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1.
Environ Pollut ; 292(Pt A): 118264, 2022 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-34606968

RESUMO

Preterm birth is the second most common cause of death in children under 5 years of age. The etiology of preterm birth has not yet been elucidated. Although maternal exposure to endocrine disrupting chemicals (EDCs) may increase the risk for preterm birth, associations have not been confirmed. We performed a meta-analysis to elucidate the relationships between maternal exposure to EDCs and preterm birth. A systematic search of PubMed, Ovid-EMBASE, and the Cochrane Library (CENTRAL) for relevant published studies providing quantitative data on the association between maternal EDC exposure and preterm birth in humans was conducted in July 2021. To calculate the overall estimates, we pooled the adjusted regression coefficients with 95% confidence intervals (CIs) from each study by the inverse variance method. A total of 59 studies were included. The pooled results indicated that maternal exposure to metals (OR, 1.23; 95% CI, 1.17 to 1.29) and phthalates (OR, 1.31; 95% CI, 1.21 to 1.42) was related to an increased risk for preterm birth. Specifically, maternal exposure to lead, cadmium, chromium, copper and manganese appeared to be correlated with an elevated risk for preterm birth. Additionally, maternal exposure to monoethyl phthalate (MEP), mono-2-ethyl-5-carboxypentyl phthalate (MECPP), monobenzyl phthalate (MBzP), and di (2-ethylhexyl) phthalate (DEHP) was also associated with preterm birth. In conclusion, maternal exposure to metals and phthalates may increase the risk for preterm birth based on current evidence.


Assuntos
Disruptores Endócrinos , Poluentes Ambientais , Ácidos Ftálicos , Nascimento Prematuro , Criança , Pré-Escolar , Exposição Ambiental , Feminino , Humanos , Recém-Nascido , Exposição Materna , Ácidos Ftálicos/toxicidade , Gravidez , Nascimento Prematuro/induzido quimicamente , Nascimento Prematuro/epidemiologia , Análise de Regressão
2.
Environ Pollut ; 292(Pt A): 118336, 2022 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-34634403

RESUMO

BACKGROUND: Studies have linked gaseous air pollutants to multiple health effects via inflammatory pathways. Several major inflammatory biomarkers, including C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) have also been considered as predictors of cardiovascular disease. However, there has been no meta-analysis to evaluate the associations between gaseous air pollutants and these typical biomarkers of inflammation to date. OBJECTIVES: To evaluate the overall associations between short-term and long-term exposures to ambient ozone (O3), nitrogen dioxide (NO2), sulfur dioxide (SO2), carbon dioxide (CO) and major inflammatory biomarkers including CRP, fibrinogen, IL-6 and TNF-α. METHODS: A meta-analysis was conducted for publications from PubMed, Web of Science, Scopus and EMBASE databases up to Feb 1st, 2021. RESULTS: The meta-analysis included 38 studies conducted among 210,438 participants. Generally, we only observed significant positive associations between short-term exposures to gaseous air pollutants and inflammatory biomarkers. For a 10 µg/m3 increase in short-term exposure to O3, NO2, and SO2, there were significant increases of 1.05% (95%CI: 0.09%, 2.02%), 1.60% (95%CI: 0.49%, 2.72%), and 10.44% (95%CI: 4.20%, 17.05%) in CRP, respectively. Meanwhile, a 10 µg/m3 increase in NO2 was also associated with a 4.85% (95%CI: 1.10%, 8.73%) increase in TNF-α. Long-term exposures to gaseous air pollutants were not statistically associated with these biomarkers, but the study numbers were relatively small. Subgroup analyses found more apparent associations in studies with better study design, higher quality, and smaller sample size. Meanwhile, the associations also varied across studies conducted in different geographical regions. CONCLUSION: Short-term exposure to gaseous air pollutants is associated with increased levels of circulating inflammatory biomarkers, suggesting that a systemic inflammatory state is activated upon exposure. More studies on long-term exposure to gaseous air pollutants and inflammatory biomarkers are warranted to verify the associations.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Ozônio , Poluentes Atmosféricos/análise , Poluição do Ar/análise , Biomarcadores , Exposição Ambiental/análise , Humanos , Inflamação/induzido quimicamente , Dióxido de Nitrogênio/análise , Ozônio/análise , Material Particulado/análise
3.
Environ Pollut ; 292(Pt B): 118351, 2022 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-34637830

