Rozprawy doktorskie na temat „Placental oxidative stress”
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Vanderlelie, Jessica, i n/a. "Placental Oxidative Stress in Preeclampsia". Griffith University. School of Medical Science, 2006. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20060918.161726.
Pełny tekst źródłaVanderlelie, Jessica. "Placental Oxidative Stress in Preeclampsia". Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365679.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Full Text
Khera, Alisha. "Selenium Supplementation Protects Placental Trophoblast Cells from Mitochondrial Oxidative Stress". Thesis, Griffith University, 2016. http://hdl.handle.net/10072/367348.
Pełny tekst źródłaThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
Hung, T. H. "In vitro hypoxia-reoxygenation as a model for placental oxidative stress in preeclampsia". Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604788.
Pełny tekst źródłaAnto, Enoch Odame. "Evaluation of suboptimal health status and prospective levels of oxidative stress biomarkers and angiogenic growth mediators with placental anatomy and pathology in normotensive and preeclamptic births". Thesis, Edith Cowan University, Research Online, Perth, Western Australia, 2020. https://ro.ecu.edu.au/theses/2317.
Pełny tekst źródłaBelhareth, Rym. "Tabac et grossesse". Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5007/document.
Pełny tekst źródłaActive smoking by the mother exposes the developing fetus to agents that can cross the placental barrier and interfere with placental functions. A wide range of immunological functions, including innate and adaptive immune responses, might be impaired. In this study, we assessed the effect of cigarette smoke extract (CSE) on macrophages isolated from human placentas (pMφs), which are major partners of innate feto-maternal immunity. I showed that CSE significantly inhibited the formation of multinucleated giant cells (MGCs). This property of CSE is specific to macrophages because the fusion of monocyte-derived macrophages is inhibited during the in vitro formation of granulomas. I also investigated particle uptake and cytokine production by pMφs exposed to CSE. CSE inhibited the uptake of zymosan, but not that of opsonized zymosan, suggesting that it interferes with phagocytic receptors, not with the phagocytic machinery of pMφs. CSE increased the release of Tumor Necrosis Factor and interleukin-33, and decreased that of interleukin-10, demonstrating that the balance between inflammatory and anti-inflammatory cytokines is affected by CSE. Furthermore, CSE enhanced the expression of metalloproteinase (MMPs) genes such as MMP-1, MMP-10 and MMP-12, known to be involved in tissue remodeling including macrophage fusion. Finally, I showed that nicotine, one of the major compounds of tobacco, did not affect the functional properties of pMφs
Guerby, Paul. "Dysfonction de la nitric oxide synthase endothéliale au cours de la pré-éclampsie : rôle du glutathion et du stress oxydant". Thesis, Toulouse 3, 2019. http://www.theses.fr/2019TOU30078.
Pełny tekst źródłaContext: During pre-eclampsia (PE), the defective trophoblastic invasion and remodeling of the uterine spiral arteries leads to poor adaptation of utero-placental circulation associated with hypoxia/reoxygenation phenomena. This induces oxidative stress and an imbalance between angiogenic/antiangiogenic factors (decrease in VEGF and PIGF vs. increase in sFlt1) responsible for abnormal placentation, endothelial dysfunction and systemic inflammation. Endothelial nitric oxide synthase dysfunction (eNOS) and decreased NO bioavailability play a critical role in the pathophysiology of PE. eNOS is the main source of placental NO production, and plays a key role in homeostasis and vascular tone regulation. Recent evidence indicates that eNOS may undergo glutathionylation in the vascular wall, and subsequent uncoupling in a prooxidant environment, this resulting in an increased generation of superoxide anion and a decreased production of NO. Objective: The purpose of this work was to study the consequences of oxidative stress on placental eNOS, in particular its glutathionylation and modification by lipid oxidation products (LPO), in relation to its dysfunction observed during PE. Materials and Methods: The modification of eNOS was studied in placental tissues obtained from preeclampsia-affected (n=13), vs normal pregnant women (n=9) and in HTR-8/SVneo human trophoblasts exposed to hypoxia/reoxygenation (H/R), or by exposure to LPO. Results: Immunofluorescence and confocal microscopy revealed a high glutathionylation of eNOS in PE placentas, reversed by dithiotreitol, which was confirmed by immunoprecipitation and western-blot experiments, with no difference in total eNOS expression between PE and normal pregnancy. Exposure of HTR8 trophoblasts to H/R conditions generates S-glutathionylation of eNOS associated with reduced NO production, and increased superoxide anion generation. NO is necessary for the invasive potential of trophoblasts, since trophoblasts exposed to H/R, or silenced for eNOS by small interfering RNAs (siRNA), showed a decreased migration capacity, which was restored by the NO donor, NOC-18. In the second part of this work, we investigated the presence of LPO in PE placentas, and hypothesized that eNOS could be a target of these agents. We show that LPO such as 4-hydroxynenal (4-HNE), and 4-oxo-2-nonenal (ONE), accumulate in PE placentas, particularly on eNOS, while no changes are observed in normal pregnancy placentas. Proteomics studies on recombinant eNOS show that ONE and 4-HNE modify several epitopes (ONE-Lys, HNE-His, HNE-Cys). The addition of 4-HNE or ONE to HTR8 inhibits NO production and cell migration, restored by the addition of NOC-18. Conclusions and perspectives: These results show that placental eNOS is an important target for oxidative stress during PE, with modifications by S-glutathionylation or adduct formation with ONE or 4-HNE, associated with a decrease in NO production. These changes could contribute to the dysfunction of placental eNOS observed during the PE. In perspective, we plan to study the consequences of oxidative stress and LPO on accelerated placental aging, which may contribute to the pathophysiology of PE, and beyond, of pathological pregnancies
LARSON, JON SCOTT. "THE VISUALIZATION, QUANTIFICATION AND MODELING OF GENOMIC INSTABILITY IN THE MOUSE AND IN CULTURED CELLS". University of Cincinnati / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1163452507.
