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1.
Ecotoxicol Environ Saf ; 203: 110928, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32888618

RESUMO

Hexavalent chromium [Cr(VI)] is seriously harmful to ecosystems and living organisms due to its strong toxicity. Role of dynamin-related protein 1 (Drp1) and Drp1-associated mitochondrial fragmentation in mitophagy and cytotoxicity after Cr(VI) exposure has not been clarified so far. We confirmed that Cr(VI) caused mitochondrial fission by up-regulating Drp1 expression and enhancing Drp1 mitochondrial translocation. By applying the intracellular Ca2+ antagonist BAPTA-AM and mitochondrial Ca2+ antagonist Ru360, we demonstrated that Cr(VI)-induced excessive mitochondrial fission was in a Ca2+-Drp1 dependent manner. The administration of Drp1 siRNA significantly suppressed the overactivation of mitophagy in Cr(VI)-induced hepatotoxicity. The specific Drp1 inhibitor mitochondrial division inhibitor-1 (Mdivi-1) blocked the overactive mitophagy and subsequently ameliorated hepatotoxicity caused by Cr(VI) in vivo. We reached the conclusion that Drp1-dependent mitochondrial fission contributes to Cr(VI)-induced mitophagy and hepatotoxicity, which may provide experimental basis for the study of chromium-associated toxicity, especially for the prevention of health damage in chromium-exposed population.


Assuntos
Doença Hepática Induzida por Substâncias e Drogas/etiologia , Cromo/toxicidade , Dinaminas/metabolismo , Poluentes Ambientais/toxicidade , Hepatócitos/efeitos dos fármacos , Dinâmica Mitocondrial/efeitos dos fármacos , Mitofagia/efeitos dos fármacos , Animais , Linhagem Celular , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/patologia , Ecossistema , Hepatócitos/metabolismo , Hepatócitos/patologia , Humanos , Camundongos , Camundongos Endogâmicos C57BL , Mitocôndrias Hepáticas/efeitos dos fármacos , Mitocôndrias Hepáticas/metabolismo , Mitocôndrias Hepáticas/patologia , RNA Interferente Pequeno/metabolismo
2.
Ecotoxicol Environ Saf ; 203: 111037, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32888596

RESUMO

Glacier studies as of late have ruffled many eyeballs, exploring this frigid ecology to understand the impact of climate change. Mapquesting the glaciers led to the discovery of concealed world of "psychrophiles" harboring in it. In the present study, the antibiotic resistance genes (ARGs) and heavy metal resistance genes (MRGs) were evaluated through both the culture-dependent and culture-independent methods. Samples were collected from two different glaciers, i.e., debris-covered glacier (Changme Khangpu) and debris-free glacier (Changme Khang). Functional metagenomics of both the glacier samples, provided evidence of presence of resistant genes against various antibiotic groups. Bacitracin resistant gene (bacA) was the predominant ARG in both the glaciers. MRGs in both the glacier samples were diversified as the genes detected were resistant against various heavy metals such as arsenic, tungsten, mercury, zinc, chromium, copper, cobalt, and iron. Unique MRGs identified from Changme Khangpu glacier were resistant to copper (cutA, cutE, cutC, cutF, cueR, copC, and copB) and chromium (yelf, ruvB, nfsA, chrR, and chrA) whereas, from Changme Khang glacier they showed resistance against cobalt (mgtA, dmef, corD, corC, corB, and cnrA), and iron (yefD, yefC, yefB, and yefA) heavy metals. ARGs aligned maximum identity with Gram-negative psychrotolerant bacteria. The cultured bacterial isolates showed tolerance to high concentrations of tested heavy metal solutions. Interestingly, some of the antibiotic resistant bacterial isolates also showed tolerance towards the higher concentrations of heavy metals. Thus, an introspection of the hypothesis of co-occurrence and/co-selection of ARGs and MRGs in such environments has been highlighted here.


Assuntos
Adaptação Biológica/genética , Antibacterianos/toxicidade , Resistência Microbiana a Medicamentos/genética , Poluentes Ambientais/toxicidade , Genes Bacterianos/efeitos dos fármacos , Camada de Gelo/microbiologia , Metais Pesados/toxicidade , Adaptação Biológica/efeitos dos fármacos , Bactérias Gram-Negativas/efeitos dos fármacos , Bactérias Gram-Negativas/genética , Camada de Gelo/química , Índia , Metagenômica , Siquim
3.
Ecotoxicol Environ Saf ; 203: 111041, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32888612

RESUMO

Although the production and use of PCB153 have been banned globally, PCB153 pollution remains because of its persistence and long half-life in the environment. There is ongoing evidence that exposure to PCB153 may influence gut microbiota health and increase the risk of host health. It is needed to illuminate whether there are associations between gut microbiota dysregulation and PCB153-induced host diseases. Importantly, it is urgently needed to find specific strains as biomarkers to monitor PCB153 pollution and associated disorders. The work aims to investigate the change of gut microbiota composition, structure and diversity and various host physiological indexes, to ravel the chain causality of PCB153, gut microbiota health and host health, and to find potential gut microbiota markers for PCB153 pollution. Here, adult female mice were administrated with PCB153. Obtained results indicated that PCB153 led to gut microbiota health deterioration. PCB153 exposure also induced obesity, hepatic lipid accumulation, abdominal adipose tissue depots and dyslipidemia in mice. Furthermore, specific gut microbiota significantly correlated with the host health indexes. This work provides support for the relationship between gut microbiota aberrance derived from PCB153 and risk of host health, and offers some indications of possible indicative functions of gut microbiota on PCB153 pollution.


