

RESUMO

Estuarine ecosystems near mega-cities are sinks of anthropogenic endocrine disrupting chemicals (EDCs). As the most important primary producer, indigenous microalgae and their secreted extracellular polymeric substances (EPSs) might interact with EDCs and contribute to their fate and risk. Tetraselmis sp. is a representative model of estuarine microalga, for which EDC toxicity and its effects on EPS synthesis have rarely been studied. Through microalgal isolation, algal cell growth tests, EDC removal and the characterization of related EPS profiles, the present work intends to clarify the comparative responses of Tetraselmis sp. to nonylphenol (NP), bisphenol A (BPA) and 17α-ethinylestradiol (EE2). The results showed that the half inhibitory concentration on cell growth was 0.190-0.313 mg/dm3 for NP, which was one order of magnitude lower than the comparable values for BPA and EE2 at 2.072-3.254 mg/dm3. Regarding chlorophyll, NP induced its degradation, EE2 led to its decreased production, and BPA had no obvious effect. Under EDC stress, only the concentrations of colloidal polysaccharides and proteins responded dose-dependently to EE2. Except for the colloidal fraction in the EE2 treatment group, the increase in neutral monosaccharides, especially glucose and galactose, was a common response to EDCs. Compared to the recalcitrant BPA, NP underwent abiotic degradation in alga-free water, and EE2 could be biodegraded in water containing this microalga. The chemical-specific responses of cell growth, chlorophyll and related EPS profiles were driven by the different fates of EDCs, and the underlying mechanism was further discussed. The results obtained in the present work are of critical importance for understanding the fate and effects of different EDCs mediated by microalgae and their related EPSs.


Assuntos
Disruptores Endócrinos , Poluentes Químicos da Água , Compostos Benzidrílicos/toxicidade , Ecossistema , Disruptores Endócrinos/análise , Disruptores Endócrinos/toxicidade , Etinilestradiol/análise , Etinilestradiol/toxicidade , Matriz Extracelular de Substâncias Poliméricas/química , Fenóis , Poluentes Químicos da Água/análise , Poluentes Químicos da Água/toxicidade
2.
Ecotoxicol Environ Saf ; 211: 111923, 2021 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-33493725

RESUMO

Bisphenol A (BPA), as a phenolic compound, is harmful to human health, and its residue in the aquatic environment also threatens the health of aquatic animals. In this research, the toxicity effects of BPA on liver tissues were evaluated in common carp (Cyprinus carpio) after long-term exposure. Fish were exposed to five concentrations of BPA (0, 0.01, 0.1, 0.5 and 2 mg/L) for 30 days. The blood and liver tissues were gathered to analyze biochemical indices and genes transcription levels. The data related to lipid metabolism showed that BPA exposure increased serum total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) levels, upregulated the expressions of fatp1, pparγ, fas, atgl, hsl, pparα, cpt1b, acox-1, and downregulated the expression of dgat1 in liver. Antioxidative parameters displayed a reduced antioxidant ability and increased lipid peroxidation after BPA exposure. Meanwhile, the upregulations of nrf2, ho-1, cyp1a and cyp1b genes revealed an adaptive response mechanism against oxidative stress-induced adverse effects. After 30 days of exposure, BPA induced apoptosis and endoplasmic reticulum stress (ERS) via upregulating the expression levels of apoptosis and ERS-related genes and increasing Ca2+ concentration in liver. Moreover, the downregulation of mtor and the upregulation of atg3, atg7, tfeb, uvrag and mcoln1 indicated that BPA could influence the normal process of autophagy. Furthermore, BPA exposure activated toll like receptors (TLRs) pathway to mediate the inflammatory response. Our results demonstrated that BPA exposure disturbed lipid metabolism, and induced oxidative stress, ERS, apoptosis, autophagy and inflammatory response in the liver of common carp. These findings contributed to the understanding of hepatotoxicity mechanism induced by BPA in fish.


Assuntos
Autofagia/efeitos dos fármacos , Compostos Benzidrílicos/toxicidade , Imunidade/efeitos dos fármacos , Metabolismo dos Lipídeos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Fenóis/toxicidade , Poluentes Químicos da Água/toxicidade , Animais , Antioxidantes/metabolismo , Apoptose , Carpas/metabolismo , Carpas/fisiologia , Estresse do Retículo Endoplasmático , Humanos , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/fisiologia , Estresse Oxidativo/efeitos dos fármacos
3.
Mar Pollut Bull ; 163: 111931, 2021 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-33418343

RESUMO

Endocrine disrupting compounds (EDCs) in marine environments has become a major environmental concern. Nonetheless, the biological effects of EDCs on organisms in coastal environments remain poorly characterized. In this study, biomonitoring of EDCs in male fish Sebastiscus marmoratus was carried out in the Maowei Sea, China. The results showed that the concentration of 4-nonylphenol (4-NP) was below the detection limit, the concentrations of 4-tert-octylphenol (4-t-OP) and bisphenol A (BPA) in seawater were moderate compared with those in other global regions, and the possible sources are the municipal wastewater discharge. Nested ANOVA analyses suggest significant differences of the brain aromatase activities and plasma vitellogenin (VTG) expression between the port area and the oyster farming area. A new fish expert system (FES) was developed for evaluating the biological effects of EDCs on fish. Our findings show that the FES is a potential tool to evaluate the biological effects of marine pollutants.