RESUMO

Particulate matter exposure and related chemical changes in drinking water have been associated with health problems and inflammatory disorders. This study aimed to examine the effect of orally administered ash-water dilution on the gut of mice under normal and inflammatory conditions. Balb/c mice received ash-released soluble and dust-suspended components in the drinking water for 14 days. On day 7, animals were intrarectally instilled with TNBS in ethanol or flagellin from Salmonella typhimurium in PBS. At sacrifice, colon segments were collected and histologic damage, mRNA expression and cytokine levels in tissue were evaluated. In addition, these parameters were also evaluated in IL-10 null mice. We found that mice that received 5% w. fine-ash dilution in the drinking water worsened colitis signs. Weight loss, shortening of the colon, tissue edema with mucosa and submucosa cell infiltration and production of pro-inflammatory cytokines and chemokines were enhanced compared to control mice. A more pronounced inflammation was observed in IL-10 null mice. In addition, markers of NLRP3-dependent inflammasome activation were found in animals exposed to ash. In conclusion, ingestion of contaminated water with dust-suspended particulate matter enhanced the inflammatory response in the gut, probably due to alteration of the gut barrier and promoting an intense contact with the luminal content. This study critically appraises the response for fine particulate matter in uncommon illnesses reported for volcanic ash pollution. We suggest actions to enable better prediction and assessment the health impacts of volcanic eruptions.


Assuntos
Colite , Erupções Vulcânicas , Animais , Colite/induzido quimicamente , Inflamação/induzido quimicamente , Camundongos , Material Particulado/toxicidade
4.
Environ Pollut ; 292(Pt B): 118381, 2022 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-34673156

RESUMO

Colon microenvironment and microbiota dysbiosis are closely related to various human metabolic diseases. In this study, a total of 72 healthy female mice were exposed to fluoride (F) (0, 25, 50 and 100 mg/L F-) in drinking water for 70 days. The effect of F on intestinal barrier and the diversity and composition in colon microbiota have been evaluated. Meanwhile, the relationship among F-induced colon microbiota alterations and antimicrobial peptides (AMPs) expression and short-chain fatty acids (SCFAs) level also been assessed. The results suggested that F decreased the goblet cells number and glycoprotein expression in colon. And further high-throughput 16S rRNA gene sequencing result demonstrated that F exposure induced the diversity and community composition of colonic microbiota significantly changes. Linear Discriminant Analysis Effect Size (LEfSe) analysis identified 11 predominantly characteristic taxa which may be the biomarker in response to F exposure. F-induced intestinal microbiota perturbations lead to the significantly decreased SCFAs levels in colon. Immunofluorescence results showed that F increased the protein expression of interleukin-17A (IL-17A) and IL-22 (P < 0.01) and disturbed the expression of interleukin-17 receptor A (IL-17RA) and IL-22R (P < 0.05 or P < 0.01). In addition, the increased expression of IL-17A and IL-22 cooperatively enhanced the mRNA expression of AMPs which response to F-induced microbiota perturbations. Collectively, destroyed microenvironment and disturbed AMPs are the primary reason of microbiota dysbiosis in colon after F exposure. Colonic homoeostasis imbalance would be helpful for finding the source of F-induced chronic systemic diseases.


Assuntos
Disbiose , Microbioma Gastrointestinal , Animais , Colo , Disbiose/induzido quimicamente , Feminino , Fluoretos , Camundongos , Proteínas Citotóxicas Formadoras de Poros , RNA Ribossômico 16S/genética
5.
J Ethnopharmacol ; 282: 114574, 2022 Jan 10.
Artigo em Inglês | MEDLINE | ID: mdl-34461187

RESUMO

ETHNOPHARMACOLOGICAL RELEVANCE: Gekko gecko is used as a traditional medicine for various diseases including respiratory disorders in northeast Asian countries, mainly Korea, Japan, and China. AIM OF THE STUDY: Allergic asthma is a chronic respiratory disease caused by an inappropriate immune response. Due to the recent spread of coronavirus disease 2019, interest in the treatment of pulmonary disorders has rapidly increased. In this study, we investigated the anti-asthmatic effects of G. gecko extract (GGE) using an established mouse model of ovalbumin-induced asthma. MATERIALS AND METHODS: To evaluate the anti-asthmatic effects of GGE, we evaluated histological changes and the responses of inflammatory mediators related to allergic airway inflammation. Furthermore, we investigated the regulatory effects of GGE on type 2 helper T (Th2) cell activation. RESULTS: Administration of GGE attenuated asthmatic phenotypes, including inflammatory cell infiltration, mucus production, and expression of Th2 cytokines. Furthermore, GGE treatment reduced Th2 cell activation and differentiation. CONCLUSIONS: These results indicate that GGE alleviates allergic airway inflammation by regulating Th2 cell activation and differentiation.


