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1.
Sci Total Environ ; 792: 148440, 2021 Oct 20.
Artigo em Inglês | MEDLINE | ID: mdl-34465058

RESUMO

Previously, we systemically confirmed that prenatal caffeine exposure (PCE) could cause intrauterine growth retardation (IUGR) and adrenal steroid synthesis dysfunction in offspring rats. However, the multi-generation inheritance of adrenal dysfunction and its epigenetic mechanism has not been reported. In this study, the PCE rat model was established, part of the pregnant rats were executed on gestational day 20, while the others were delivered normally and the fetal rats were reared into adulthood. The PCE female rats of filial generation 1 (F1) were mated with wild males to produce F2 offspring, and the same way to produce F3 offspring. All the adult female rats of three generations were sacrificed for the related detection. Results showed that PCE could decrease fetal weight, increase IUGR rate, and elevate serum corticosterone level. Meanwhile, the expression of fetal adrenal GR, DNMT3a/3b, miRNA let-7c increased while those of CTCF, H19, and StAR decreased, and the total methylation rate of the H19 promoter region was enhanced. We used SW-13 cells to clarify the molecular mechanism and found that cortisol-induced in vitro changes of these indexes were consistent with those in vivo. We confirmed that high level of cortisol through activating GR, on the one hand, promoted let-7 expression and inhibited StAR expression; on the other hand, caused high methylation and low expression of H19 by down-regulating CTCF and up-regulating DNMT3a/3b, then enhanced let-7 inhibitory effect on StAR by "molecular sponge" effect. Finally, in vivo experiments showed that the adrenal steroid synthesis function and H19/let-7 axis presented the glucocorticoid-dependent changes in the adult female F1, F2, and F3. In conclusion, PCE can cause female adrenal dysfunction with matrilineal multi-generation inheritance, which is related to the programming alteration of the H19/let-7 axis. This study provides a novel perspective to explain the multi-generation inheritance of fetal-originated disease in IUGR offspring.


Assuntos
Cafeína , Efeitos Tardios da Exposição Pré-Natal , Animais , Corticosterona , Feminino , Retardo do Crescimento Fetal/induzido quimicamente , Masculino , Gravidez , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Ratos , Ratos Wistar
2.
Int J Mol Sci ; 22(16)2021 Aug 16.
Artigo em Inglês | MEDLINE | ID: mdl-34445488

RESUMO

Prenatal alcohol exposure (PAE) can have immediate and long-lasting toxic and teratogenic effects on an individual's development and health. As a toxicant, alcohol can lead to a variety of physical and neurological anomalies in the fetus that can lead to behavioral and other impairments which may last a lifetime. Recent studies have focused on identifying mechanisms that mediate the immediate teratogenic effects of alcohol on fetal development and mechanisms that facilitate the persistent toxic effects of alcohol on health and predisposition to disease later in life. This review focuses on the contribution of epigenetic modifications and intercellular transporters like extracellular vesicles to the toxicity of PAE and to immediate and long-term consequences on an individual's health and risk of disease.


Assuntos
Etanol/toxicidade , Desenvolvimento Fetal/efeitos dos fármacos , Efeitos Tardios da Exposição Pré-Natal/genética , Teratogênese/genética , Adolescente , Desenvolvimento do Adolescente/efeitos dos fármacos , Adulto , Epigênese Genética/efeitos dos fármacos , Vesículas Extracelulares/efeitos dos fármacos , Vesículas Extracelulares/genética , Feminino , Regulação da Expressão Gênica/efeitos dos fármacos , Humanos , Gravidez
3.
Nutrients ; 13(8)2021 Aug 22.
Artigo em Inglês | MEDLINE | ID: mdl-34445045

RESUMO

In recent years, strong evidence has emerged that exposure to a maternal high-fat diet (HFD) provokes changes in the structure, function, and development of the offspring's brain and may induce several neurodevelopmental and psychiatric illnesses. The aims of this study were to evaluate the effects of a maternal HFD during pregnancy and lactation on depressive-like behavior and Cnr1 gene expression (encoding the CB1 receptor) in brain structures of rat offspring and to investigate the epigenetic mechanism involved in this gene expression. We found that a maternal HFD during pregnancy and lactation induced a depressive-like phenotype at postnatal days (PNDs) 28 and 63. We found that a maternal HFD decreased the Cnr1 mRNA levels in the prefrontal cortex with the increased levels of miR-212-5p and methylation of CpG islands at the Cnr1 promoter and reduced the level of Cnr1 gene expression in the dorsal striatum with an increased level of miR-154-3p in adolescent male offspring. A contrasting effect of a maternal HFD was observed in the hippocampus, where upregulation of Cnr1 gene expression was accompanied by a decrease of miR-154-3p (at PNDs 28 and 63) and miR-212-5p (at PND 63) expression and methylation of CpG islands at the Cnr1 promoter in male offspring. In summary, we showed that a maternal HFD during pregnancy and lactation triggered several epigenetic mechanisms in the brains of rat offspring, which may be related to long-lasting alterations in the next generation and produce behavioral changes in offspring, including a depressive-like phenotype.