Assuntos
Disruptores Endócrinos , Perciformes , Poluentes Químicos da Água , Animais , Compostos Benzidrílicos/análise , Compostos Benzidrílicos/toxicidade , China , Disruptores Endócrinos/análise , Disruptores Endócrinos/toxicidade , Monitoramento Ambiental , Masculino , Poluentes Químicos da Água/análise , Poluentes Químicos da Água/toxicidade
4.
Environ Pollut ; 271: 116380, 2021 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-33387779

RESUMO

A vast amount of evidence indicates that bisphenol A (BPA) and phthalates are widely distributed in the environment since these compounds are mass-produced for the manufacture of plastics and plasticizers. These compounds belong to a large group of substances termed endocrine-disrupting chemicals (EDC). It is well known that humans and living organisms are unavoidably and unintentionally exposed to BPA and phthalates from food packaging materials and many other everyday products. BPA and phthalates exert their effect by interfering with hormone synthesis, bioavailability, and action, thereby altering cellular proliferation and differentiation, tissue development, and the regulation of several physiological processes. In fact, these EDC can alter fetal programming at an epigenetic level, which can be transgenerational transmitted and may be involved in the development of various chronic pathologies later in the adulthood, including metabolic, reproductive and degenerative diseases, and certain types of cancer. In this review, we describe the most recent proposed mechanisms of action of these EDC and offer a compelling selection of experimental, epidemiological and clinical studies, which show evidence of how exposure to these pollutants affects our health during development, and their association with a wide range of reproductive, metabolic and neurological diseases, as well as hormone-related cancers. We stress the importance of concern in the general population and the urgent need for the medical health care system to closely monitor EDC levels in the population due to unavoidable and involuntary exposure to these pollutants and their impact on human health.


Assuntos
Disruptores Endócrinos , Exposição Ambiental , Adulto , Compostos Benzidrílicos/toxicidade , Política de Saúde , Humanos , Fenóis/toxicidade
5.
Environ Pollut ; 271: 116304, 2021 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-33401208

RESUMO

Epidemiological studies have demonstrated that the general population's exposure to bisphenol A (BPA) substitutes is ubiquitous. Bisphenol F (BPF), one of the main BPA substitutes, is increasingly replacing BPA in plastics for food and beverage applications. Accumulating evidence suggests that BPA exposure is associated with nonalcoholic fatty liver disease (NAFLD)-like changes. However, the potential effects of BPF on lipid homeostasis remain poorly understood. In the present study, an epidemiological analysis with LC-MS-MS revealed that the BPF concentrations in the serum of NAFLD patients were significantly higher than those in a control group. Supporting this result, using Oil Red O, BODIPY 493/503, LipidTox Deep Red staining and gas chromatography-time-of-flight mass spectrometry (TOF-MS) assays, we found that BPF exposure induced NAFLD-like changes, with obvious lipid droplet deposition, triglyceride (TG) and fatty acids increase in mouse livers. Meanwhile, lipid droplet deposition and TG increase induced by BPF were also observed in HepG2 cells, accompanied by autophagic flux blockade, including autophagosome accumulation and the decreased degradation of SQSTM1/p62. Using adenoviruses dual-reporter plasmid RFP-GFP-LC3, RFP-GFP-PLIN2 transfection, AO staining, and EGFR degradation assays, we demonstrated that BPF treatment impaired lysosomal degradative capacity, since BPF treatment obviously impaired lysosomal acidification, manifested as decreased lysosomal hydrolase cathepsin L (CTSL) and mature cathepsin D (CTSD) in HepG2 and mouse liver issues. Additionally, v-ATPase D, a multi-subunit enzyme that mediates acidification of eukaryotic intracellular organelles, significantly decreased after BPF exposure in both the vitro and in vivo studies. This study ascertained a novel mechanism involving dysfunctional of lysosomal degradative capacity induced by BPF, which contributes to lipophagic disorders and causes lipid droplet deposition. This work provides evidence that lysosomes may be a target organelle where BPF exerts its potential toxicity; therefore, novel intervention strategies targeting lysosome are promising for BPF-induced NAFLD-like changes.