Assuntos
Antiasmáticos/uso terapêutico , Asma/tratamento farmacológico , Medicina Tradicional do Leste Asiático , Muco/metabolismo , Ovalbumina , Extratos Vegetais/uso terapêutico , Animais , Asma/induzido quimicamente , Asma/patologia , Líquido da Lavagem Broncoalveolar , COVID-19 , Citocinas/metabolismo , Feminino , Citometria de Fluxo , Imunoglobulina E/imunologia , Mediadores da Inflamação/metabolismo , Pulmão/patologia , Camundongos , Camundongos Endogâmicos BALB C , Pandemias , Células Th2/efeitos dos fármacos , Células Th2/imunologia , Triptaminas/farmacologia
6.
J Hazard Mater ; 421: 126704, 2022 01 05.
Artigo em Inglês | MEDLINE | ID: mdl-34325292

RESUMO

Cadmium (Cd) is a toxic environmental pollutant and induces toxic effects to organism. Nevertheless, the mechanism of Cd-induced toxicity in swine remains obscure. To explore this, 10 healthy 6-week-old weaned swine were placed into two groups stochastically, the Cd group was treated with a commercial diet containing 20 mg/kg Cd for 40 days. The results of histopathological and ultrastructural observations showed typical necrosis features and inflammatory cell infiltration in Cd group. Excessive Cd suppressed T-AOC and SOD activities, increased MDA content and ROS levels. Cd diet elevated the expression of RIPK1, RIPK3, and MLKL to activate the RIPK3-dependent necroptosis pathway. Results of Th1 and Th2 cytokines indicated that the levels of IL-4, IL-6 and IL10 was increased, while the level of IFN-γ was decreased, illustrating Th1/Th2 immune imbalance leads to aggravate inflammatory responses. Cd activated the TNF-α/NF-κB pathway and induced inflammatory responses via increasing the expression of HO-1, IL-1ß, iNOS, COX2. Heat shock proteins were notably elevated in response to inflammatory reactions. And these effects were inhibited by necrostatin-1 (Nec-1) and N-acetyl-cysteine (NAC). Altogether, these data demonstrated that Cd induced necroptosis and inflammation to aggravate small intestine injury in swine by increasing the excessive accumulation of ROS and imbalanced Th1/Th2, respectively.


Assuntos
NF-kappa B , Necroptose , Animais , Cádmio/toxicidade , Inflamação/induzido quimicamente , Intestino Delgado/metabolismo , NF-kappa B/genética , NF-kappa B/metabolismo , Estresse Oxidativo , Suínos , Fator de Necrose Tumoral alfa
7.
J Hazard Mater ; 421: 126710, 2022 01 05.
Artigo em Inglês | MEDLINE | ID: mdl-34332479

RESUMO

The particulate matter (PM) in livestock houses, one of the primary sources of atmospheric PM, is not only detrimental to the respiratory health of animals and farmworkers but also poses a threat to the public environment and public health and warrants increased attention. In this study, we investigated the variation in the pulmonary microbiome and metabolome in broiler chickens exposed to PM collected from a broiler house. We examined the pulmonary microbiome and metabolome in broilers, observing that PM induced a visible change in α and ß diversity. A total of 66 differential genera, including unclassified_f_Ruminococcaceae and Campylobacter, were associated with pulmonary inflammation. Untargeted metabolomics was utilised to identify 63 differential metabolites induced by PM and correlated with differential bacteria. We observed that PM resulted in injury of the broiler lung and disruption of the microbial community, as well as causing changes in the observed metabolites. These results imply that perturbations to the microbiome and metabolome may play pivotal roles in the mechanism underlying PM-induced broiler lung damage.


Assuntos
Metaboloma , Microbiota , Animais , Galinhas , Inflamação/induzido quimicamente , Pulmão , Material Particulado/toxicidade
8.
Chemosphere ; 286(Pt 1): 131545, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34293563

RESUMO

Several studies have reported exposure of humans to various endocrine disrupting chemicals (EDCs) worldwide. However, there is a lack of data regarding EDC exposures in humans living in Southeast Asian countries, such as the Philippines. Hence, this study measured levels of 41 EDCs in women residing in the Greater Manila Area, home to the second largest city in Southeast Asia. Urine samples from women with versus without breast cancer were analyzed for 11 phthalate metabolites, 8 environmental phenols, and 10 bisphenols, while serum samples were analyzed for 12 perfluoroalkyl substances (PFAS). Out of the four groups of EDCs analyzed, PFAS were significantly associated with breast cancer (adjusted OR = 13.63, 95% CI: 3.24-94.88 p-trend = 0.001 for PFDoA; adjusted OR = 9.26, 95% CI 2.54-45.10, p-trend = 0.002 for PFDA; and adjusted OR = 2.66, 95% CI: 0.95-7.66, p-trend = 0.004 for PFHxA). Long-chain PFAS levels were positively correlated with age and were significantly higher in women from Region IV-A, a heavily industrialized region, than from the National Capital Region. Overall, this study showed baseline information regarding the level of EDCs in Filipinas, providing a glimpse of EDC exposure in women living in a megalopolis city in Southeast Asia.