Assuntos
Dislipidemias/induzido quimicamente , Monitoramento Ambiental/métodos , Poluentes Ambientais/toxicidade , Microbioma Gastrointestinal/efeitos dos fármacos , Obesidade/induzido quimicamente , Bifenilos Policlorados/toxicidade , Animais , Biomarcadores/análise , Colo/microbiologia , Dislipidemias/metabolismo , Dislipidemias/microbiologia , Feminino , Conteúdo Gastrointestinal/microbiologia , Microbioma Gastrointestinal/genética , Expressão Gênica/efeitos dos fármacos , Fígado/efeitos dos fármacos , Fígado/metabolismo , Camundongos , Camundongos Endogâmicos C57BL , Obesidade/metabolismo , Obesidade/microbiologia , RNA Ribossômico 16S
4.
Ecotoxicol Environ Saf ; 203: 110974, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32888622

RESUMO

Ammonia (NH3), an environmental pollutant, poses a serious threat to human and avian health. Although previous studies have showed that NH3 caused kidney injury, the molecular mechanisms of nephrotoxicity induced by NH3 remain unclear. To explore the mechanisms of NH3 nephrotoxicity, a total of 36 broiler chicks at one day of age were exposed to NH3. After 42 days of exposure, blood samples were collected to determine creatinine and uric acid; and kidney samples were weighted and then collected to detect ultrastructural changes, oxidative stress parameters, ATPases, necroptosis- and mitochondrial dynamics-related genes. The results showed that chickens exposed to NH3 showed lower relative kidney weight and an increase concentration in serum creatinine and uric acid. NH3 exposure caused nephrocyte necrosis and increased the expression of necroptosis-related genes (TNF-α, RIPK1, RIPK3, MLKL, and JNK). Besides, the activities of antioxidant systems (SOD, CAT, GSH-Px, and T-AOC) were reduced, whereas the concentrations of H2O2 and MDA were elevated. Lower activities of ATPases were obtained in NH3 treatment groups. Furthermore, the mitochondrial fission-related genes drp1 and mff were activated, and mitochondrial fusion-related genes opa1, mfn1 and mfn2 were suppressed after NH3 exposure. Based on the above results, we conclude that NH3 caused-oxidative stress and mitochondrial dysfunction mediated nephrocyte necroptosis in chickens. This study may provide new insight into NH3 nephrotoxicity.


Assuntos
Amônia/toxicidade , Poluentes Ambientais/toxicidade , Rim/efeitos dos fármacos , Dinâmica Mitocondrial/efeitos dos fármacos , Necroptose/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Animais , Antioxidantes/metabolismo , Galinhas , Expressão Gênica/efeitos dos fármacos , Humanos , Peróxido de Hidrogênio/metabolismo , Rim/ultraestrutura , Testes de Função Renal , Dinâmica Mitocondrial/genética , Tamanho do Órgão/efeitos dos fármacos , Estresse Oxidativo/genética , Proteína Serina-Treonina Quinases de Interação com Receptores/genética
5.
Ecotoxicol Environ Saf ; 205: 111338, 2020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-32956867

RESUMO

Lead (Pb) is well-recognized for its great hazards to human and wildlife health. It has negative influences on multiple organs and systems of birds. Especially, lead exposure caused adverse impacts on bird reproduction. In this study, one week old female Japanese quails were randomly allocated into four groups and each group was respectively fed with 0, 50 ppm, 500 ppm and 1000 ppm Pb in drinking water for 36 days to determine the effects of chronic lead exposure on ovarian development and function. The results showed that Pb did accumulate in the ovary and ovarian development was delayed by high dose lead exposure (500 ppm and 1000 ppm). Moreover, high Pb dosage induced ovarian histopathological damages characterized by granulosa cells disorganization, follicle atresia and interstitial cell degeneration. Meanwhile, the concentration of estradiol (E2) was significantly decreased and mRNA levels of genes involved with ovarian steroidogenesis were significantly down-regulated by high concentration Pb. In addition, Pb exposure caused increasing cell apoptosis and significant changes of the expression of genes involved with cell death in the ovary. High dose Pb exposure also inhibited thyroid hormone release and disrupted ovarian thyroid deiodination apart from causing thyroid histopathological injury such as follicular deformation and atrophy. The study indicated that Pb might cause ovarian malfunction by inducing ovary and thyroid microstructural damages, thyroid hormone and estrogen release inhibition and ovarian steroidogenesis disruption.