Assuntos
Depressão/genética , Dieta Hiperlipídica/efeitos adversos , Fenômenos Fisiológicos da Nutrição Materna/genética , Efeitos Tardios da Exposição Pré-Natal/genética , Receptor CB1 de Canabinoide/metabolismo , Animais , Comportamento Animal , Encéfalo/metabolismo , Epigênese Genética , Feminino , Expressão Gênica , Lactação/genética , Masculino , Gravidez , Ratos
4.
Int J Mol Sci ; 22(15)2021 Jul 28.
Artigo em Inglês | MEDLINE | ID: mdl-34360870

RESUMO

BACKGROUND: Metformin is commonly used to treat gestational diabetes mellitus. This study investigated the effect of maternal metformin intervention during obese glucose-intolerant pregnancy on the gonadal white adipose tissue (WAT) of 8-week-old male and female mouse offspring. METHODS: C57BL/6J female mice were provided with a control (Con) or obesogenic diet (Ob) to induce pre-conception obesity. Half the obese dams were treated orally with 300 mg/kg/d of metformin (Ob-Met) during pregnancy. Gonadal WAT depots from 8-week-old offspring were investigated for adipocyte size, macrophage infiltration and mRNA expression of pro-inflammatory genes using RT-PCR. RESULTS: Gestational metformin attenuated the adiposity in obese dams and increased the gestation length without correcting the offspring in utero growth restriction and catch-up growth caused by maternal obesity. Despite similar body weight, the Ob and Ob-Met offspring of both sexes showed adipocyte hypertrophy in young adulthood. Male Ob-Met offspring had increased WAT depot weight (p < 0.05), exaggerated adipocyte hyperplasia (p < 0.05 vs. Con and Ob offspring), increased macrophage infiltration measured via histology (p < 0.05) and the mRNA expression of F4/80 (p < 0.05). These changes were not observed in female Ob-Met offspring. CONCLUSIONS: Maternal metformin intervention during obese pregnancy causes excessive adiposity, adipocyte hyperplasia and WAT inflammation in male offspring, highlighting sex-specific effects of prenatal metformin exposure on offspring WAT.


Assuntos
Animais Recém-Nascidos/metabolismo , Diabetes Gestacional , Metformina/farmacologia , Obesidade Materna , Efeitos Tardios da Exposição Pré-Natal , Adiposidade , Animais , Diabetes Gestacional/tratamento farmacológico , Diabetes Gestacional/metabolismo , Feminino , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Obesidade Materna/tratamento farmacológico , Obesidade Materna/metabolismo , Gravidez , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Efeitos Tardios da Exposição Pré-Natal/patologia , Fatores Sexuais
5.
Environ Pollut ; 285: 117376, 2021 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-34380208

RESUMO

Despite the abundance of epidemiological evidence concerning the association between pesticide exposure and adverse health outcomes including acute childhood leukemia (AL), evidence remains inconclusive, and is inherently limited by heterogeneous exposure assessment and multiple statistical testing. We performed a literature search of peer-reviewed studies, published until January 2021, without language restrictions. Summary odds ratios (OR) and 95% confidence intervals (CI) were derived from stratified random-effects meta-analyses by type of exposure and outcome, exposed populations and window of exposure to address the large heterogeneity of existing literature. Heterogeneity and small-study effects were also assessed. We identified 55 eligible studies (n = 48 case-control and n = 7 cohorts) from over 30 countries assessing >200 different exposures of pesticides (n = 160,924 participants). The summary OR for maternal environmental exposure to pesticides (broad term) during pregnancy and AL was 1.88 (95%CI: 1.15-3.08), reaching 2.51 for acute lymphoblastic leukemia (ALL; 95%CI: 1.39-4.55). Analysis by pesticide subtype yielded an increased risk for maternal herbicide (OR: 1.41, 95%CI: 1.00-1.99) and insecticide (OR: 1.60, 95%CI: 1.11-2.29) exposure during pregnancy and AL without heterogeneity (p = 0.12-0.34). Meta-analyses of infant leukemia were only feasible for maternal exposure to pesticides during pregnancy. Higher magnitude risks were observed for maternal pesticide exposure and infant ALL (OR: 2.18, 95%CI: 1.44-3.29), and the highest for infant acute myeloid leukemia (OR: 3.42, 95%CI: 1.98-5.91). Overall, the associations were stronger for maternal exposure during pregnancy compared to childhood exposure. For occupational or mixed exposures, parental, and specifically paternal, pesticide exposure was significantly associated with increased risk of AL (ORparental: 1.75, 95%CI: 1.08-2.85; ORpaternal: 1.20, 95%CI: 1.07-1.35). The epidemiological evidence, supported by mechanistic studies, suggests that pesticide exposure, mainly during pregnancy, increases the risk of childhood leukemia, particularly among infants. Sufficiently powered studies using repeated biomarker analyses are needed to confirm whether there is public health merit in reducing prenatal pesticide exposure.