Assuntos
Neoplasias da Mama , Disruptores Endócrinos , Poluentes Ambientais , Fluorcarbonetos , Neoplasias da Mama/induzido quimicamente , Neoplasias da Mama/epidemiologia , Feminino , Humanos , Filipinas
9.
Chemosphere ; 286(Pt 1): 131495, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34293567

RESUMO

Certain endocrine disruptor chemicals are involved in the pathogenesis of polycystic ovary syndrome (PCOS), a hormonal disease related to infertility in women. Phthalates are the most common plasticizers found in several consumer products. Experimental and epidemiologic evidence suggests that some phthalates disrupt endocrine functions in reproductive mechanisms and development. We previously measured the levels of eight phthalate metabolites in the urine of 599 Saudi women who underwent in vitro fertilization (IVF) treatment and were enrolled in a prospective study (2015-2017). The current nested case-control study aimed to determine the association between urinary levels of phthalate metabolites and PCOS. Overall, 441 women from the IVF study were identified as eligible for this study. Women in the case group included those diagnosed with PCOS (N = 82). The control group comprised those unable to conceive due to male azoospermia or who underwent preimplantation genetic diagnosis (N = 359). Most urinary phthalate metabolite levels were several-fold higher than those reported in national surveys from other countries. The ratio of luteinizing hormone to follicle-stimulating hormone, an index of PCOS, was significantly higher in the case than in the control group, with no indication of its association with phthalate metabolites. The logistic regression model was applied after adjusting for confounders to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for each metabolite modeled as a natural logarithm (ln). For each ln-unit increase in the sum of the four di (2-ethylhexyl) phthalate (∑4DEHP) metabolites as well as two individual metabolites, mono-(2-ethyl-5-oxohexyl) phthalate and mono-(2-ethyl-5-carboxypentyl) phthalate, the odds of PCOS increased by 40.5% [OR = 1.405 (95% CI: 1.025, 1.925)], 41.1% [OR = 1.055 (95% CI: 1.055, 1.885)], and 38.6% [OR = 1.386 (95% CI: 1.033, 1.86)], respectively. In contrast, the % odds of PCOS decreased marginally significantly by 44% [OR = 0.560 (95% CI: 0.313, 1.002)] with an ln-unit increase of %MEHP4, the ratio of mono-(2-ethylhexyl) phthalate to ∑4DEHP. These findings suggest that DEHP may contribute to PCOS, and further investigation is required to understand the underlying mechanisms.


Assuntos
Poluentes Ambientais , Síndrome do Ovário Policístico , Estudos de Casos e Controles , Feminino , Fertilização In Vitro , Humanos , Masculino , Ácidos Ftálicos , Síndrome do Ovário Policístico/induzido quimicamente , Síndrome do Ovário Policístico/epidemiologia , Estudos Prospectivos
10.
Chemosphere ; 286(Pt 1): 131614, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34325257

RESUMO

Particulate matter (PM)-induced airway inflammation contributes to the development and exacerbation of chronic airway diseases. Circular RNA (circRNA) is a new class of non-coding RNA that participates in gene regulation in various respiratory diseases, but the regulatory role of circRNA in PM-induced airway inflammation has not been fully elucidated. In this study, we performed the human circRNA microarray to reveal differentially expressed circRNAs in PM-induced human bronchial epithelial cells (HBECs). A total of 176 upregulated and 15 downregulated circRNAs were identified. Of these, a new circRNA termed circTXNRD1 was upregulated by PM exposure in a dose- and time-dependent manner. Knockdown of circTXNRD1 significantly attenuated PM-induced expression of proinflammatory cytokine interleukin 6 (IL-6). CircRNA pull-down, dual-luciferase reporter assay and fluorescence in situ hybridization showed that circTXNRD1 acted as an endogenous sponge to decrease miR-892a levels in HBECs. Downregulation of miR-892a could increase cyclooxygenase-2 (COX-2) expression and eventually promote IL-6 secretion in PM-induced HBECs. Taken together, our findings reveal circTXNRD1 as a novel inflammatory mediator in PM-induced inflammation in HBECs via regulating miR-892a/COX-2 axis. These results provide new insight into the biological mechanism underlying PM-induced inflammation in chronic airway diseases.