Assuntos
Hepatopatia Gordurosa não Alcoólica , Animais , Compostos Benzidrílicos/toxicidade , Humanos , Gotículas Lipídicas , Lisossomos , Camundongos , Hepatopatia Gordurosa não Alcoólica/induzido quimicamente , Fenóis
6.
Sci Total Environ ; 758: 144003, 2021 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-33321361

RESUMO

Bisphenol A-BPA, a widespread plastic additive, is an emerging contaminant of high concern and a potential endocrine disruptor in mammals. BPA also represents a potential threat for aquatic species, especially for larval stages. In the marine bivalve Mytilus galloprovincialis, BPA has been previously shown to affect early larval development and gene transcription. In this work, the effects of BPA (0.05-0.5-5 µM) were further investigated at different times post fertilization (24-28-32-48 hpf). BPA induced concentration-dependent alterations in deposition of the organic matrix and calcified shell at different larval stages, as shown by double calcofluor/calcein staining, resulting in altered phenotypes at 48hpf. Transcription of Tyrosinase-TYR, that plays a key role in remodelling of the shell organic matrix, and of HOX1, a member of homeobox genes involved in larval shell formation and neurogenesis, were evaluated by In Situ Hybrydization-ISH. BPA altered the spatial pattern of expression of both genes, with distinct effects depending on the concentration and developmental stage. Moreover, BPA affected the time course of mRNA levels for TYR from 24 to 48hpf. BPA impaired development of serotonin-5-HT-immunoreactive neurons at different times pf; at 48hpf, the reduction in the number of serotoninergic neurons was associated with developmental delay and downregulation of the 5-HT receptor-5-HTR. All the effects were observed from the lowest concentration tested, corresponding to detectable BPA levels in contaminated coastal waters. These data demonstrate that BPA interferes with key processes occurring during the first developmental stages of mussels, thus representing a potential threat for natural populations.


Assuntos
Mytilus , Animais , Compostos Benzidrílicos/toxicidade , Larva , Fenóis/toxicidade
7.
Chemosphere ; 263: 128020, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33297044

RESUMO

Bisphenol A (BPA) is an endocrine-disrupting compound that impairs testosterone synthesis in male mammals. A circadian clock gene deficiency leads to diminished fertility and even infertility in male mice. However, whether circadian clock signaling pathways mediate the suppressive effect of BPA on testosterone synthesis in Leydig cells (LCs) remains unknown. The present study aims to detect the effect of BPA on cellular circadian clock and testosterone synthesis in mouse LCs, and examine the mechanisms underlying NR1D1 signaling. BPA treatment significantly attenuated the transcription levels of Nr1d1 and steroidogenic genes (Hsd3b2 and Hsd17b3) in TM3 cells, but increased other circadian clock gene levels (Per2 and Dbp). BPA treatment also significantly downregulated NR1D1 and StAR protein expression, but upregulated BMAL1 protein expression in TM3 cells. Furthermore, there was a marked decline in testosterone production in BPA-treated TM3 cells. Intraperitoneal injection of BPA profoundly reduced NR1D1 and StAR protein levels and steroidogenic gene transcription levels (Cyp11a1, Hsd3b2, and Hsd17b3), while enhancing BMAL1 protein and other circadian clock gene (Per2 and Dbp) levels in mouse testes. Notably, serum testosterone levels were also drastically reduced in BPA-treated mice. Moreover, SR9009, an NR1D1 agonist, augmented testosterone production in TM3 cells via elevated expression of steroidogenic genes (StAR, Cyp11a1 and Hsd17b3). Conversely, Nr1d1 knockdown inhibited testosterone accumulation and attenuated steroidogenic gene expression. Moreover, treatment with SR9009 partially reversed the BPA effect on the circadian clock and testosterone production. Taken together, our study demonstrates that BPA perturbs testosterone production, at least partially, via inhibiting NR1D1 signaling in LCs.


Assuntos
Células Intersticiais do Testículo , Testosterona , Fatores de Transcrição ARNTL , Animais , Compostos Benzidrílicos/toxicidade , Masculino , Camundongos , Membro 1 do Grupo D da Subfamília 1 de Receptores Nucleares , Fenóis
8.
Chemosphere ; 263: 128203, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33297166

RESUMO

This study summarizes the knowledge about effects of bisphenol A (BPA) and its analogues on reproduction of pigs and some parameters of their offspring during period 2011-2020. Bisphenols are known as one of the most harmful environmental toxicants with endocrine-disrupting properties. One study in the reference period related to male reproductive system. Treatment with an antagonist of G-protein coupled estrogen receptor (GPER) - G15, and bisphenol A and its analogues, tetrabromobisphenol A (TBBPA) and tetrachromobisphenol A (TCBPA) diversely disrupted protein molecules controlling the biogenesis and function of microRNA in Leydig cells. Nine studies examined the effect of BPA, bisphenol S (BPS) or fluorene-9-bisphenol (BHPF) on female reproductive system. From the possible protective effect's point of view seems to be perspective the administration of melatonin in BPA-exposed oocytes. Finally, two studies were found to evaluate the maternal exposure to BPA on offspring's meat quality, muscle metabolism and oxidative stress. Administration of methyl donor improved antioxidant enzymes activity and reduced oxidative stress in piglets.


