MARIANA MATERA VERAS
Projetos de Pesquisa
Unidades Organizacionais
LIM/05 - Laboratório de Poluição Atmosférica Experimental, Hospital das Clínicas, Faculdade de Medicina - Líder
15 resultados
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- Concentrated ambient fine particulate matter (PM2.5) exposure induce brain damage in pre and postnatal exposed mice(2020) DOMENICO, Marlise Di; BENEVENUTO, Sarah Gomes de Menezes; TOMASINI, Paula Pellenz; YARIWAKE, Victor Yuji; ALVES, Nilmara de Oliveira; RAHMEIER, Francine Luciano; FERNANDES, Marilda da Cruz; MOURA, Dinara Jaqueline; SALDIVA, Paulo Hilario Nascimento; VERAS, Mariana MateraAir pollution is a public health concern that has been associated with adverse effects on the development and functions of the central nervous system (CNS). However, studies on the effects of exposure to pollutants on the CNS across the entire developmental period still remain scarce. In this study, we investigated the impacts of prenatal and/or postnatal exposure to fine particulate matter (PM2.5) from Sao Paulo city, on the brain structure and behavior of juvenile male mice. BALB/c mice were exposed to PM2.5 concentrated ambient particles (CAP) at a daily concentration of 600 mu g/m(3) during the gestational [gestational day (GD) 1.5-18.5] and the postnatal periods [postnatal day (PND) 22-90] to filtered air (FA) in both periods (FA/FA), to CAP only in the postnatal period (FA/CAP), to CAP only in the gestational period (CAP/FA), and to CAP in both periods (CAP/CAP). Behavioral tests were performed when animals were at PND 30 and PND 90. Glial activation, brain volume, cortical neuron number, serotonergic and GABAergic receptors, as well as oxidative stress, were measured. Mice at PND 90 presented greater behavioral changes in the form of greater locomotor activity in the FA-CAP and CAP-CAP groups. In general, these same groups explored objects longer and the CAP-FA group presented anxiolytic behavior. There was no difference in total brain volume among groups, but a lower corpus callosum (CC) volume was observed in the CAP-FA group. Also, the CAP-CAP group presented an increase in microglia in the cortex and an increased in astrocytes in the cortex, CC, and C1A and dentate gyrus of hippocampus regions. Gene expression analysis showed a decrease in BDNF in the hippocampus of CAP-CAP group. Treatment of immortalized glial cells with non-cytotoxic doses of ambient PM2.5 increased micronuclei frequencies, indicating genomic instability. These findings highlight the potential for negative neurodevelopmental outcomes induced by exposure to moderate levels of PM2.5 in Sao Paulo city.
- Epoxiconazole-Induced Degeneration in Rat Placenta and the Effects of Estradiol Supplementation(2013) MORENO, Maria Cecilia Rey; FUSSELL, Karma C.; GROETERS, Sibylle; SCHNEIDER, Steffen; STRAUSS, Volker; STINCHCOMBE, Stefan; FEGERT, Ivana; VERAS, Mariana; RAVENZWAAY, Bennard vanEpoxiconazole (CAS-No. 133855-98-8) was recently shown to cause both a marked depletion of maternal estradiol blood levels and a significantly increased incidence of late fetal mortality when administered to pregnant rats throughout gestation (GD 7-18 or 21); estradiol supplementation prevented this epoxiconazole effect in rats (Stinchcombe et al., 2013), indicating that epoxiconazole-mediated estradiol depletion is a critical key event for induction of late fetal resorptions in rats. For further elucidation of the mode of action, the placentas from these modified prenatal developmental toxicity experiments with 23 and 50 mg/kg bw/d epoxiconazole were subjected to a detailed histopathological examination. This revealed dose-dependent placental degeneration characterized by cystic dilation of maternal sinuses in the labyrinth, leading to rupture of the interhemal membrane. Concomitant degeneration occurred in the trophospongium. Both placentas supporting live fetuses and late fetal resorptions were affected; the highest degree of severity was observed in placentas with late resorptions. Placental degeneration correlated with a severe decline in maternal serum estradiol concentration. Supplementation with 0.5 and 1.0 g of the synthetic estrogen estradiol cyclopentylpropionate per day reduced the severity of the degeneration in placentas with live fetuses. The present study demonstrates that both the placental degeneration and the increased incidence of late fetal resorptions are due to decreased levels of estrogen, since estrogen supplementation ameliorates the former and abolishes the latter. Birth Defects Res (Part B) 98:208-221, 2013. (c) 2013 Wiley Periodicals, Inc.