Pełny tekst źródłaNunes, Priscila Rezeck. "Efeito do estresse oxidativo sobre autofagia em tecido placentário". Botucatu, 2017. http://hdl.handle.net/11449/148980.
Pełny tekst źródłaResumo: Introdução: A gestação é uma condição fisiológica que pode apresentar maior suscetibilidade ao desequilíbrio entre fatores pró e antioxidativos, evoluindo assim com dano celular e resposta inflamatória. A autofagia é um processo que elimina organelas e proteínas danificadas do citoplasma, com potente mecanismo anti-inflamatório responsável pela manutenção da homeostase celular. A autofagia pode controlar a inflamação por meio da inibição da ativação do inflamassoma, complexo essencial para a liberação de citocinas pró-inflamatórias. Assim, alterações nesses processos podem relacionar-se com disfunções celulares e doenças sistêmicas. Objetivos: Este projeto teve como objetivo avaliar se a exposição de explantes placentários a diferentes concentrações de peróxido de hidrogênio (H2O2) é capaz de induzir autofagia e levar a ativação do inflamassoma NLRP3. Métodos: Explantes placentários de gestantes normais obtidos após o parto foram cultivados em diferentes concentrações de H2O2 por 4 e 24 h após a avaliação da viabilidade dos mesmos nesses períodos. As enzimas superóxido dismutase (SOD) e catalase foram avaliadas nos sobrenadantes das culturas após 4 h. As expressões gênicas de marcadores de autofagia (LC3-II, beclin-1 e p62), do inflamassoma (NLRP3 e caspase-1) e das citocinas IL-1β, IL-10 e TNF-α foram avaliadas por RT-qPCR. Os níveis de gonadotrofina coriônica (hCG), proteína de choque térmico 70 (Hsp70) e citocinas IL-1β, IL-10 e TNF-α foram determinados por ensaio imunoenz... (Resumo completo, clicar acesso eletrônico abaixo)
Mestre
Nunes, Priscila Rezeck [UNESP]. "Efeito do estresse oxidativo sobre autofagia em tecido placentário". Universidade Estadual Paulista (UNESP), 2017. http://hdl.handle.net/11449/148980.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Introdução: A gestação é uma condição fisiológica que pode apresentar maior suscetibilidade ao desequilíbrio entre fatores pró e antioxidativos, evoluindo assim com dano celular e resposta inflamatória. A autofagia é um processo que elimina organelas e proteínas danificadas do citoplasma, com potente mecanismo anti-inflamatório responsável pela manutenção da homeostase celular. A autofagia pode controlar a inflamação por meio da inibição da ativação do inflamassoma, complexo essencial para a liberação de citocinas pró-inflamatórias. Assim, alterações nesses processos podem relacionar-se com disfunções celulares e doenças sistêmicas. Objetivos: Este projeto teve como objetivo avaliar se a exposição de explantes placentários a diferentes concentrações de peróxido de hidrogênio (H2O2) é capaz de induzir autofagia e levar a ativação do inflamassoma NLRP3. Métodos: Explantes placentários de gestantes normais obtidos após o parto foram cultivados em diferentes concentrações de H2O2 por 4 e 24 h após a avaliação da viabilidade dos mesmos nesses períodos. As enzimas superóxido dismutase (SOD) e catalase foram avaliadas nos sobrenadantes das culturas após 4 h. As expressões gênicas de marcadores de autofagia (LC3-II, beclin-1 e p62), do inflamassoma (NLRP3 e caspase-1) e das citocinas IL-1β, IL-10 e TNF-α foram avaliadas por RT-qPCR. Os níveis de gonadotrofina coriônica (hCG), proteína de choque térmico 70 (Hsp70) e citocinas IL-1β, IL-10 e TNF-α foram determinados por ensaio imunoenzimático (ELISA) após 24 h de cultura. Resultados: Os níveis de LDH foram crescentes conforme o tempo de cultura, sendo que as culturas de 24 h apresentaram-se com viabilidade celular adequada para o estudo. Os níveis proteicos de catalase e Hsp70, bem como a expressão gênica de LC3-II, beclin-1 e p62 apresentaram níveis crescentes e relacionados às maiores concentrações de H2O2. As concentrações proteicas de SOD, hCG e TNF-α foram maiores nas culturas com 100 µM de H2O2. A expressão gênica de TNF-α, IL-1β, NLRP3 e caspase-1 foram elevadas em 1000 µM de H2O2. Além disso, a expressão proteica de IL-1β também foi maior nessa concentração. As concentrações gênicas e proteicas de IL-10 decresceram de acordo com o aumento da concentração de H2O2. Conclusões: Os resultados obtidos demonstraram que o H2O2 é capaz de induzir o estado de estresse oxidativo placentário, induzir autofagia, ativar o inflamassoma e assim aumentar a produção de citocinas inflamatórias.