Assuntos
Coturnix/metabolismo , Poluentes Ambientais/toxicidade , Estradiol/metabolismo , Expressão Gênica/efeitos dos fármacos , Chumbo/toxicidade , Ovário/efeitos dos fármacos , Hormônios Tireóideos/metabolismo , Adolescente , Animais , Apoptose/efeitos dos fármacos , Coturnix/genética , Coturnix/crescimento & desenvolvimento , Relação Dose-Resposta a Droga , Poluentes Ambientais/metabolismo , Estradiol/genética , Feminino , Células da Granulosa/efeitos dos fármacos , Células da Granulosa/patologia , Humanos , Chumbo/metabolismo , Folículo Ovariano/efeitos dos fármacos , Folículo Ovariano/patologia , Ovário/crescimento & desenvolvimento , Ovário/metabolismo , Ovário/patologia , Distribuição Aleatória , Reprodução/efeitos dos fármacos , Reprodução/genética , Glândula Tireoide/efeitos dos fármacos , Glândula Tireoide/metabolismo , Glândula Tireoide/patologia , Hormônios Tireóideos/genética
6.
Ecotoxicol Environ Saf ; 205: 111300, 2020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-32961492

RESUMO

Bacterial resistance caused by the abuse of antibiotics has attracted worldwide attention. However, there are few studies exploring bacterial resistance under the environmental exposure condition of antibiotics that is featured by low-dose and mixture. In this study, sulfonamides (SAs), sulfonamide potentiators (SAPs) and tetracyclines (TCs) were used to determine the effects of antibiotics on plasmid RP4 conjugative transfer of Escherichia coli (E. coli) under single or combined exposure, and the relationship between the effects of antibiotics on conjugative transfer and growth was investigated. The results show that the effects of single or binary antibiotics on plasmid RP4 conjugative transfer all exhibit a hormetic phenomenon. The linear regression reveals that the concentrations of the three antibiotics promoting conjugative transfer are correlated with the concentrations promoting growth and the physicochemical properties of the compounds. The combined effects of SAs-SAPs and SAs-TCs on plasmid conjugative transfer are mainly synergistic and antagonistic. While SAPs provide more effective concentrations for the promotion of conjugative transfer in SAs-SAPs mixtures, SAs play a more important role in promoting conjugative transfer in SAs-TCs mixtures. Mechanism explanation shows that SAs, SAPs and TCs inhibit bacterial growth by acting on their target proteins DHPS, DHFR and 30S ribosomal subunit, respectively. This study indicates that toxic stress stimulates the occurrence of conjugative transfer and promotes the development of bacterial resistance, which will provide a reference for resistance risk assessment of antibiotic exposure.


Assuntos
Antibacterianos/toxicidade , Conjugação Genética/efeitos dos fármacos , Poluentes Ambientais/toxicidade , Escherichia coli/efeitos dos fármacos , Hormese , Plasmídeos , Antagonismo de Drogas , Sinergismo Farmacológico , Escherichia coli/genética , Escherichia coli/crescimento & desenvolvimento , Plasmídeos/efeitos dos fármacos , Plasmídeos/genética , Sulfonamidas/toxicidade , Tetraciclinas/toxicidade
7.
Ecotoxicol Environ Saf ; 202: 110910, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32800245

RESUMO

Microplastics (MPs) are ubiquitous in the environment and more abundant in the marine environment. Consequently, increasing focus has been put on MPs in oceans and seas, while little importance has been attached to their presence in freshwaters and soils. Therefore, this paper aimed to provide a comprehensive review of the occurrence, analysis and ecotoxicology of MPs. The abundance and distribution of MPs in several typical freshwater systems of China were summarized. It suggested that the surface water of Poyang Lake contained the highest concentration of 34 items/L MPs among all the 8 freshwater systems, and the content of MPs in sediments were higher than that of the surface water. Net-based zooplankton sampling methods are the most frequently utilized sampling methods for MPs, and density separation, elutriation and digestion are three major pretreatment methods. Fourier transform infrared spectroscopy, Raman spectroscopy and pyrolysis-gas chromatography coupled to mass spectrometry are often used to identify the polymer types of MPs. Besides, MPs might damage the digestive tract of various organisms and negatively inhibit their growth, feeding and reproduction. The ways of human exposure to MPs are by ingestion, inhalation and dermal exposure, digestive and respiratory system might be adversely influenced. However, potential health risks of MPs to humans are remained insufficiently researched. Overall, by showing the presence of MPs in freshwaters and soils as well as possible ecotoxicological effects on the environment and humans, this paper provided a framework for future research in this field.