Assuntos
Exposição Ocupacional , Praguicidas , Leucemia-Linfoma Linfoblástico de Células Precursoras , Efeitos Tardios da Exposição Pré-Natal , Estudos de Casos e Controles , Exposição Ambiental , Feminino , Humanos , Lactente , Masculino , Exposição Materna , Exposição Paterna , Leucemia-Linfoma Linfoblástico de Células Precursoras/induzido quimicamente , Leucemia-Linfoma Linfoblástico de Células Precursoras/epidemiologia , Gravidez , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Fatores de Risco
6.
Behav Neurol ; 2021: 6301458, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34336001

RESUMO

Prenatal exposure to buprenorphine renders offspring vulnerable to cerebral impairments. In this study, our data demonstrate, for the first time, that prenatal exposure to buprenorphine escalates astrocyte activation concurrent with indications of endoplasmic reticulum (ER) stress in the hippocampi of neonates, and this can be prevented by the coadministration of dextromethorphan with buprenorphine. Furthermore, dextromethorphan can inhibit the accumulation of GPR37 in the hippocampus of newborns caused by buprenorphine and is accompanied by the proapoptotic ER stress response that involves the procaspase-3/CHOP pathway. Primary astrocyte cultures derived from the neonates of the buprenorphine group also displayed aberrant ER calcium mobilization and elevated basal levels of cyclooxygenase-2 (COX-2) at 14 days in vitro while showing sensitivity to lipopolysaccharide-activated expression of COX-2. Similarly, these long-lasting defects in the hippocampus and astrocytes were abolished by dextromethorphan. Our findings suggest that prenatal exposure to buprenorphine might instigate long-lasting effects on hippocampal and astrocytic functions. The beneficial effects of prenatal coadministration of dextromethorphan might be, at least in part, attributed to its properties in attenuating astrocyte activation and hippocampal ER stress in neonates.


Assuntos
Buprenorfina , Efeitos Tardios da Exposição Pré-Natal , Apoptose , Astrócitos , Dextrometorfano/toxicidade , Estresse do Retículo Endoplasmático , Feminino , Humanos , Recém-Nascido , Gravidez , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente
7.
Artigo em Inglês | MEDLINE | ID: mdl-34444080

RESUMO

The evidence supporting the idea that natural disaster-related prenatal maternal stress (PNMS) influences the child's development has been accumulating for several years. We conducted a meta-analytical review to quantify this effect on different spheres of child development: birth outcomes, cognitive, motor, physical, socio-emotional, and behavioral development. We systematically searched the literature for articles on this topic (2756 articles retrieved and 37 articles included in the systematic review), extracted the relevant data to calculate the effect sizes, and then performed a meta-analysis for each category of outcomes (30 articles included across the meta-analyses) and meta-regressions to determine the effect of some factors of interest on the association between PNMS and child development: type of PNMS (objective, psychological, cognitive, diet), type of natural disaster (ice storm, flood/cyclone), type of report (maternal, third-party observer, medical), timing of exposure (preconception exposure included or not) and child age at assessment (under 10 or 10 years and older). We found that PNMS significantly influences all spheres of child development. Higher PNMS levels were associated with longer gestational age, larger newborns, and higher BMI and adiposity levels, as well as worse cognitive, motor, socio-emotional, and behavioral outcomes.


Assuntos
Desastres , Desastres Naturais , Efeitos Tardios da Exposição Pré-Natal , Criança , Desenvolvimento Infantil , Feminino , Humanos , Recém-Nascido , Gravidez , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Estresse Psicológico
8.
Arch Oral Biol ; 130: 105245, 2021 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-34438320