- The effects of particulate ambient air pollution on the murine umbilical cord and its vessels: A quantitative morphological and immunohistochemical study(2012) VERAS, Mariana Matera; GUIMARAES-SILVA, Rosane Maria; CALDINI, Elia Garcia; SALDIVA, Paulo H. N.; DOLHNIKOFF, Marisa; MAYHEW, Terry M.Previous studies have shown that particulate matter (PM) compromise birth weight and placental morphology. We hypothesized that exposing mice to ambient PM would affect umbilical cord (UC) morphology. To test this, mice were kept in paired open-top exposure chambers at the same location and ambient conditions but, in one chamber, the air was filtered (F) and, in the other, it was not (NF). UCs were analysed stereologically and by immunohistochemistry to localize isoprostane and endothelin receptors. The cords of mice from NF chambers were smaller in volume due to loss of mucoid connective tissue and decrease in volume of collagen. These structural changes and in umbilical vessels were associated with greater volumes of regions immunostained for isoprostane, ETAR and ETBR. Findings indicate that the adverse effects of PM on birth weight may be mediated in part by alterations in UC structure or imbalances in the endogenous regulators of vascular tone and oxidative stress.
- Chronic exposure to PM2.5 aggravates SLE manifestations in lupus-prone mice(2021) YARIWAKE, Victor Yuji; TORRES, Janaina Iannicelli; SANTOS, Amandda Rakell Peixoto dos; FREITAS, Sarah Cristina Ferreira; ANGELIS, Katia De; FARHAT, Sylvia Costa Lima; CAMARA, Niels Olsen Saraiva; VERAS, Mariana MateraBackground Air pollution causes negative impacts on health. Systemic lupus erythematosus (SLE) is an autoimmune disease with diverse clinical manifestations and multifactorial etiology. Recent studies suggest that air pollution can trigger SLE and induce disease activity. However, this association has not been deeply investigated. Thus, the aim of this study was to evaluate whether exposure to fine particulate matter (PM2.5) exacerbates SLE manifestations, focusing on renal complications, in a lupus-prone animal model. Female NZBWF1 mice were exposed daily to 600 mu g/m(3) of inhaled concentrated ambient particles (CAP) or filtered air (FA). Survival rate, body weight, weight of organs (kidney, spleen, thymus, liver and heart), blood cell count, proteinuria, kidney stereology, renal histopathology, gene expression and oxidative stress were analyzed. Results Female NZBW mice exposed to CAP showed decreased survival, increased circulating neutrophils, early onset of proteinuria and increased kidney weight with renal cortex enlargement when compared to NZBW mice exposed to FA. Conclusions This work shows that air pollution aggravates some SLE manifestations in lupus-prone mice. These results reinforce the need of reducing air pollutant levels in order to promote a better quality of life for individuals diagnosed with SLE.