Assuntos
Monitoramento Ambiental , Poluentes Ambientais/análise , Microplásticos/análise , Animais , China , Ecotoxicologia , Monitoramento Ambiental/métodos , Poluentes Ambientais/toxicidade , Cromatografia Gasosa-Espectrometria de Massas , Humanos , Lagos/química , Microplásticos/toxicidade , Oceanos e Mares , Plásticos/química , Solo , Espectroscopia de Infravermelho com Transformada de Fourier , Poluentes Químicos da Água/análise , Zooplâncton
8.
J Toxicol Environ Health B Crit Rev ; 23(6): 276-291, 2020 08 17.
Artigo em Inglês | MEDLINE | ID: mdl-32741292

RESUMO

Exposure to environmental pollutants may produce impairment of male reproductive health. The epidemiological literature evaluating potential consequences of human exposure to per- and polyfluoroalkyl substances (PFAS) has grown in recent years with concerns for both pre- and postnatal influences. The aim of this systematic review was to assess available evidence on associations between PFAS exposures in different stages of life and semen quality, reproductive hormones, cryptorchidism, hypospadias, and testicular cancer. A systematic search of literature published prior to March 9th, 2020, was performed in the databases PubMed and Embase®. Predefined criteria for eligibility were applied by two authors screening study records independently. Among the 242 study records retrieved in the literature search, 26 studies were eligible for qualitative assessment. While several investigations suggested weak associations for single compounds and specific outcomes, a lack of consistency across studies limited conclusions of overall evidence. The current gap in knowledge is particularly obvious regarding exposures prior to adulthood, exposure to combinations of both PFAS and other types of environmental chemicals, and outcomes such as cryptorchidism, hypospadias, and testicular cancer. Continued efforts to clarify associations between PFAS exposure and male reproductive health through high-quality epidemiological studies are needed.


Assuntos
Criptorquidismo/induzido quimicamente , Exposição Ambiental/efeitos adversos , Poluentes Ambientais/toxicidade , Fluorcarbonetos/toxicidade , Hipospadia/induzido quimicamente , Saúde Reprodutiva , Sêmen/efeitos dos fármacos , Neoplasias Testiculares/induzido quimicamente , Hormônios Esteroides Gonadais/metabolismo , Humanos , Masculino
9.
Bull Environ Contam Toxicol ; 105(3): 381-386, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32794125

RESUMO

Selenium represents an essential trace nutrient that is necessary for biological functions. Deficiencies can induce disease, but excess can induce toxicity. Selenium deficiency is a major concern in underdeveloped countries, while also posing as a toxic pollutant in waterways surrounding landfills, agricultural areas, and fossil fuel production sites. We examined the microbiome of selenomethionine (SeMet) fed American alligators (Alligator mississippiensis) at the beginning and end of a 7-week exposure experiment. Alligators were randomly divided into three groups: control and 1000 or 2000 ppm SeMet. DNA from before exposure (oral and cloaca swabs) and post-exposure (oral, cloaca, small & large intestines) sampling were extracted and amplified for bacterial 16 s rRNA. While treatment did not seem to have much effect, we observed a predominance of Fusobacteriaceae and Porpyromonodaceae across all tissue types. Cetobacterium and Clostridium are the most abundant genera as potential indicators of the aquatic and carrion feeding lifestyle of alligators.


Assuntos
Jacarés e Crocodilos/microbiologia , Exposição Dietética , Poluentes Ambientais/toxicidade , Microbiota , Selenometionina/toxicidade , Animais , Antioxidantes , Selênio , Oligoelementos
10.
Zhonghua Yu Fang Yi Xue Za Zhi ; 54(7): 798-803, 2020 Jul 06.
Artigo em Chinês | MEDLINE | ID: mdl-32842306

RESUMO

With the increasing number of environmental chemicals, the risk assessment system based on animal toxicity testing is difficult to satisfy the current demands and needs to be reformed urgently. With the wide application of high-throughput screening technology, the advantage of exposomics in risk assessment is gradually emerging. Exposomics aims to study the health effects of mixed environmental exposure at different stages of life (especially in the early stage of life) through the dynamic monitoring of external and internal exposure levels. Exposomics is introduced into risk assessment to systematically study gene-environment interaction so as to provide a reliable basis for the construction of exposure-biomarker-disease network. This review summarized the importance and application prospect of exposomics in risk assessment of environmental chemicals in terms of the research progress, application in risk assessment and existing problems, opportunities and challenges.


Assuntos
Exposição Ambiental , Poluentes Ambientais/toxicidade , Animais , Biomarcadores , Monitoramento Ambiental , Medição de Risco , Testes de Toxicidade
11.
Ecotoxicol Environ Saf ; 205: 111149, 2020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-32829210

RESUMO

Exposure to heavy metals was reported to be associated with heart rate variability (HRV) alteration. However, possible pathway of such association remains unclear. In this research, we investigated the possible role of lipid peroxidation in the associations between urinary heavy metals and HRV. We performed a cross-sectional study using baseline data of Wuhan-Zhuhai cohort. Urinary heavy metals (including lead, barium, antimony, cadmium, zinc, copper, iron and manganese), urinary 8-iso-prostaglandin-F2α levels (common biomarker for lipid peroxidation) and HRV indices (SDNN, r-MSSD, low frequency, high frequency and total power) were measured among 3022 participants. We conducted multivariable linear regression models to quantify associations between urinary 8-iso-prostaglandin-F2α (8-iso-PGF2α) and heavy metals or HRV indices. The potential role of 8-iso-PGF2α in the association of urinary heavy metals with HRV was evaluated through mediation analyses. After adjusting for potential confounders, urinary manganese, iron, copper, zinc, cadmium, antimony and barium were identified to be negatively associated with one or more HRV parameters. Each one-unit growth of log-transformed levels of urinary manganese, iron, copper, zinc, antimony and barium was associated with a 1.9%, 1.5%, 4.7%, 4.0%, 2.7% and 1.3% decrease in SDNN, respectively. We observed positive dose-response relationships between all eight urinary heavy metals and 8-iso-PGF2α, as well as negative association of urinary 8-iso-PGF2α with SDNN and total power (all P trend<0.05). The proportions mediated by 8-iso-PGF2α on SDNN were 4.6% for manganese, 9.3% for iron, 19.8% for antimony and 11.0% for barium. The proportions mediated by 8-iso-PGF2α on total power were 6.9% for manganese and 10.1% for cadmium (all P value < 0.05). This study suggested that urinary manganese, iron, copper, zinc, cadmium, antimony and barium were negatively associated with HRV indices. Lipid peroxidation may partly mediate the associations of urinary manganese, iron, cadmium, antimony and barium with specific HRV indices.