RESUMO

OBJECTIVE: To examine whether maternal chewing affects prenatal stress-induced behavioral alternations associated with the changes in apoptosis-related proteins and serotonin pathway of the mouse offspring. DESIGN: Pregnant mice were assigned to control, stress, and stress/chewing groups. Stress mice were placed in restraint tubes, from gestational day 12 until parturition. Stress/chewing mice were given a wooden stick for chewing during stress period. Morris water maze and hole-board tests were applied for behavioral alterations in one-month-old male pups. Hippocampal mRNA expression of B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X protein (Bax) was analyzed by quantitative real-time PCR. Serotonin and tryptophan hydroxylase expression level in the dorsal raphe nucleus was investigated immunohistochemically. RESULTS: Prenatal stress impaired the spatial learning, induced anxiety-like behavior, increased the ratio of hippocampal Bax/Bcl-2 expression, and decreased the expression of serotonin and tryptophan hydroxylase in dorsal raphe nucleus of the offspring. Maternal chewing ameliorated prenatal stress-induced cognitive impairment, anxiety-like behavior, and attenuated the increased ratio of hippocampal Bax/Bcl-2 expression, and the downregulated serotonin signaling in dorsal raphe nucleus of the offspring. CONCLUSIONS: Our results indicate that maternal chewing could improve prenatal stress-related anxiety-like behavior and cognitive impairment in mouse offspring, at least in part by affecting hippocampal apoptotic response and central serotonin pathway.


Assuntos
Disfunção Cognitiva , Efeitos Tardios da Exposição Pré-Natal , Animais , Ansiedade , Cognição , Feminino , Hipocampo , Masculino , Mastigação , Camundongos , Gravidez , Serotonina , Estresse Psicológico/complicações
9.
Nutrients ; 13(7)2021 Jul 16.
Artigo em Inglês | MEDLINE | ID: mdl-34371944

RESUMO

Animal studies have shown that exposure to excess sugar during the prenatal and postnatal periods may alter early brain structure in rat pups. However, evidence in humans is lacking. The aim of this study was to determine associations of maternal total and added sugar intake in pregnancy with early brain tissue organization in infants. Adolescent mothers (n = 41) were recruited during pregnancy and completed 24 h dietary recalls during the second trimester. Diffusion tensor imaging was performed on infants using a 3.0 Tesla Magnetic Resonance Imaging Scanner at 3 weeks. Maps of fractional anisotropy (FA) and mean diffusivity (MD) were constructed. A multiple linear regression was used to examine voxel-wise associations across the brain. Adjusting for postmenstrual age, sex, birth weight, and total energy intake revealed that maternal total and added sugar consumption were associated inversely and diffusely with infant MD values, not FA values. Inverse associations were distributed throughout all of the cortical mantle, including the posterior periphery (Bs = -6.78 to -0.57, Ps < 0.001) and frontal lobe (Bs = -4.72 to -0.77, Ps ≤ 0.002). Our findings suggest that maternal total and added sugar intake during the second trimester are significantly associated with features of brain tissue organization in infants, the foundation for future functional outcomes.


Assuntos
Encéfalo/anatomia & histologia , Encéfalo/diagnóstico por imagem , Açúcares da Dieta , Efeitos Tardios da Exposição Pré-Natal , Fenômenos Fisiológicos da Nutrição Pré-Natal , Adolescente , Anisotropia , Imagem de Tensor de Difusão , Feminino , Humanos , Recém-Nascido , Imageamento por Ressonância Magnética , Masculino , Mães , Gravidez , Segundo Trimestre da Gravidez , Estudos Prospectivos , Adulto Jovem
10.
Medicine (Baltimore) ; 100(34): e26986, 2021 Aug 27.
Artigo em Inglês | MEDLINE | ID: mdl-34449468

RESUMO

BACKGROUND: Maternal tobacco exposure during pregnancy is known to cause a potential hazard to the offspring's health. So far, published studies have shown no consistent results with whether tobacco exposure in utero is causally linked to the development of allergic rhinitis in offspring. The aim of this study was to comprehensively evaluate the association between maternal tobacco exposure during pregnancy and allergic rhinitis in offspring by meta-analysis and to provide reference for clinical work. METHODS: Literatures were searched in CNKI, Wanfang Data, VIP, SinoMed, PubMed, Web of science and Embase up to September 30,2020. Screening, inclusion, quality assessment, data extraction and data analysis of the literatures were conducted. Meta-analysis was performed with Revman 5.3 and State15.1 software. Odds ratio (OR) and 95%CI were used as observation indicators. RESULTS: We had retrieved 16 articles with 22 independent datasets and 11,49,879 sample size. When all the studies were analyzed together, the results showed that maternal smoking exposure during pregnancy would increase the risk of allergic rhinitis in offspring (OR = 1.13, 95%CI:1.02-1.26), especially maternal passive smoking during pregnancy (OR = 1.39, 95%CI:1.05-1.84). But subgroup analysis showed that maternal active smoking during pregnancy was only significantly associated with offspring allergic rhinitis in cross-sectional studies (OR = 1.24, 95%CI:1.07-1.45) and study done in America study (OR = 1.22, 95%CI:1.05-1.42). CONCLUSIONS: Tobacco exposure during pregnancy could increase the risk of allergic rhinitis in offspring. The importance of avoiding prenatal tobacco exposure should be emphasized more for the health of next generation in the public.