- Inhalation of fine particulate matter during pregnancy increased IL-4 cytokine levels in the fetal portion of the placenta(2015) MELO, Juliana Oliveira de; SOTO, Sonia Fatima; KATAYAMA, Isis Akemi; WENCESLAU, Camilla Ferreira; PIRES, Amanda Gonalves; VERAS, Mariana Matera; FURUKAWA, Luzia N. S.; CASTRO, Isac de; SALDIVA, Paulo Hilario Nascimento; HEIMANN, Joel ClaudioThis study aimed to verify the development of placental and systemic inflammation in rats exposed to fine particulate matter before or during pregnancy. Wistar rats were exposed to filtered air ( control) or to a load of 600 mu g/m(3) of fine particles in the air. The gene expression of IL-1 beta, IL-4, IL-6, IL-10, INF-gamma, TNF-alpha and Toll-like receptor 4 in the placenta was evaluated. The serum and placental concentrations of IL-1 beta, IL-4, IL-6, IL-10, INF-gamma and TNF-alpha were measured. The total and differential blood leukocyte and blood platelet count was assessed. Compared to control animals, IL-4 content was elevated in the fetal portion of the placenta in rats exposed to air pollution before and during pregnancy. Increased IL-4 suggests that a placental inflammatory reaction may have occurred in response to exposure to fine particulate matter and that this cytokine was responsible, among possibly others factors, for resolution of the inflammatory reaction.
- Air pollution and DOHaD: The health of the next generation with emphasis on the Brazilian population(2023) SALDIVA, Paulo Hilario Nascimento; SANTEE, Kadija; FAJERSTZJAN, Lais; VERAS, Mariana MateraIt is established in the scientific literature that environmental air pollution has acute and chronic harmful consequences on human health. In recent decades, studies showed that the harmful effects of bad air quality can impair future generations. Early exposure to bad air quality (in uterus, infant, and early childhood) can increase the susceptibility to noncommunicable diseases (NCDs) across the lifespan. Brazil and other countries do not meet health safety standards recommended by the World Health Organization, exposing large population to air pollution and its risks. Controlling air quality is crucial in order to face the increase in NCDs and protect the health of the population. Reducing air pollution should be considered a public health policy to prevent and manage NCDs, alongside with well-established recommendations for changes in lifestyle (eating healthy food, exercising, stopping tobacco smoking, etc.).
- Fine particulate matters from air pollution exacerbate renal ischemia reperfusion injury(2022) SANCHES, T.; PARRA, A. C.; VERAS, M.; BUTTER, L. M.; CLAESSEN, N.; ROELOFS, J.; FLORQUIN, S.; KERS, J.; ANDRADE, L.; TAMMARO, A.
- Recreational use of marijuana during pregnancy and negative gestational and fetal outcomes: An experimental study in mice(2017) BENEVENUTO, Sarah G.; DOMENICO, Marlise D.; MARTINS, Marco Antonio G.; COSTA, Natalia S.; SOUZA, Ana Rosa L. de; COSTA, Jose L.; TAVARES, Marina F. M.; DOLHNIKOFF, Marisa; VERAS, Mariana MateraThe prevalence of marijuana use among pregnant women is high. However, the effects on gestation and fetal development are not well known. Epidemiological and experimental studies present conflicting results because of the route of administration, dose, time of exposure, species used, and how Cannabis toxicity is tested (prepared extracts, specific components, or by pyrolysis). In this study, we experimentally investigated the effects of maternal inhalation of Cannabis sativa smoke representing as nearly as possible real world conditions of human marijuana use. Pregnant mice (n=20) were exposed (nose-only) daily for 5 min to marijuana smoke (0.2 g of Cannabis) from gestational day (GD) 5.5 to GD17.5 or filtered air. Food intake and maternal weight gain were recorded. Ultrasound biomicroscopy was performed on 10.5 and 16.5dpc. On GD18.5, half of the dams were euthanized for the evaluation of term fetus, placenta, and resorptions. Gestation length, parturition, and neonatal outcomes were evaluated in the other half. Five minutes of daily (low dose) exposure during pregnancy resulted in reduced birthweight, and litter size was not altered; however, the number of male pups per litter was higher. Besides, placental wet weight was increased and fetal to placental weight ratio was decreased in male fetuses, showing a sex-specific effect. At the end of gestation, females from the Cannabis group presented reduced maternal net body weight gain, despite a slight increase in their daily food intake compared to the control group. In conclusion, our results indicate that smoking marijuana during pregnancy even at low doses can be embryotoxic and fetotoxic.