Assuntos
MicroRNAs , RNA Circular , Ciclo-Oxigenase 2/genética , Células Epiteliais , Humanos , Hibridização in Situ Fluorescente , Inflamação/induzido quimicamente , Inflamação/genética , MicroRNAs/genética , Material Particulado/toxicidade , RNA/genética
11.
Chemosphere ; 286(Pt 2): 131833, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34426128

RESUMO

Due to the poor living and healthcare conditions, preterm birth (PTB) in rural population is a pressing health issue. However, PTB studies in rural population are rare. To explore the effects of air pollutants on PTB in rural population, we collected 697,316 medical records during 2014-2016 based on the National Free Preconception Health Examination Project. Logistic regression models were used to estimate the association between air pollutants and PTB and the modifying effects of demographic characteristics. Relative contribution and principal component analysis-generalized linear model (PCA-GLM) analysis were used to explore the most significant air pollutant and gestational period. Our results demonstrated that PTB risk is positively associated with exposure to air pollutants including PM10, PM2.5, SO2, NO2, and CO, while negatively associated with O3 exposure (P < 0.05). In addition, we found that NO2 was the largest contributor to the risk of PTB caused by air pollutants (26.5%). The third trimester of pregnancy was the most sensitive exposure window. PCA-GLM analysis showed that the first component (a combination of PM, SO2, NO2, and CO) increased the risk of PTB. Moreover, we found that rural women who are younger, had higher educated, multi-parity, or smoke appeared to be more sensitive to the association between air pollutants exposure and PTB (P-interaction<0.05). Our findings suggested that increased air pollutants except O3 were associated with elevated PTB risk, especially among vulnerable mothers. Therefore, the effects of air pollutants exposure on PTB should be mitigated by restricting emission sources of NO2 and SO2 in rural population, especially during the third trimester.


Assuntos
Poluentes Atmosféricos , Poluição do Ar , Nascimento Prematuro , Efeitos Tardios da Exposição Pré-Natal , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , China/epidemiologia , Feminino , Humanos , Recém-Nascido , Exposição Materna/estatística & dados numéricos , Material Particulado/análise , Material Particulado/toxicidade , Gravidez , Nascimento Prematuro/induzido quimicamente , Nascimento Prematuro/epidemiologia , População Rural
12.
Chemosphere ; 286(Pt 2): 131802, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34426134

RESUMO

BACKGROUND: Spontaneous abortion (SAB) brings serious physical and psychological sequelae to women and their families. Though a growing body of individual studies have suggested the possible linkage between chronic particulate matter (PM) exposure and risks of SAB, the provided results were rather contradictory. We therefore performed an evidence-based meta-analysis. METHODS: We systematically searched the PubMed, EMBASE and Web of Science databases for available studies published before February 1, 2021 which reported associations between PM exposure and SAB. Corresponding models were applied to combine relative risks (RRs) and their confidence intervals (CIs) from eligible studies according to heterogeneity test. The GRADEpro app was used to evaluate the certainty of evidence. Sensitivity analyses and a publication bias assessment were also utilized to determine the stability of results. RESULTS: Of the initial 2358 citations, 6 papers examining the chronic effects of PM exposure were deemed eligible and a total population of approximately 723,000 was observed. Pooled RR for SAB risks associated with a 10 µg/m3 increase in fine particulate matter (PM2.5) and particulate matter ≤ 10 µm in aerodynamic diameter (PM10) were 1.20 (95%CI: 1.01-1.40) and 1.09 (95%CI: 1.02-1.15), respectively. The GRADE results of PM2.5 and PM10 were both categorized as "moderate" certainty evidence. CONCLUSION: Our findings revealed a significant increase of SAB hazards related with maternal PM exposure, and this study may therefore provide new evidence for personal protection to improve reproductive health.


Assuntos
Aborto Espontâneo , Poluentes Atmosféricos , Poluição do Ar , Aborto Espontâneo/induzido quimicamente , Aborto Espontâneo/epidemiologia , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Exposição Ambiental/análise , Exposição Ambiental/estatística & dados numéricos , Feminino , Humanos , Material Particulado/análise , Gravidez
13.
Chemosphere ; 286(Pt 2): 131811, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34365169

RESUMO

As humans are always exposed to multiple pesticides, it is necessary to conduct risk assessments for pesticide mixtures. Due to data limitations, in this study, we introduced a disease-specific screening-level modeling framework to simulate the cumulative cancer risk (CR) of carcinogenic pesticides, which was developed based on the lognormal dose-response (LDR) curve of chemicals with disease-specific modes of action (MOAs). The simulated results of a case study indicate that the cumulative CR can be at least two orders of magnitude higher than the simulated CRs of individual pesticides. The comparison between the LDR model and the linear extrapolation (or cancer slope factor, CSF) model indicates that the CSF model can greatly overestimate population cancer risks. In addition, we applied our model to evaluate current regulatory standards of carcinogenic pesticide mixtures, and the results indicate that current standards for the selected jurisdictions can control the cumulative cancer risks within the acceptable level. However, the CSF model suggests that all selected jurisdictions cannot protect population health against the carcinogenic pesticide mixture, which is due to the nature of the low-dose linear extrapolation that triggers an initial slope when the effect dose is close to zero. Thus, we concluded that although the MOAs of pesticides in human bodies must be evaluated in future studies, our disease-specific model can be a useful and practical tool for cancer risk assessment and regulatory management of pesticide mixtures.