Assuntos
Exposição Ambiental/estatística & dados numéricos , Poluentes Ambientais/toxicidade , Frequência Cardíaca , Peroxidação de Lipídeos , Metais Pesados/toxicidade , Adulto , Antimônio , Biomarcadores/metabolismo , Cádmio , Cobre , Estudos Transversais , Dinoprosta/análogos & derivados , Exposição Ambiental/análise , Poluentes Ambientais/metabolismo , Feminino , Humanos , Ferro , Masculino , Manganês , Metais Pesados/metabolismo , Pessoa de Meia-Idade , Zinco
12.
Ecotoxicol Environ Saf ; 204: 111058, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32739676

RESUMO

Skeletal fluorosis causes growth plate impairment and growth retardation during bone development. However, the mechanism of how fluoride impairs chondrocyte is unclear. To explore the effect of fluoride on chondrocyte differentiation and the regulation of circadian clock signaling pathway during chondrogenesis, we treated ATDC5 cells with fluoride and carried out a series of experiments. 10-3 M fluoride inhibited cell viability and significantly decreased the expression of Sox9 and Col2a1 (P < 0.05). Fluoride inhibited proteoglycan synthesis and decreased significantly the expression of Aggrecan, Ihh and Col10a1 (P < 0.05). Meanwhile, fluoride significantly inhibited the expression of Bmal1 and disrupted circadian clock signaling pathway (P < 0.05). Furthermore, fluoride disrupted the time-dependent expression of circadian clock molecules and stage-specific differentiation markers. Overexpression of Bmal1 by lentivirus reversed the adverse effects of fluoride on chondrogenesis. These results suggested that fluoride inhibited chondrocyte viability and delayed chondrocyte differentiation. Fluoride delayed chondrogenesis partly via interfering with Bmal1 and circadian clock signaling pathway. Nevertheless, the specific mechanism of circadian clock in fluoride-induced cartilage damage needs to be further studied.


Assuntos
Diferenciação Celular/efeitos dos fármacos , Condrócitos/efeitos dos fármacos , Condrogênese/efeitos dos fármacos , Relógios Circadianos , Poluentes Ambientais/toxicidade , Fluoretos/toxicidade , Animais , Técnicas de Cultura de Células , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Condrócitos/citologia , Condrócitos/metabolismo , Condrogênese/fisiologia , Colágeno Tipo X/genética , Colágeno Tipo X/metabolismo , Lâmina de Crescimento/efeitos dos fármacos , Lâmina de Crescimento/metabolismo , Camundongos , Fatores de Transcrição SOX9/genética , Fatores de Transcrição SOX9/metabolismo , Transdução de Sinais
13.
Ecotoxicol Environ Saf ; 204: 111063, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32791358

RESUMO

The lipocalins genes have been assigned for involving in the responses of organisms to various stress factors. The function of lipocalins under PCB18 stress was addressed by pathway complementation in the Oryza sativa L. OsTIL-silenced mutant. The growth of wild type (WT) and OsTIL-silenced mutant (MT) callus were suppressed by PCB18, and MT varieties were inhibited more seriously than WT varieties. Meanwhile, only WT varieties showed "Hormesis" effect. Compared with WT (3 day > 90.0%, 6 day ≤45.5%), MT varieties kept high removing efficiency by HPLC analysis. Varied gene transcription after OsTIL silencing was demonstrated between two varieties, especially obvious under PCB stress. Silenced OsTIL induced more protective gene transcriptions by qPCR analysis, OsVDE at 3 day, OsCHL, OsZEP1, OsZEP2 and OsUN at 6 day and OsZEP2 at 9 day. PCB18 stress further irritated these genes transcription in MT varieties. The defense stagy in WT varieties was that the transcriptions of lipocalins were inhibited to reduce PCB18 accumulation and toxicity. OsTIL could effectively limit PCB18 accumulation and toxicity. After TIL lacking, OsCHL, OsZEP1, OsZEP2 and OsUN in mutant were strongly evoked to against PCB stress. Remarkably, OsUN and OsZEP2 gene expressions were responded to PCB18 stress in both two varieties.