Assuntos
Disruptores Endócrinos , Animais , Compostos Benzidrílicos/toxicidade , Disruptores Endócrinos/toxicidade , Feminino , Células Intersticiais do Testículo , Masculino , Fenóis , Suínos
9.
Chemosphere ; 263: 128307, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33297244

RESUMO

Bisphenol A (BPA) and Diethylhexyl Phthalate (DEHP) are well-studied endocrine disrupting chemicals (EDCs), however, the effects of mixtures of these EDCs are not. To assess the consequences of prenatal exposure to a mixture of these EDCs, dams were orally administered either saline (control), BPA (5 µg/kg BW/day), high dose DEHP (HD-D; 7.5 mg/kg BW/day), or a combination of BPA with HD-D in experiment 1; saline, BPA (5 µg/kg BW/day), low-dose DEHP (LD-D; 5 µg/kg BW/day) or a combination of BPA with LD-D in experiment 2. Gestational weights, number of abortions, litter size and weights, number of live births and stillbirths were recorded. Morphometric measures were obtained at birth and body weight, food and water intake were monitored weekly from postnatal weeks 3-12. Offspring were sacrificed at 16-24 weeks of age and organ weights were measured. The abortion rate of dams exposed to HD-D and the mixtures, BPA + LD-D and BPA + HD-D were higher at 9, 14 and 27% respectively. Prenatal exposure to BPA or HD-D significantly decreased relative thymus weights in male but not female offspring. Apoptotic cells were detected in thymus sections of both male and female offspring prenatally exposed to DEHP. Relative heart weights increased in BPA + HD-D exposed male offspring compared to the other groups. The results indicate that a mixture of BPA and DEHP, produced a pronounced effect on pregnancy outcomes. Male offspring appear to be more susceptible to the programming effects of these EDCs or their mixture suggesting a need to reconsider the possible additive, antagonistic or synergistic effects of EDC mixtures.


Assuntos
Dietilexilftalato , Disruptores Endócrinos , Efeitos Tardios da Exposição Pré-Natal , Animais , Compostos Benzidrílicos/toxicidade , Dietilexilftalato/toxicidade , Disruptores Endócrinos/toxicidade , Feminino , Humanos , Masculino , Fenóis , Gravidez , Resultado da Gravidez , Ratos , Ratos Sprague-Dawley
10.
Chemosphere ; 262: 128045, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33182117

RESUMO

The vulnerability to environmental insults is heightened at early stages of development. However, the neurotoxic potential of bisphenol A (BPA) and bisphenol S (BPS) at developmental windows remains unclear. To investigate the mechanisms mediating the developmental neurotoxicity, zebrafish embryos were treated with 0.01, 0.03, 0.01, 0.3, 1 µM BPA/BPS. Also, we used Tg(HuC:GFP) zebrafish to investigate whether BPA/BPS could induce neuron development. The reduction in body length, and increased heart rate were significant in 0.3 and 1 µM BPA/BPS groups. The green fluorescence protein (GFP) intensity increased at 72 hpf and 120 hpf in Tg(HuC:GFP) larvae which was consistent with the increased mRNA expression of elval3 following BPS treatments, an indication of the plausible effect of BPS on embryonic neuron development. Additionally, BPA/BPS treatments elicited hyperactivity and reduced static time in zebrafish larvae, suggesting behavioral alterations. Moreover, qRT-PCR results showed that BPA and BPS could interfere with the normal expression of development-related genes vegfa, wnt8a, and mstn1 at the developmental stages. The expression of neurodevelopment-related genes (ngn1, elavl3, gfap, α1-tubulin, mbp, and gap43) were significantly upregulated in BPA and BPS treatments, except for the remarkable downregulation of mbp and gfap elicited by BPA at 48 (0.03 µM) and 120 hpf (0.3 µM) respectively; ngn1 at 48 hpf for 0.1 µM BPS. Overall, our results highlighted that embryonic exposure to low concentrations of BPA/BPS could be deleterious to the central nervous system development and elicit behavioral abnormalities in zebrafish at developmental stages.