Assuntos
Exposição Materna/efeitos adversos , Rinite Alérgica/epidemiologia , Poluição por Fumaça de Tabaco/efeitos adversos , Estudos Transversais , Feminino , Humanos , Razão de Chances , Gravidez , Efeitos Tardios da Exposição Pré-Natal
11.
Int J Mol Sci ; 22(15)2021 Jul 27.
Artigo em Inglês | MEDLINE | ID: mdl-34360774

RESUMO

Trimethyltin (TMT) is an irreversible neurotoxicant. Because prenatal TMT exposure has been reported to induce behavioral changes, this study was conducted to observe gender differences and epigenetic changes using a mouse model. In behavioral testing of offspring at 5 weeks of age, the total times spent in the center, corner, or border zones in the male prenatal TMT-exposed mice were less than those of control unexposed mice in the open-field test. Female TMT-exposed mice scored lower on total numbers of arm entries and percentages of alternations than controls in the Y-maze test with lower body weight. We found that only TMT-exposed males had fewer copies of mtDNA in the hippocampus and prefrontal cortex region than controls. Additional epigenetic changes, including increased 5-methyl cytosine/5-hydroxymethyl cytosine levels in the male TMT hippocampus, were observed. After methylation binding domain (MBD) sequencing, multiple signaling pathways related to metabolism and neurodevelopment, including FoxO signaling, were identified by pathway analysis for differentially methylated regions (DMRs). Increased FOXO3 and decreased ASCL1 expression were also observed in male TMT hippocampi. This study suggests that sex differences and epigenetics should be more carefully considered in prenatal toxicology studies.


Assuntos
Metilação de DNA/efeitos dos fármacos , Hipocampo/metabolismo , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Compostos de Trimetilestanho/toxicidade , Animais , Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo , Feminino , Proteína Forkhead Box O3/metabolismo , Regulação da Expressão Gênica/efeitos dos fármacos , Hipocampo/patologia , Masculino , Camundongos , Gravidez , Efeitos Tardios da Exposição Pré-Natal/patologia , Caracteres Sexuais
12.
Nutrients ; 13(7)2021 Jul 04.
Artigo em Inglês | MEDLINE | ID: mdl-34371812

RESUMO

There is growing evidence that bone health may be programmed in the first years of life. Factors during the prenatal period, especially maternal nutrition, may have an influence on offspring's skeletal development and thus the risk of osteoporosis in further life, which is an increasing societal, health and economic burden. However, it is still inconclusive which early life factors are the most important and to what extent they may affect bone health. We searched through three databases (PubMed, Google Scholar, Cochrane Library) and after eligibility criteria were met, the results of 49 articles were analyzed. This narrative review is an overall summary of up-to-date studies on maternal diet, nutritional status, and birth-related factors that may affect offspring bone development, particularly bone mineral density (BMD). Maternal vitamin D status and diet in pregnancy, anthropometry and birth weight seem to influence BMD, however other factors such as subsequent growth may mediate these associations. Due to the ambiguity of the results in the analyzed studies, future, well-designed studies are needed to address the limitations of the present study.


Assuntos
Densidade Óssea , Dieta/efeitos adversos , Exposição Materna/efeitos adversos , Fenômenos Fisiológicos da Nutrição Materna , Efeitos Tardios da Exposição Pré-Natal/fisiopatologia , Adulto , Peso ao Nascer , Desenvolvimento Ósseo , Criança , Pré-Escolar , Estudos de Coortes , Feminino , Humanos , Lactente , Recém-Nascido , Estado Nutricional , Estudos Observacionais como Assunto , Osteoporose/etiologia , Osteoporose/fisiopatologia , Gravidez , Efeitos Tardios da Exposição Pré-Natal/etiologia , Ensaios Clínicos Controlados Aleatórios como Assunto
13.
Eur J Epidemiol ; 36(8): 861-872, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34420151