Assuntos
Neoplasias , Praguicidas , Carcinógenos/toxicidade , Detecção Precoce de Câncer , Humanos , Neoplasias/induzido quimicamente , Praguicidas/toxicidade , Medição de Risco
14.
Chemosphere ; 286(Pt 2): 131791, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34371361

RESUMO

Exposure to acrolein was reported to be related with adverse health effects. However, the associations between acrolein exposure and blood lipids remain largely unknown. We assessed the associations of urinary acrolein metabolites with blood lipids using data from the National Health and Nutrition Examination Survey (NHANES) and further investigated the existence of mediation by systemic inflammation in the associations. Urinary acrolein metabolites, N-acetyl-S-(carboxyethyl)-l-cysteine (CEMA) and N-acetyl-S-(3-hydroxypropyl)-l-cysteine (3-HPMA), blood lipids, and serum high sensitivity C-reactive protein (hs-CRP) were measured in the NHANES. The associations of urinary acrolein metabolites with blood lipids and dyslipidemia and hs-CRP were estimated by multiple linear and logistic regression models. Mediation analysis was conducted to evaluate the mediating effects of hs-CRP on the associations between urinary acrolein metabolites and blood lipids. We found urinary CEMA+3-HPMA (∑acrolein) was significantly associated with higher levels of serum triglycerides (TG), hs-CRP, and lower levels of high-density lipoprotein cholesterol (HDL-C). Each 1-unit increment in ln-transformed level of ∑acrolein was associated with a 0.06 mmol/L increment in TG and 0.02 mmol/L decrement in HDL-C (all P <0.05). A positive dose-response relationship was observed between urinary ∑acrolein and dyslipidemia risk. In addition, hs-CRP significantly mediated the associations of urinary ∑acrolein with serum TG and HDL-C, with mediated proportions of 22.12% and 41.41%, respectively. In conclusion, acrolein exposure is associated with the levels of serum TG, HDL-C, and hs-CRP. Hs-CRP may mediate acrolein-associated alterations of blood lipids. Our results indicated that decreased exposure to acrolein may reduce systemic inflammation and dyslipidemia risk.


Assuntos
Acroleína , Lipídeos , HDL-Colesterol , Humanos , Inflamação/induzido quimicamente , Inquéritos Nutricionais
15.
Chemosphere ; 286(Pt 3): 131844, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34392196

RESUMO

The etiology of hypospadias and cryptorchidism, which are the two most common genital anomalies in males, has not been elucidated. Although prenatal exposure to endocrine-disrupting chemicals (EDCs) may increase the risks of hypospadias and cryptorchidism, the associations have not been confirmed. Therefore, we performed a meta-analysis to establish the relationships between prenatal exposure to EDCs and male genital anomalies. A systematic search of PubMed, EMbase, and Cochrane Library CENTRAL for relevant published studies providing quantitative data on the associations between prenatal EDCs exposure and hypospadias/cryptorchidism in humans was conducted. In total, sixteen case-controlled studies were included. Prenatal exposure to overall EDCs was associated with an increased risk of hypospadias in males (OR, 1.34, 95 % CI 1.12 to 1.60). Although there was no statistically significant association between overall EDCs exposure and cryptorchidism (OR, 1.11, 95 % CI 0.99 to 1.24), exposure to phenol substances was associated with an increased risk of cryptorchidism (OR, 1.81, 95 % CI, 1.12 to 2.93). Using the GRADE tool, we found the overall evidence to be of moderate certainty. In conclusion, the current evidence suggests prenatal EDCs exposure may increase the risk of hypospadias in males.


Assuntos
Criptorquidismo , Disruptores Endócrinos , Hipospadia , Estudos de Casos e Controles , Criptorquidismo/induzido quimicamente , Criptorquidismo/epidemiologia , Disruptores Endócrinos/toxicidade , Feminino , Genitália , Humanos , Hipospadia/induzido quimicamente , Hipospadia/epidemiologia , Masculino , Gravidez
16.
Chemosphere ; 286(Pt 2): 131645, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34426127