Assuntos
Compostos Benzidrílicos/toxicidade , Embrião não Mamífero/efeitos dos fármacos , Desenvolvimento Embrionário/efeitos dos fármacos , Neurogênese/efeitos dos fármacos , Fenóis/toxicidade , Sulfonas/toxicidade , Poluentes Químicos da Água/toxicidade , Peixe-Zebra , Animais , Embrião não Mamífero/metabolismo , Larva/efeitos dos fármacos , Larva/metabolismo , Peixe-Zebra/metabolismo , Proteínas de Peixe-Zebra/metabolismo
11.
Ecotoxicol Environ Saf ; 207: 111299, 2021 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-32927158

RESUMO

The analogues of biphenol A (BPA), including bisphenol S (BPS) and bisphenol B (BPB), are commonly used to replace the application of BPA in containers and wrappers of daily life. However, their safeties are questioned due to their similar chemical structure and possible physiological effects as BPA. To investigate the neurotoxic effects of BPA, BPS, and BPB as well as their underlying mechanism, IMR-32 cell line from male and SK-N-SH cell line from female were exposed respectively to BPA, BPS and BPB with concentrations of 1 nM, 10 nM, 100 nM, 1 µM, 10 µM, and 100 µM for 24 h. Additionally, 24 h exposure of BPA combining epigallocatechin gallate (EGCG) (4 µM and 8 µM for IMR-32 and SK-N-SH respectively) were conducted. Results demonstrated that BPs exposure could promote reactive oxygen species production and increase level of malondialdehyde (MDA) while decrease levels of superoxide dismutase (SOD). Intensive study revealed that after exposure to BPA mitochondrial membrane potential (MMP) dropped down and the protein expression levels of Bak-1, Bax, cytochrome c and Caspase-3 were up-regulated but Bcl-2 were down-regulated significantly. Moreover, apoptosis rate was raised and cell activity declined remarkably in the neuroblastoma cells. All the effects induced by BPA could be alleviated by the adding of EGCG, which similar alleviations could be inferred in IMR-32 and SK-N-SH cells induced by BPS and BPB. Furthermore, BPS showed lower neurotoxic effects compared to BPA and BPB. Interestingly, the neurotoxic effects of BPA on IMR-32 cells were significantly higher than those on SK-N-SH cells. In conclusion, the results suggested that BPA, BPS and BPB could induce oxidative stress and apoptosis via mitochondrial pathway in the neuroblastoma cells and male is more susceptible to BPs than female.


Assuntos
Apoptose/efeitos dos fármacos , Compostos Benzidrílicos/toxicidade , Disruptores Endócrinos/toxicidade , Mitocôndrias/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Fenóis/toxicidade , Sulfonas/toxicidade , Caspase 3/metabolismo , Linhagem Celular Tumoral , Relação Dose-Resposta a Droga , Feminino , Humanos , Masculino , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Caracteres Sexuais
12.
Chemosphere ; 262: 127880, 2021 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-32777607

RESUMO

BACKGROUND: Bisphenol A (BPA) is a well-known endocrine disruptor that affects male fertility. However, the main biological events through which BPA affects spermatogenesis remain to be identified. METHODS: Adult male mice were treated by feeding with drinking water containing BPA (0.2 µg/ml, 20 µg/ml, 200 µg/ml, respectively) for two months. Testes were collected for protein extraction or for immunohistochemical analysis. Epididymal spermatozoa were collected for sperm quality evaluation and male fertility assay by in vitro fertility (IVF). Serums were collected for detection of testosterone levels. Proteins associated with germ cell proliferation, meiosis, blood-testis barrier, and steroidogenesis production were examined in BPA-treated and control mice testes. CCK8 assay was used to detect the effect of BPA on the proliferation of GC-1 and GC-2 cells. RESULTS: The BPA-treated mice were characterized by decreased sperm quality, serum testosterone levels and, sub-fertile phenotype characterizing with low pregnancy rates and reduced fertilization efficiency. In lower BPA (0.2 µg/ml) treatment, PCNA and PLZF were down-expressed that indicated impaired germ cell proliferation. SYCP3 was down-expressed in BPA-treated mice, but expressions of other proteins associated with meiosis and blood-testis barrier were not significantly altered. CYP11A1 and HSD3B1 were down-expressed in BPA-treated mice that demonstrated reduced steroidogenesis activity. BPA has a concentration-dependent inhibition effect on the proliferation of GC-1 and GC-2 cells. Conclusively, low doses BPA exposure reduced mice sperm quality mainly by impairing germ cell proliferation, leading to reduced male fertility. The study would provide relevant information for investigation on molecular mechanisms and protective strategy on male production.