Assuntos
Poluentes Ambientais/toxicidade , Lipocalinas/genética , Oryza/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Bifenilos Policlorados/toxicidade , Ativação Transcricional/efeitos dos fármacos , Regulação da Expressão Gênica de Plantas , Inativação Gênica , Genes de Plantas , Oryza/genética , Oryza/crescimento & desenvolvimento , Estresse Oxidativo/genética
14.
Ecotoxicology ; 29(8): 1128-1137, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32827288

RESUMO

Mercury exposure can disrupt development of the cerebellum, part of the brain essential for coordination of movement through a complex environment, including flight. In precocial birds, such as fowl, the cerebellum develops embryonically, and the chick is capable of leaving the nest within hours of hatching. However, most birds, including all songbirds, are altricial, and spend weeks in the nest between hatching and fledging. The objective of this study was to describe the normal development of the cerebellum in a model altricial songbird so as to determine the effect of exposure to mercury on cerebellar maturation. Adult zebra finch (Taeniopygia guttata) pairs were fed either a control diet, or a diet augmented with one of four treatment-levels of methylmercury (0.3-2.4 µg/g wet weight), and their offspring, the subjects of this study, were fed the same diet by parents. We documented, for the first time, the schedule of cerebellar development in an altricial bird, and compared stages of development among methylmercury-exposed groups. For all treatments of methylmercury, the age of completion of cellular migration was later than for control zebra finches, indicating a delay in cerebellar maturation. Displaced (heterotopic) Purkinje neurons, a pathology typical of methylmercury exposure in developing vertebrate brains, were more numerous in methylmercury-exposed birds, and persisted at least until the age of independence. Delays in maturation of the cerebellum could delay fledging in altricial bird species, with potential serious implications for the fitness of exposed individuals, as predation rates in the nest are often very high.


Assuntos
Cerebelo/crescimento & desenvolvimento , Poluentes Ambientais/toxicidade , Tentilhões , Mercúrio/toxicidade , Animais , Cerebelo/efeitos dos fármacos , Feminino , Masculino
15.
PLoS One ; 15(8): e0237705, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32833973

RESUMO

Polychlorinated biphenyls (PCBs) are environmental pollutants and endocrine disruptors, harmfully affecting reproductive, endocrine, neurological and immunological systems. This broad influence has implications for processes such as wound healing, which is modulated by the immunological response of the body. Conversely, while PCBs can be linked to diminished wound healing, outside of PCB pollution systems, exercise has been shown to accelerate wound healing. However, the potential for moderate intensity exercise to modulate or offset the harmful effects of a toxin like PCB are yet unknown. A key aim of the present study was to examine how PCB exposure at different doses (0, 100, 500, 1000 ppm i.p.) altered wound healing in exercised versus non-exercised subgroups of mice. We examined PCB effects on immune function in more depth by analyzing the concentrations of cytokines, interleukin-1ß (IL-1ß), tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6) and granulocyte macrophage colony stimulating factor (GM-CSF) in these wounds inflicted by punch biopsy. Mice were euthanized at Day 3 or Day 5 after PCB injection (n = 3-6) and skin excised from the wound area was homogenized and analyzed for cytokine content. Results revealed that wound healing was not signficantly impacted by either PCB exposure or exercise, but there were patterns of delays in healing that depended on PCB dose. Changes in cytokines were also observed and depended on PCB dose and exercise experience. For example, IL-1ß concentrations in Day 5 mice without PCB administration were 33% less in exercised mice than mice not exercised. However, IL-1ß concentrations in Day 3 mice administered 100 ppm were 130% greater in exercised mice than not exercisedmice. Changes in the other measured cytokines varied with mainly depressions at lesser PCB doses and elevations at higher doses. Exercise had diverse effects on cytokine levels, but increased cytokine levels in the two greater doses. Explanations for these diverse effects include the use of young animals with more rapid wound healing rates less affected by toxin exposure, as well as PCB-mediated compensatory effects at specific doses which could actually enhance immune function. Future work should examine these interactions in more detail across a developmental time span. Understanding how manipulating the effects of exposure to environemntal contaminants using behavioral modification could be very useful in certain high risk populations or exposed individuals.


Assuntos
Disruptores Endócrinos/toxicidade , Poluentes Ambientais/toxicidade , Condicionamento Físico Animal/fisiologia , Bifenilos Policlorados/toxicidade , Cicatrização/imunologia , Animais , Citocinas/imunologia , Citocinas/metabolismo , Modelos Animais de Doenças , Feminino , Humanos , Camundongos , Pele/imunologia , Pele/lesões , Pele/metabolismo , Cicatrização/efeitos dos fármacos
16.
Ecotoxicol Environ Saf ; 204: 111049, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32758698