RESUMO

Human health effects of airborne lower-chlorinated polychlorinated biphenyls (LC-PCBs) are largely unexplored. Since PCBs may cross the placenta, maternal exposure could potentially have negative consequences for fetal development. We aimed to determine if exposure to airborne PCB during pregnancy was associated with adverse birth outcomes. In this cohort study, exposed women had lived in PCB contaminated apartments at least one year during the 3.6 years before conception or the entire first trimester of pregnancy. The women and their children were followed for birth outcomes in Danish health registers. Logistic regression was performed to estimate odds ratios (OR) for changes in secondary sex ratio, preterm birth, major congenital malformations, cryptorchidism, and being born small for gestational age. We performed linear regression to estimate difference in birth weight among children of exposed and unexposed mothers. All models were adjusted for maternal age, educational level, ethnicity, and calendar time. We identified 885 exposed pregnancies and 3327 unexposed pregnancies. Relative to unexposed women, exposed women had OR 0.97 (95% CI 0.82, 1.15) for secondary sex ratio, OR 1.13 (95% CI 0.76, 1.67) for preterm birth, OR 1.28 (95% CI 0.81, 2.01) for having a child with major malformations, OR 1.73 (95% CI 1.01, 2.95) for cryptorchidism and OR 1.23 (95% CI 0.88, 1.72) for giving birth to a child born small for gestational age. The difference in birth weight for children of exposed compared to unexposed women was - 32 g (95% CI-79, 14). We observed an increased risk of cryptorchidism among boys after maternal airborne LC-PCB exposure, but due to the proxy measure of exposure, inability to perform dose-response analyses, and the lack of comparable literature, larger cohort studies with direct measures of exposure are needed to investigate the safety of airborne LC-PCB exposure during pregnancy.


Assuntos
Poluentes Atmosféricos/toxicidade , Anormalidades Congênitas/etiologia , Exposição Ambiental/efeitos adversos , Crescimento/efeitos dos fármacos , Exposição Materna/efeitos adversos , Bifenilos Policlorados/efeitos adversos , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Adulto , Estudos de Coortes , Anormalidades Congênitas/epidemiologia , Dinamarca/epidemiologia , Feminino , Seguimentos , Humanos , Lactente , Recém-Nascido , Recém-Nascido Pequeno para a Idade Gestacional , Bifenilos Policlorados/análise , Gravidez , Resultado da Gravidez , Nascimento Prematuro , Efeitos Tardios da Exposição Pré-Natal/epidemiologia
14.
Nutrients ; 13(7)2021 Jul 13.
Artigo em Inglês | MEDLINE | ID: mdl-34371892

RESUMO

Probiotic and prebiotic products have shown potential health benefits, including for the prevention of adverse pregnancy outcomes. The incidence of adverse effects in pregnant people and their infants associated with probiotic/prebiotic/synbiotic intake, however, remains unclear. The objectives of this study were to evaluate the evidence on adverse effects of maternal probiotic, prebiotic, and/or synbiotic supplementation during pregnancy and lactation and interpret the findings to help inform clinical decision-making and care of this population. A systematic review was conducted following PRISMA guidelines. Scientific databases were searched using pre-determined terms, and risk of bias assessments were conducted to determine study quality. Inclusion criteria were English language studies, human studies, access to full-text, and probiotic/prebiotic/synbiotic supplementation to the mother and not the infant. In total, 11/100 eligible studies reported adverse effects and were eligible for inclusion in quantitative analysis, and data were visualised in a GOfER diagram. Probiotic and prebiotic products are safe for use during pregnancy and lactation. One study reported increased risk of vaginal discharge and changes in stool consistency (relative risk [95% CI]: 3.67 [1.04, 13.0]) when administering Lactobacillus rhamnosus and L. reuteri. Adverse effects associated with probiotic and prebiotic use do not pose any serious health concerns to mother or infant. Our findings and knowledge translation visualisations provide healthcare professionals and consumers with information to make evidence-informed decisions about the use of pre- and probiotics.


Assuntos
Lactação , Prebióticos , Efeitos Tardios da Exposição Pré-Natal , Probióticos/uso terapêutico , Simbióticos , Feminino , Humanos , Lactente , Recém-Nascido , Prebióticos/efeitos adversos , Gravidez , Probióticos/efeitos adversos , Medição de Risco , Fatores de Risco , Simbióticos/efeitos adversos
15.
Nutrients ; 13(7)2021 Jul 13.
Artigo em Inglês | MEDLINE | ID: mdl-34371900

RESUMO

Excess caloric intake and body fat accumulation lead to obesity, a complex chronic disease that represents a significant public health problem due to the health-related risk factors. There is growing evidence showing that maternal obesity can program the offspring, which influences neonatal phenotype and predispose offspring to metabolic disorders such as obesity. This increased risk may also be epigenetically transmitted across generations. Thus, there is an imperative need to find effective reprogramming approaches in order to resume normal fetal development. Polyphenols are bioactive compounds found in vegetables and fruits that exert its anti-obesity effect through its powerful anti-oxidant and anti-inflammatory activities. Polyphenol supplementation has been proven to counteract the prejudicial effects of maternal obesity programming on progeny. Indeed, some polyphenols can cross the placenta and protect the fetal predisposition against obesity. The present review summarizes the effects of dietary polyphenols on obesity-induced maternal reprogramming as an offspring anti-obesity approach.