Assuntos
Compostos Benzidrílicos/toxicidade , Disruptores Endócrinos/toxicidade , Fenóis/toxicidade , Espermatozoides/fisiologia , Animais , Proliferação de Células/efeitos dos fármacos , Disruptores Endócrinos/metabolismo , Epididimo/efeitos dos fármacos , Feminino , Fertilidade/efeitos dos fármacos , Masculino , Camundongos , Gravidez , Espermatogênese/efeitos dos fármacos , Espermatozoides/efeitos dos fármacos , Testículo/efeitos dos fármacos , Testes de Toxicidade Crônica
13.
Sci Total Environ ; 750: 141685, 2021 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-32862004

RESUMO

Human exposure to bisphenol A (BPA) is unavoidable in daily life. Recently, research has showen that BPA could induce oxidative imbalance, thereby causing reproductive toxicity and liver dysfunction. Accumulated evidence has demonstrated that metformin possesses strong anti-oxidative properties. This study aimed to study the mechanism underlying the hepatic-protective effect of metformin on liver injury induced by BPA in rats via the UPLC-MS/MS metabolomics approach. Forty-two male rats were randomly divided into six groups (n = 7), namely the saline group (control), the corn oil group (vehicle), the metformin group (Met), the bisphenol A group (BPA), the bisphenol A and metformin group (BPA + Met), and the bisphenol A and diammonium glycyrrhizinate (positive control) group (BPA + DG). Serum was collected for biochemical analysis and metabolomics, and liver tissue was collected for histopathology and metabolomics in each group. We found that metformin could significantly reduce the levels of liver function enzymes (ALT, AST and GGT) and ameliorate inflammatory cell infiltration and hepatocyte necrosis induced by BPA. On the other hand, metformin could significantly enhance the total antioxidant capacity in BPA rats. Notably, metabolomics data indicated that the principal altered metabolic pathways based on the 26 differential metabolites in liver tissue, and 21 in serum among vehicle, BPA and BPA + Met groups, respectively, including cysteine and methionine metabolism, glutathione metabolism, and arginine biosynthesis and purine metabolism. Additionally, metformin significantly increased cystathionine ß synthase (CBS) and cystathionine γ lyase (CSE), thus reducing serum levels of homocysteine and increasing hepatic levels of cysteine and glutathione in BPA-treated rats. Overall, this study's results provided new insights into the role and mechanism of metformin in BPA-induced liver injury in rats.


Assuntos
Cistationina gama-Liase , Metformina , Animais , Compostos Benzidrílicos/toxicidade , Cromatografia Líquida , Cistationina beta-Sintase/metabolismo , Cistationina gama-Liase/metabolismo , Humanos , Fígado/metabolismo , Masculino , Metformina/toxicidade , Fenóis , Ratos , Espectrometria de Massas em Tandem , Regulação para Cima
14.
Sci Total Environ ; 753: 141949, 2021 Jan 20.
Artigo em Inglês | MEDLINE | ID: mdl-32891999

RESUMO

Bisphenol S (BPS) is the major substitute for the production of bisphenol A (BPA)-free products and detected in both food and environment. Although the relationship between BPA exposure and increased risk of obesity and diabetes has been noted, the potential influence of BPS is not fully understood. Herein, a non-targeted lipidomic study was performed to explore BPA/BPS exposure actions using the 3T3-L1 preadipocyte differentiation model, and revealed the comprehensive lipidome disturbance induced by either BPA or BPS exposure at different doses of 0.01, 1 and 100 µM. BPA was more potent than BPS in disturbance of lipid metabolism. A considerable similarity of BPS exposure to BPA was discovered. The key lipid remodeling in response to exposure was found to involve the cardiolipins, phosphatidylglycerols and fatty acids metabolic pathways, providing novel clues of potential mechanism in which both BPA and BPS exposure could be associated with increased risk of insulin resistance. Our study supplies the perspective into the lipidome response to environmental stress induced by BPA/BPS, and shows that BPA-free products are not necessarily safer. Substitution of BPA by its structural analog BPS should be therefore performed with caution.


Assuntos
Compostos Benzidrílicos , Lipidômica , Animais , Compostos Benzidrílicos/toxicidade , Camundongos , Fenóis/toxicidade , Sulfonas
15.
Sci Total Environ ; 753: 141805, 2021 Jan 20.
Artigo em Inglês | MEDLINE | ID: mdl-32911163