RESUMO

The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide. Perinatal development is a critical window for altered, lifelong health trajectory, and evidence supports the role of perinatal programming in chronic metabolic diseases. To examine the impact of diet and bisphenol A (BPA) on the developmental trajectory of NAFLD in offspring, we exposed dams from pre-gestation through lactation to a human-relevant dose of oral BPA coupled with intake of high fat Western or Mediterranean-style diets. We assessed hepatic steatosis by quantifying hepatic triglycerides (TGs) and metabolic health by measuring body weight, relative organ weights, and serum hormone levels in dams and offspring at postnatal day 10 (PND10) and 10-months of age. In dams, consumption of the Western or Mediterranean diet increased hepatic TGs 1.7-2.4-fold, independent of BPA intake. Among offspring, both perinatal diet and BPA exposure had a greater impact on metabolic outcomes than on hepatic steatosis. At PND10, serum leptin levels were elevated 2.6-4.8-fold in pups exposed to the Mediterranean diet, with a trend for sex-specific effects on body and organ weights. At 10-months, sex-specific increases in organ weight and hormone levels were observed in mice perinatally exposed to Western + BPA or Mediterranean + BPA. These findings suggest lifestage-specific interaction of perinatal exposures to experimental diets and BPA on offspring metabolic health without effects on NAFLD later in life. Importantly, alterations in dam phenotype by diet and BPA exposure appear to impact offspring health trajectory, emphasizing the need to define dam diet in assessing effects of environmental exposures on offspring health.


Assuntos
Hepatopatia Gordurosa não Alcoólica , Efeitos Tardios da Exposição Pré-Natal , Animais , Compostos Benzidrílicos/toxicidade , Dieta Hiperlipídica/efeitos adversos , Feminino , Masculino , Camundongos , Hepatopatia Gordurosa não Alcoólica/induzido quimicamente , Fenóis , Gravidez
17.
J Sci Food Agric ; 102(1): 434-444, 2022 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-34143895

RESUMO

BACKGROUND: The incidence of inflammatory bowel disease (IBD) continues to increase worldwide. Multiple factors, including diet, loss of the intestinal barrier function, and imbalance of the immune system can cause IBD. A balanced diet is important for maintaining a healthy bowel and preventing IBD from occurring. The effects of probiotic Lactobacillus gasseri-fermented Maillard reaction products (MRPs) prepared by reacting whey protein with galactose on anti-inflammation and intestinal homeostasis were investigated in this study, which compared MPRs and probiotics separately. RESULTS: In an animal colitis model induced by 2% dextran sulfate sodium (DSS), FWG administration alleviated colon length loss and maintained intestinal immune system homeostasis as reflected by down-regulated interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-α output, and metallopeptidase-9, and epithelial barrier balance as reflected by up-regulated occludin, E-cadherin, and zonula occludens-1 production in the colon. Furthermore, the expression of splenic cytokines such as IL-6, TNF-α, and IL-10 was up-regulated in the FWG-treated mice in a comparable amount to the control group to ensure the balance of immune responses. CONCLUSION: This study showed that the use of FWG protects the intestines from colitis caused by DSS and maintains immune balance. FWG increased antioxidant enzyme activity, increased intestinal permeability, and regulated the balance of pro- and anti-inflammatory cytokines in the intestines and spleen. Continued intake of FWG can alleviate IBD symptoms through the preservation of mucosal immune responses, epithelial junction and homeostasis through the regulated splenic cytokines. © 2021 Society of Chemical Industry.


Assuntos
Colite/tratamento farmacológico , Produtos Finais de Glicação Avançada/administração & dosagem , Lactobacillus gasseri/metabolismo , Probióticos/administração & dosagem , Animais , Anti-Inflamatórios/administração & dosagem , Colite/induzido quimicamente , Colite/imunologia , Colite/fisiopatologia , Colo/efeitos dos fármacos , Colo/imunologia , Sulfato de Dextrana/efeitos adversos , Modelos Animais de Doenças , Galactose/metabolismo , Produtos Finais de Glicação Avançada/metabolismo , Homeostase/efeitos dos fármacos , Humanos , Interleucina-10/genética , Interleucina-10/imunologia , Interleucina-6/genética , Interleucina-6/imunologia , Mucosa Intestinal/efeitos dos fármacos , Mucosa Intestinal/imunologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Junções Íntimas/genética , Junções Íntimas/imunologia , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/imunologia , Proteínas do Soro do Leite/metabolismo
18.
Biol Trace Elem Res ; 200(1): 164-171, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-33661473