Assuntos
Tecido Adiposo/metabolismo , Fármacos Antiobesidade/administração & dosagem , Metabolismo Energético , Obesidade Materna/metabolismo , Obesidade Pediátrica/prevenção & controle , Polifenóis/administração & dosagem , Efeitos Tardios da Exposição Pré-Natal , Tecido Adiposo/fisiopatologia , Adiposidade , Animais , Dieta Saudável , Epigênese Genética , Feminino , Regulação da Expressão Gênica no Desenvolvimento , Humanos , Masculino , Fenômenos Fisiológicos da Nutrição Materna , Estado Nutricional , Obesidade Materna/genética , Obesidade Materna/fisiopatologia , Obesidade Pediátrica/genética , Obesidade Pediátrica/metabolismo , Obesidade Pediátrica/fisiopatologia , Gravidez , Fatores de Risco
16.
Br J Nurs ; 30(15): 890-893, 2021 Aug 12.
Artigo em Inglês | MEDLINE | ID: mdl-34379462

RESUMO

Fetal alcohol syndrome (FAS) and fetal alcohol spectrum disorders (FASDs) are caused by prenatal alcohol exposure (PAE). They cause epigenetic changes, permanent neurodevelopmental deficits, and anomalies in growth and facial structure. This article enforces the need for health and social care professionals to have a greater understanding and awareness of how FAS and FASD may impact on the individual, the family and the community, to enable them to provide the most effective preventive and supportive care possible.


Assuntos
Transtornos do Espectro Alcoólico Fetal , Efeitos Tardios da Exposição Pré-Natal , Feminino , Transtornos do Espectro Alcoólico Fetal/prevenção & controle , Pessoal de Saúde , Humanos , Gravidez
17.
Zhejiang Da Xue Xue Bao Yi Xue Ban ; 50(3): 279-289, 2021 Jun 25.
Artigo em Inglês | MEDLINE | ID: mdl-34402257

RESUMO

To investigate the effects of maternal exposure to 13 chemicals mixture (CM) during pregnancy on pregnancy outcome and health status of maternal/offspring mice. C57BL/6 pregnant mice were given drinking water containing carbaryl dimethoate glyphosate methomyl methyl parathion triadimefon aspartame sodium benzoate calcium disodium ethylene diamine tetra-acetate ethylparaben butylparaben bisphenol A and acacia gum The effects of CM exposure on pregnancy outcome, health status of dams/offspring, levels of circulating inflammatory cytokines in dams/offspring and emotional related behaviors of offspring were evaluated. CM exposure during pregnancy had no significant effect on pregnancy outcome, liver function, body weight of the dams in late pregnancy and uterine/ovarian weight after delivery, however, it led to an increase in maternal serum IFN-γ level (<0.05). CM exposure during pregnancy had no significant effect on the liver function of offspring, but increased the serum IFN-γ, prefrontal cortex IFN-γ, and TNF-α and hippocampus IFN-γ levels in the offspring(all <0.01). In addition, the offspring of CM group showed significant abnormal emotion-related (autism-like) behaviors in adulthood, especially in male offspring. Low dose CM exposure during pregnancy may induce inflammation status in dams/offspring, and lead to autism-like behaviors in offspring, indicating the potential effects of low dose CM exposure on human maternal and infant health.


Assuntos
Transtorno Autístico , Efeitos Tardios da Exposição Pré-Natal , Adulto , Animais , Transtorno Autístico/induzido quimicamente , Feminino , Humanos , Masculino , Exposição Materna/efeitos adversos , Camundongos , Camundongos Endogâmicos C57BL , Fenótipo , Gravidez , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente
18.
Artigo em Inglês | MEDLINE | ID: mdl-34360212

RESUMO

(1) This longitudinal study aimed to investigate the link between prenatal alcohol exposure and prenatal maternal depression with the offspring's low-grade inflammatory status. (2) Prenatal alcohol exposure was determined via maternal self-report during the 3rd trimester of pregnancy (self-report+: n = 29) and the meconium alcohol metabolite Ethyl Glucuronide (EtG), collected at birth (≥30 ng/g: n = 23). The Edinburgh Postnatal Depression Scale (EPDS) was used to screen for prenatal maternal depressive symptoms during the 3rd trimester (≥10: n = 35). Fifteen years later, 122 adolescents (M = 13.32 years; 48.4% female) provided blood samples for the analysis of high sensitivity C-reactive protein (hsCRP; M = 0.91; SD = 1.28). (3) Higher hsCRP levels were found in EtG positive adolescents (p = 0.036, ηp2 = 0.04) and an inverse non-significant dose-response relation with hsCRP (r = -0.35, p = 0.113). For maternal self-reported prenatal alcohol consumption (p = 0.780, ηp2 = 0.00) and prenatal depressive symptoms (p = 0.360, ηp2 = 0.01) no differences for hsCRP levels between the affected and unaffected groups were found. (4) Adolescents with prenatal alcohol exposure are at risk for low-grade systemic inflammation. The EtG biomarker may be more accurate compared to self-reports. The findings suggest that prenatal maternal depression does not evoke low-grade systemic inflammation.