RESUMO

Seahorses, with brood pouch in adult males, are a bioindicator species that exhibit specialized reproductive strategy of "male pregnancy". Bisphenol A (BPA), one of the most pervasive endocrine-disrupting chemicals (EDCs), is hazardous for reproductive, immune, and neurological systems. However, no evidence of BPA toxicity to the male-pregnant animals is available. Herein, the reproductive toxicity of BPA was evaluated in lined seahorses (Hippocampus erectus) following exposure to environmentally relevant concentrations (10, 100, and 1000 µg/L) through physiological, histological, and transcriptional analyses. Our results indicated BPA bioaccumulation to be positively correlated with exposure doses in both sexes. Ovarian failure was only observed in the high-dose BPA treatment group, accompanied by the apoptosis of follicular cells and up-regulation of pro-apoptotic genes. However, brood pouches maintenance were surprisingly inhibited at low concentration, and transcriptomic analysis revealed disturbed profiles of genes involved in the extracellular matrix and cell-cell adhesion pathways. Interestingly, seahorse testes were less sensitive to BPA exposure than that in other teleosts. Thus, our study suggests that BPA at environmentally relevant concentrations might cause reproductive dysfunction in seahorses, potentially exerting adverse effects on the seahorse population since most of them inhabit shallow coastal areas with prevalent estrogenic contaminants.


Assuntos
Disruptores Endócrinos , Smegmamorpha , Animais , Compostos Benzidrílicos/toxicidade , Bioacumulação , Disruptores Endócrinos/toxicidade , Feminino , Masculino , Fenóis/toxicidade
16.
Chemosphere ; 268: 129273, 2021 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-33352513

RESUMO

Due to its widespread applications and its ubiquitous occurrence in the environment, bisphenol A (BPA) and its alternatives have gained increasing attention, especially in terms of human safety. Like BPA, alternatives such as bisphenol S (BPS), bisphenol F (BPF), and bisphenol AF (BPAF) have also been identified to be endocrine-disrupting chemicals (EDCs). Hence, in this study, we reviewed the literature of BPA and its alternatives mainly published between the period 2018-2020, including their occurrences in the environment, human exposure, and adverse health effects. The review shows that bisphenols are prevalent in the environment with BPA, BPS, and BPF being the most ubiquitous in the environment worldwide, though BPA remains the most abundant bisphenol. However, the levels of BPS and BPF in different environmental media have been constantly increasing and their fates and health risks are being evaluated. The studies show that humans and animals are exposed to bisphenols in many different ways through inhalation and ingestion and the exposure can have serious health effects. Urinary bisphenols (BPs) levels were frequently reported to be positively associated with different health problems such as cancer, infertility, cardiovascular diseases, diabetes and neurodegenerative diseases. Our literature study also shows that BPs generate reactive oxygen species and disrupt various signalling pathways, which could lead to the development of chronic diseases. Activated carbon-based and chitosan-based sorbents have been widely utilized in the removal of BPA in aqueous solutions. In addition, enzymes and microorganisms have also been getting much attention due to their high removal efficiencies.


Assuntos
Compostos Benzidrílicos , Disruptores Endócrinos , Animais , Compostos Benzidrílicos/toxicidade , Carvão Vegetal , Disruptores Endócrinos/toxicidade , Humanos , Fenóis , Água
17.
J Toxicol Sci ; 45(10): 639-650, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33012732

RESUMO

Bisphenol A (BPA), an endocrine disruptor with estrogenic effects, is widely used as a raw material for manufacturing polycarbonate plastic and epoxy resins. Prenatal and postnatal exposure to BPA affects brain morphogenesis. However, the effects of prenatal and postnatal BPA exposure on postnatal neurogenesis in mice are poorly understood. In this study, we developed a mouse model of prenatal and postnatal BPA exposure and analyzed its effects on hippocampal neurogenesis. The hippocampal dentate gyrus is vulnerable to chemical exposure, as neurogenesis continues in this region even after birth. Our results showed that in mice, prenatal and postnatal BPA exposure decreased the number of type-1, 2a, 2b, and 3 neural progenitor cells, as well as in granule cells, in the hippocampal dentate gyrus on postnatal days 16 and 70. The effect of prenatal and postnatal BPA exposure on neural progenitors were affected at all differentiation stages. In addition, prenatal and postnatal BPA exposure affects the maintenance of long-term memory on postnatal day 70. Our results suggest that neurodevelopmental toxicity due to prenatal and postnatal BPA exposure might affect postnatal morphogenesis and functional development of the hippocampal dentate gyrus.