RESUMO

Dietary cholesterol causes atherosclerosis along with a reduction of copper concentrations in the atherosclerosis wall. This study was to determine the relationship between aorta copper concentrations and the severity of atherosclerotic lesions as well as copper homeostasis in multiple organs in cholesterol-fed rabbits. Male New Zealand white rabbits, 10-week-old and averaged 2.0 kg, were fed a diet containing 1% (w/w) cholesterol or the same diet without cholesterol as controls. Twelve weeks after the feeding, aortic atherosclerotic lesions, serum cholesterol, and multiple organ copper concentrations were measured. Compared to controls, rabbits fed cholesterol-supplemented diet displayed higher serum cholesterol levels and developed atherosclerosis. Copper concentrations in the cholesterol-fed rabbits were increased in the serum and kidney but decreased in the atherosclerosis wall and multiple organs, including heart, liver, spleen, and lung. Furthermore, aorta copper concentrations negatively correlated, respectively, with the severity of the atherosclerotic lesion (r = - 0.64, p = 0.01), the microscope atherosclerotic lesion area (r = - 0.60, p = 0.02), and the stenosis of the lumen (r = - 0.54, p = 0.04). Dietary cholesterol not only causes atherosclerosis but also disturbs copper homeostasis in multiple organ systems. The negative correlation between aorta copper concentrations and the severity of atherosclerotic lesions suggests a vicious cycle between copper reduction and the pathogenesis of atherosclerosis. These changes in copper homeostasis would be additive to atherosclerosis as a risk factor for cardiovascular disease in humans.


Assuntos
Aterosclerose , Colesterol na Dieta , Animais , Aorta , Aterosclerose/induzido quimicamente , Cobre , Homeostase , Masculino , Coelhos
19.
Environ Pollut ; 292(Pt B): 118418, 2022 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-34737028

RESUMO

Animals must partition limited resources between their own growth and subsequent reproduction. Endocrine disruptors (ED) may cause maternal metabolic disorders that decrease successful reproduction and might be responsible for multi- and transgenerational effects in amphibians. We found that the frog Silurana (Xenopus) tropicalis, exposed to environmentally relevant concentrations of benzo[a]pyrene and triclosan throughout its life cycle, produced F1 females with delayed sexual maturity and decreased size and weight. These F1 females displayed a marked metabolic syndrome associated with decreased fasting plasma cholesterol and triglyceride concentrations and decreased gonadal development. F1 females from F0 exposed animals also had decreased reproductive investment highlighted by a decrease of oocyte lipid reserves associated with significant F2-tadpole mortality. F2 females from F0 exposed animals also displayed a marked metabolic syndrome but were able to correctly direct liver lipid metabolism to the constitution of fat bodies and oocyte yolk stores. In addition, the F2 females produced progeny that had normal mortality levels at 5 days post hatching compared to the controls suggesting a good reproductive investment. Our data confirmed that these ED, at concentrations often found in natural ponds, can induce multi- and transgenerational metabolic disorders in the progeny of amphibians that are not directly exposed. We present a hypothesis to explain the transmission of the metabolic syndrome across generations through modification of egg reserves. However, when high mortality occurred at the tadpole stage, surviving females were able to cope with metabolic costs and produce viable progeny through sufficient investment in the contents of oocyte reserves.


Assuntos
Doenças Metabólicas , Triclosan , Animais , Benzo(a)pireno/toxicidade , Feminino , Doenças Metabólicas/induzido quimicamente , Reprodução , Triclosan/toxicidade , Xenopus laevis
20.
Environ Pollut ; 292(Pt B): 118469, 2022 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-34752792

RESUMO

Although it is a probable human carcinogen, propylene oxide is widely applied in industry and daily life. However, data on neurodevelopmental effects of propylene oxide exposure among children are extremely limited. We aimed to determine the urinary concentrations of propylene oxide metabolite among school-aged children and evaluate the potential association of propylene oxide exposure with risk of dyslexia. A total of 355 dyslexic children and 390 controls were recruited from three cities (Jining, Wuhan, and Hangzhou) in China, between 2017 and 2020. Urinary N-acetyl-S-(2-hydroxypropyl)-L-cysteine (i.e., 2-hydroxypropyl mercapturic acid; 2-HPMA) was measured as the biomarker of propylene oxide exposure. The detection frequency of 2-HPMA was 100%. After adjusting for potential confounders, the odds ratio (OR) for dyslexia per 2-fold increase in urinary 2-HPMA was 1.19 [95% confidence interval (95% CI): 1.01, 1.40, P = 0.042]. Compared with the lowest quartile of urinary 2-HPMA concentrations, children with the highest quartile of 2-HPMA had a 1.63-fold (95% CI: 1.03, 2.56, P = 0.036) significantly increased risk of dyslexia, with a dose-response relationship (P-trend = 0.047). This study provides epidemiological data on the potential association between propylene oxide exposure and the risk of dyslexia in children. Further studies are warranted to confirm the findings and reveal the underlying biological mechanisms.


Assuntos
Dislexia , Compostos de Epóxi , Acetilcisteína , Criança , Cidades , Dislexia/induzido quimicamente , Dislexia/epidemiologia , Humanos
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