- Hypoxia: From Placental Development to Fetal Programming(2017) FAJERSZTAJN, Lais; VERAS, Mariana MateraHypoxia may influence normal and different pathological processes. Low oxygenation activates a variety of responses, many of them regulated by hypoxia-inducible factor 1 complex, which is mostly involved in cellular control of O-2 consumption and delivery, inhibition of growth and development, and promotion of anaerobic metabolism. Hypoxia plays a significant physiological role in fetal development; it is involved in different embryonic processes, for example, placentation, angiogenesis, and hematopoiesis. More recently, fetal hypoxia has been associated directly or indirectly with fetal programming of heart, brain, and kidney function and metabolism in adulthood. In this review, the role of hypoxia in fetal development, placentation, and fetal programming is summarized. Hypoxia is a basic mechanism involved in different pregnancy disorders and fetal health developmental complications. Although there are scientific data showing that hypoxia mediates changes in the growth trajectory of the fetus, modulates gene expression by epigenetic mechanisms, and determines the health status later in adulthood, more mechanistic studies are needed. Furthermore, if we consider that intrauterine hypoxia is not a rare event, and can be a consequence of unavoidable exposures to air pollution, nutritional deficiencies, obesity, and other very common conditions (drug addiction and stress), the health of future generations may be damaged and the incidence of some diseases will markedly increase as a consequence of disturbed fetal programming. (C) 2017 Wiley Periodicals, Inc.
- Allergic sensitization and exposure to ambient air pollution beginning early in life lead to a COPD-like phenotype in young adult mice(2022) COSTA, Natalia de Souza Xavier; TELES, Aila Mirtes; BRITO, Jose Mara de; LOPES, Thais de Barros Mendes; ROSSI, Renata Calciolari; MAGALHAES, Fernanda; COSTA, Arantes; SARAIVA-ROMANHOLO, Beatriz Mangueira; PERINI, Adenir; FURUYA, Tatiane Katsue; CARRASCO, Alexis German Murillo; VERAS, Mariana Matera; SALDIVA, Paulo Hilaroi Nascimento; CHAMMAS, Roger; MAUAD, ThaisThe perinatal period and early infancy are considered critical periods for lung development. During this period, adversities such as environmental exposures, allergic sensitization, and asthma are believed to impact lung health in adulthood. Therefore, we hypothesized that concomitant exposure to allergic sensitization and urban -derived fine particulate matter (PM2.5) in the early postnatal period of mice would cause more profound alter-ations in lung alveolarization and growth and differently modulate lung inflammation and gene expression than either insult alone in adult life. BALB/c mice were sensitized with ovalbumin (OVA) and exposed to PM2.5 from the fifth day of life. Then, we assessed lung responsiveness, inflammation in BALF, lung tissue, and alveolari-zation by stereology. In addition, we performed a transcriptomic analysis of lung tissue on the 40th day of life. Our results showed that young adult mice submitted to allergic sensitization and exposure to ambient PM2.5 since early life presented decreased lung growth with impaired alveolarization, a mixed neutrophilic-eosinophilic pattern of lung inflammation, increased airway responsiveness, and increased expression of genes linked to neutrophil recruitment when compared to animals that were OVA-sensitized or PM(2.5 )exposed only. Both, early life allergic sensitization and PM2.5 exposure, induced inflammation and impaired lung growth, but concomitant exposure was associated with worsened inflammation parameters and caused alveolar enlargement. Our experimental data provide pathological support for the hypothesis that allergic or environmental insults in early life have permanent adverse consequences for lung growth. In addition, combined insults were associated with the development of a COPD-like phenotype in young adult mice. Together with our data, current evidence points to the urgent need for healthier environments with fewer childhood disadvantage factors during the critical windows of lung development and growth.