Assuntos
Animais Recém-Nascidos , Compostos Benzidrílicos/toxicidade , Giro Denteado/efeitos dos fármacos , Disruptores Endócrinos/toxicidade , Hipocampo/efeitos dos fármacos , Exposição Materna/efeitos adversos , Troca Materno-Fetal/efeitos dos fármacos , Células-Tronco Neurais/efeitos dos fármacos , Neurogênese/efeitos dos fármacos , Fenóis/toxicidade , Animais , Diferenciação Celular/efeitos dos fármacos , Feminino , Masculino , Camundongos , Modelos Animais , Gravidez
19.
Ecotoxicol Environ Saf ; 205: 111318, 2020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-32979806

RESUMO

The retention of polyether sulfone (PES) and bisphenol A (BPA) in wastewater has received extensive attention. The effects of PES and BPA on the removal of organic matter by anaerobic granular sludge were investigated. We also analyzed the changes in the electron transport system and the effects on the composition of extracellular polymeric substances (EPS), as well as alternations of the microbial community in the anaerobic granular sludge. In the experimental groups which received BPA, the removal of the chemical oxygen demand (COD) were significantly suppressed, which an average removal efficiency of less than 65%, 30% lower than that of the control group. In the loosely-bound EPS (LB-EPS) excitation-emission matrix (EEM) spectra, the absorption peak of tryptophan disappeared when the BPA pollutants was added, which it was present in the control group without added pollutants. The addition of PES and BPA also affected protease, acetate kinase, and coenzyme F420 activities in the anaerobic granular sludge. Especially, the coenzyme F420 reduced from 0.0045 to 0.0017 µmol/L in the presence of PES and BPA. The relative abundance of Spirochaetes decreased in the presence of PES and BPA, while the relative abundance of Bacteroidetes increased from 12.98% to 22.87%. At the genus level, in the presence of PES and BPA, the relative abundance of Acinetobacter increased from 2.20% to 9.64% and Hydrogenophaga decreased sharply from 15.58% to 0.12%.


Assuntos
Compostos Benzidrílicos/análise , Microplásticos/análise , Fenóis/análise , Polímeros/química , Sulfonas/química , Eliminação de Resíduos Líquidos , Anaerobiose , Compostos Benzidrílicos/toxicidade , Análise da Demanda Biológica de Oxigênio , Matriz Extracelular de Substâncias Poliméricas , Microbiota/efeitos dos fármacos , Microplásticos/toxicidade , Fenóis/toxicidade , Plásticos , Esgotos/química , Águas Residuárias
20.
Life Sci ; 260: 118410, 2020 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-32926927

RESUMO

AIMS: Methylsulfonylmethane (MSM), is an organosulfur compound, has many health benefits. Bisphenol-A (BPA) and γ-radiation (R) are two risky environmental contaminants that human beings are exposed to in everyday life. This work aims at unveiling the modulatory role of MSM in combating BPA and R co-exposure induced neurodegenerative disorder (Alzheimer's (AD)-mimic neurotoxicity). MAIN METHODS: Female rats were randomly divided into five groups. One group was normal control and the other four groups were subjected to subacute BPA intoxication and/or exposed to fractionated weekly doses of R for 4 weeks and either untreated or treated with MSM concomitantly. KEY FINDINGS: BPA and R co-exposure induced typical hallmarks of neurodegenerative disorders as revealed by tremendously elevated oxidative stress, extensive neuroinflammation (tumor necrosis factor -α and interleukin-1ß), elevated AD markers (amyloid-beta (Aß42), acetylcholinesterase (AchE) activity and tau-phosphorylation) in cortex and hippocampus as well as up-regulation of microglial pro-inflammatory triggering receptor expressed on myeloid cell-2(TREM-2)/DNAX-activating protein of 12 kDa (DAP-12)/spleen-tyrosine kinase (Syk) pathway and its downstream targets (PLC-γ/DAG/p38-MAPK) in hippocampus. Also, neurodegenerative lesions were revealed in histopathological examination of cortex and hippocampus coupled with marked Aß deposition in hippocampus. Whereas, MSM treatment improved histopathological insults and ameliorated level of oxidative stress, neuroinflammation and AD markers as well as modulated TREM-2/DAP-12/Syk pathway. SIGNIFICANCE: Our data suggest that MSM afforded neuroprotection against BPA and R; supporting its potential application in the associated neurodegenerative disorders.


Assuntos
Compostos Benzidrílicos/toxicidade , Dimetil Sulfóxido/farmacologia , Raios gama/efeitos adversos , Regulação da Expressão Gênica/efeitos dos fármacos , Glicoproteínas de Membrana/metabolismo , Doenças Neurodegenerativas/tratamento farmacológico , Fenóis/toxicidade , Receptores Imunológicos/metabolismo , Sulfonas/farmacologia , Quinase Syk/metabolismo , Animais , Anti-Inflamatórios/farmacologia , Estrogênios não Esteroides/toxicidade , Feminino , Glicoproteínas de Membrana/genética , Proteínas de Membrana/genética , Proteínas de Membrana/metabolismo , Doenças Neurodegenerativas/etiologia , Doenças Neurodegenerativas/patologia , Ratos , Ratos Wistar , Receptores Imunológicos/genética , Quinase Syk/genética
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