RESUMO

Recent studies identified a novel programmed and regulated cell death that was characterized by a necrotic cell death morphology, termed necroptosis. Lead (Pb) is known as a persistent inorganic environmental pollutant that affects the health of humans and animals worldwide. However, there are no detailed reports of Pb-induced necroptosis of immune tissue. Selenium (Se) is a trace element that antagonizes the toxicity of heavy metals. Here, chickens were randomly divided into four groups, treated with Pb ((CH3OO)2Pb, 150 mg/kg) and/or Se (Na2SeO3, 2 mg/kg), aim to study the effect and mechanism of necroptosis in Pb-induced spleen injury and the antagonistic effects of Se on Pb toxicity. Our results showed that Pb exposure evidently increased the accumulation of Pb in spleen and caused necroptosis by upregulating the expression of RIP1, RIP3 and MLKL, and decreasing Caspase8 expression. Meanwhile, Pb treatment inhibited the activities of SOD, GPX, and CAT, caused the accumulation of NO and MDA, and induced oxidative stress, which promoted the expression of MAPK/NF-κB pathway genes (ERK, JNK, P38, NF-κB and TNF-α) and activated HSPs (HSP27, HSP40, HSP60, HSP70 and HSP90). However, the increased content of Pb in spleen and Pb-caused necroptosis were inhibited by Se cotreatment. Overall, we conclude that Se can prevent Pb-induced necroptosis by restoring antioxidant functions and blocking the MAPK/NF-κB pathway and HSPs activation in chicken spleen.


Assuntos
Galinhas/fisiologia , Poluentes Ambientais/toxicidade , Chumbo/toxicidade , Necroptose/efeitos dos fármacos , Substâncias Protetoras/farmacologia , Selênio/farmacologia , Baço/efeitos dos fármacos , Animais , Proteínas Aviárias/metabolismo , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Feminino , Proteínas de Choque Térmico/metabolismo , NF-kappa B/metabolismo , Distribuição Aleatória , Transdução de Sinais/efeitos dos fármacos , Baço/fisiologia
17.
Biomed Environ Sci ; 33(6): 403-413, 2020 Jun 20.
Artigo em Inglês | MEDLINE | ID: mdl-32641203

RESUMO

Objective: To verify the health advisory for short-term exposure to phenol. Methods: The method of this validation experiment was the same as the US Environmental Protection Agency (EPA) methodology for toxicology experiments used to determine phenol drinking water equivalent level (DWEL). Pregnant female Sprague-Dawley rats were administered phenol in distilled water by gavage at daily doses of 15, 30, 60, 120, and 240 mg/kg body weight (b.w.) from implantation (the 6th day post-mating) to the day prior to the scheduled caesarean section (the 20th day of pregnancy). The following information was recorded: general behavior; body weight; number of corpus luteum, live birth, fetus, stillbirth, and implantation; fetal gender; body weight; body length; tail length; and abnormalities and pathomorphological changes in the dams. Results: In the 60 mg/kg b.w. dose group, the mortality of pregnant rats increased with increasing doses, suggesting maternal toxicity. Fetal and placental weights decreased as phenol dose increased from 30 mg/kg b.w., and were significantly different compared those in the vehicle control group, which suggested developmental toxicity in the fetuses. However, the phenol-exposed groups showed no significant change in other parameters compared with the vehicle control group ( P > 0.05). Conclusion: Despite using the same method as the US EPA, a different NOEAL of 15 mg/(kg·d) was obtained in this study.


Assuntos
Poluentes Ambientais/toxicidade , Desenvolvimento Fetal/efeitos dos fármacos , Fenol/toxicidade , Animais , Relação Dose-Resposta a Droga , Feminino , Gravidez , Ratos , Ratos Sprague-Dawley , Testes de Toxicidade Aguda
18.
Ecotoxicol Environ Saf ; 203: 110975, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32678756

RESUMO

Manganese (Mn) produces cholinergic neuronal loss in basal forebrain (BF) region that was related to cognitive dysfunction induced after single and repeated Mn treatment. All processes that generate cholinergic neuronal loss in BF remain to be understood. Mn exposure may produce the reduction of BF cholinergic neurons by increasing amyloid beta (Aß) and phosphorylated Tau (pTau) protein levels, altering heat shock proteins' (HSPs) expression, disrupting proteasome P20S activity and generating oxidative stress. These mechanisms, described to be altered by Mn in regions different than BF, could lead to the memory and learning process alteration produced after Mn exposure. The research performed shows that single and repeated Mn treatment of SN56 cholinergic neurons from BF induces P20S inhibition, increases Aß and pTau protein levels, produces HSP90 and HSP70 proteins expression alteration, and oxidative stress generation, being the last two effects mediated by NRF2 pathway alteration. The increment of Aß and pTau protein levels was mediated by HSPs and proteasome dysfunction. All these mechanisms mediated the cell decline observed after Mn treatment. Our results are relevant because they may assist to reveal the processes leading to the neurotoxicity and cognitive alterations observed after Mn exposure.