Assuntos
Depressão , Efeitos Tardios da Exposição Pré-Natal , Adolescente , Consumo de Bebidas Alcoólicas/efeitos adversos , Depressão/epidemiologia , Feminino , Humanos , Recém-Nascido , Inflamação , Estudos Longitudinais , Masculino , Exposição Materna/efeitos adversos , Mecônio , Gravidez
19.
Int J Mol Sci ; 22(15)2021 Aug 03.
Artigo em Inglês | MEDLINE | ID: mdl-34361111

RESUMO

Maternal smoking is a risk factor of preterm prelabor rupture of the fetal membranes (pPROM), which is responsible for 30% of preterm births worldwide. Cigarettes induce oxidative stress and inflammation, mechanisms both implicated in fetal membranes (FM) weakening. We hypothesized that the receptor for advanced glycation end-products (RAGE) and its ligands can result in cigarette-dependent inflammation. FM explants and amniotic epithelial cells (AECs) were treated with cigarette smoke condensate (CSC), combined or not with RAGE antagonist peptide (RAP), an inhibitor of RAGE. Cell suffering was evaluated by measuring lactate dehydrogenase (LDH) medium-release. Extracellular HMGB1 (a RAGE ligand) release by amnion and choriodecidua explants were checked by western blot. NF-κB pathway induction was determined by a luciferase gene reporter assay, and inflammation was evaluated by cytokine RT-qPCR and protein quantification. Gelatinase activity was assessed using a specific assay. CSC induced cell suffering and HMGB1 secretion only in the amnion, which is directly associated with a RAGE-dependent response. CSC also affected AECs by inducing inflammation (cytokine release and NFκB activation) and gelatinase activity through RAGE engagement, which was linked to an increase in extracellular matrix degradation. This RAGE dependent CSC-induced inflammation associated with an increase of gelatinase activity could explain a pathological FM weakening directly linked to pPROM.


Assuntos
Âmnio/patologia , Células Epiteliais/patologia , Regulação da Expressão Gênica/efeitos dos fármacos , Inflamação/patologia , Efeitos Tardios da Exposição Pré-Natal/patologia , Fumaça/efeitos adversos , Adulto , Âmnio/efeitos dos fármacos , Âmnio/imunologia , Âmnio/metabolismo , Células Cultivadas , Células Epiteliais/efeitos dos fármacos , Células Epiteliais/imunologia , Células Epiteliais/metabolismo , Feminino , Humanos , Inflamação/induzido quimicamente , Inflamação/metabolismo , Gravidez , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente , Efeitos Tardios da Exposição Pré-Natal/imunologia , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Receptor para Produtos Finais de Glicação Avançada
20.
Sci Rep ; 11(1): 15658, 2021 08 02.
Artigo em Inglês | MEDLINE | ID: mdl-34341434

RESUMO

The COVID-19 pandemic represents a collective trauma that may have enduring stress effects during sensitive periods, such as pregnancy. Prenatal stress may result in epigenetic signatures of stress-related genes (e.g., the serotonin transporter gene, SLC6A4) that may in turn influence infants' behavioral development. In April 2020, we launched a longitudinal cohort study to assess the behavioral and epigenetic vestiges of COVID-19-related prenatal stress exposure in mothers and infants. COVID-19-related prenatal stress was retrospectively assessed at birth. SLC6A4 methylation was assessed in thirteen CpG sites in mothers and infants' buccal cells. Infants' temperament was assessed at 3-month-age. Complete data were available from 108 mother-infant dyads. Greater COVID-19-related prenatal stress was significantly associated with higher infants' SLC6A4 methylation in seven CpG sites. SLC6A4 methylation at these sites predicted infants' temperament at 3 months.


Assuntos
COVID-19 , Metilação de DNA , Pandemias , Efeitos Tardios da Exposição Pré-Natal , SARS-CoV-2/metabolismo , Proteínas da Membrana Plasmática de Transporte de Serotonina , Estresse Fisiológico , Adulto , COVID-19/epidemiologia , COVID-19/genética , COVID-19/metabolismo , Feminino , Humanos , Recém-Nascido , Estudos Longitudinais , Masculino , Gravidez , Efeitos Tardios da Exposição Pré-Natal/epidemiologia , Efeitos Tardios da Exposição Pré-Natal/genética , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Proteínas da Membrana Plasmática de Transporte de Serotonina/genética , Proteínas da Membrana Plasmática de Transporte de Serotonina/metabolismo
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