Assuntos
Peptídeos beta-Amiloides/metabolismo , Prosencéfalo Basal/efeitos dos fármacos , Neurônios Colinérgicos/efeitos dos fármacos , Poluentes Ambientais/toxicidade , Proteínas de Choque Térmico HSP70/metabolismo , Proteínas de Choque Térmico HSP90/metabolismo , Manganês/toxicidade , Complexo de Endopeptidases do Proteassoma/metabolismo , Proteínas tau/metabolismo , Animais , Prosencéfalo Basal/metabolismo , Prosencéfalo Basal/patologia , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Neurônios Colinérgicos/metabolismo , Neurônios Colinérgicos/patologia , Relação Dose-Resposta a Droga , Poluentes Ambientais/metabolismo , Manganês/metabolismo , Camundongos , Estresse Oxidativo/efeitos dos fármacos
19.
Chemosphere ; 257: 127035, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32702804

RESUMO

Human exposure to environmental chemicals might play a role in the pathogenesis of unexplained recurrent spontaneous abortion (URSA). Bisphenol A (BPA) and bisphenol S (BPS) have been suggested to affect reproductive health. However, the mechanism remains unclear. To explore the association between BPA and BPS exposure and oxidative stress and immune homeostasis, we conducted a cross-sectional study and revealed BPA and BPS levels in relation to these two factors which were supposed to be implicated in miscarriage. 111 URSA patients were recruited and we analyzed urinary BPA and BPS concentrations, oxidative stress biomarkers (8-hydroxydeoxyguanosine and 8-isoprostane) and serum immune balance biomarkers (IL-1ß, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70, IL-13, TNF-α, TGF-ß and IFN-γ). Multivariable linear regression models were used to evaluate the correlation between bisphenols exposure and outcome biomarkers. After adjustment for age, BMI, menstrual cycle, and parity history, creatinine-adjusted BPA was significantly associated with increases in 8-isoprostane (ß = 0.74, 95% CI = 0.07, 1.41; p = 0.031) and IFN-γ (ß = 0.18, 95% CI = 0.00, 0.36; p = 0.046). No statistical correlation between BPS and biomarkers of oxidative stress or immune balance was observed when all participants were analyzed. Further analysis revealed that in the subgroup of BPS > limit of detection (0.01 ng/ml), creatinine-adjusted BPS was significantly associated with increases in IL-10 (ß = 0.22, 95% CI = 0.00, 0.45; p = 0.048). Our findings suggested that BPA and BPS exposure might be related to oxidative stress and immune imbalance in URSA patients. Overall, our work might suggest potential pathogenic and aetiological associations among the bisphenols, biomarkers and URSA, which offers hypotheses for further studies.


Assuntos
Aborto Espontâneo/epidemiologia , Compostos Benzidrílicos/toxicidade , Poluentes Ambientais/toxicidade , Exposição Materna/estatística & dados numéricos , Fenóis/toxicidade , Sulfonas/toxicidade , Adulto , Biomarcadores/sangue , Estudos Transversais , Dinoprosta/análogos & derivados , Feminino , Humanos , Interleucina-10/metabolismo , Interleucina-1beta/metabolismo , Estresse Oxidativo/fisiologia , Gravidez
20.
PLoS One ; 15(7): e0236394, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32702712

RESUMO

BACKGROUND: Maldescended testes or cryptorchidism is a genital birth defect that affects 2-9% of all male new-borns. Over the last 40 years there have been reports of increased prevalence in countries like the US, the UK and the Scandinavian countries. This possible increase has in some studies been linked to a foetal exposure to chemical pollutants. In this matched case-control study, we analysed maternal serum samples in early pregnancy for three different organochlorine compounds, to investigate whether the levels were associated with the risk of cryptorchidism. METHOD: Maternal serum samples taken during the first trimester of pregnancy from 165 cases (boys born with cryptorchidism) and 165 controls, matched for birth year and maternal age, parity and smoking habits during the pregnancy, were retrieved from the Southern Sweden Maternity Biobank. The samples were analysed for 2,2',4,4',5,5'-hexachlorobiphenyl (PCB-153), dichlorodiphenyltrichloroethane (p,p'-DDE) and hexachlorobenzene (HCB), using gas chromatography mass spectrometry. Associations between exposure and cryptorchidism were evaluated by conditional logistic regression. RESULTS: We found no statistically significantly associations between exposure to these compounds and cryptorchidism, either when the exposure variables were used as a continuous variable, or when the exposure levels were divided in quartiles. CONCLUSION: We found no evidence of an association between maternal levels of PCB-153, p,p'-DDE or HCB during the pregnancy and the risk of having cryptorchidism in the sons.


Assuntos
Criptorquidismo/sangue , Poluentes Ambientais/sangue , Hidrocarbonetos Clorados/sangue , Exposição Materna/efeitos adversos , Adulto , Estudos de Casos e Controles , Criptorquidismo/induzido quimicamente , Criptorquidismo/epidemiologia , Criptorquidismo/patologia , Diclorodifenil Dicloroetileno/sangue , Diclorodifenil Dicloroetileno/toxicidade , Poluentes Ambientais/toxicidade , Feminino , Cromatografia Gasosa-Espectrometria de Massas , Hexaclorobenzeno/sangue , Hexaclorobenzeno/toxicidade , Humanos , Hidrocarbonetos Clorados/toxicidade , Recém-Nascido , Masculino , Bifenilos Policlorados/sangue , Bifenilos Policlorados/toxicidade , Gravidez , Efeitos Tardios da Exposição Pré-Natal/sangue , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Suécia/epidemiologia
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