Introduction: Pregnancy is a physiological condition characterized by increased susceptibility to oxidative stress, which can lead to cell damage and inflammatory response. Autophagy is a process that removes damaged organelles and proteins from the cytoplasm. It works as potent anti-inflammatory mechanism, responsible for maintaining cellular homeostasis. Autophagy can control inflammatory responses by regulating the activation of inflammasome, an essential complex for pro-inflammatory cytokine release. Objectives: The aim of this study was to evaluate whether placental explants exposure to hydrogen peroxide (H2O2) is able to induce autophagy and inflammasome activation. Methods: Placental explants achieved from normal pregnant women after delivery were cultured in different concentrations of H2O2 for 4 and 24 h after viability evaluation for these periods. Superoxide dismutase (SOD) and catalase were evaluated in culture supernatants after 4 h. Gene expressions of autophagy markers (LC3-II, beclin-1 and p62), inflammasome (NLRP3 and caspase-1) and IL-1β, IL-10 and TNF-α were assessed by RT-qPCR. Levels of chorionic gonadotrophin (hCG), heat shock protein (Hsp70) and IL-1β, IL-10 and TNF-α were determined by enzyme-linked immunosorbent assay (ELISA) after 24 h of culture. Results: LDH levels were increased according to culture time, and the 24 h cultures presented adequate cell viability for the study. The protein levels of catalase and Hsp70, as well as the gene expression of LC3-II, beclin-1 and p62 presented increasing levels and related to the higher concentrations of H2O2. Protein concentrations of SOD, hCG and TNF-α were higher in cultures with 100 μM of H2O2. Gene expression of TNF-α, IL-1β, NLRP3 and caspase-1 were raised in 1000 μM of H2O2. In addition, IL-1β protein expression was also higher at this concentration. Gene and protein concentrations of IL-10 decreased as the H2O2 concentration increased. Conclusions: Our results demonstrate that H2O2 is able to induce a state of placental oxidative stress, induce autophagy, activate the inflammasome and then increase the production of inflammatory cytokines.
FAPESP: 2014/25611-5
Spada, Ana Paula Machado [UNESP]. "Avaliação do estresse oxidativo no sangue e na placenta de ratas com diabete de intensidade moderada". Universidade Estadual Paulista (UNESP), 2009. http://hdl.handle.net/11449/99250.
Pełny tekst źródłaCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Objetivo: avaliar o estresse oxidativo no sangue e na placenta de ratas com diabete de intensidade moderada. Métodos: O diabete foi induzido em ratas Wistar recém-nascidas (grupo diabete moderado) no dia do nascimento (dia 0) por streptozotocin (100 mg/kg, via subcutênea). As ratas do grupo nãodiabético (controle) receberam somente tampão citrato. Na vida adulta, as ratas (diabéticas e controle) foram submetidas ao acasalamento e o dia de diagnóstico positivo de prenhez foi considerado dia 0. A glicemia foi determinada nos dias 0, 7, 14 e 21 de prenhez. No 21º dia de prenhez, as ratas foram anestesiadas e dessangradas para determinação das atividades enzimáticas de superóxido dismutase (SOD), glutationa peroxidase (GSH-Px) e glutationa redutase (GSH-Rd) e das concentrações de grupos tiólicos (SH) e de espécies reativas ao ácido tiobarbitúrico (TBARS). Em seguida, as placentas foram retiradas e processadas para determinação das atividades de SOD e catalase e concentração de TBARS, gluationa reduzida e grupos tiólicos. Resultados: Ratas com diabete induzido no período neonatal (grupo diabético) apresentaram glicemia superior a 120mg/dl no dia 0 de prenhez e foi observada hiperglicemia no 14º dia de prenhez. A análise do estresse oxidativo em hemáceas lavadas mostrou que no grupo diabético houve aumento significativo na atividade da GSH-Px. No tecido placentário a atividade da catalase foi significativamente maior em ratas com diabete moderado. Conclusão: Frente às condições experimentais analisadas, o aumento dos biomarcadores do sistema antioxidante em ratas com diabete de intensidade moderada foram suficientes para conter o estresse oxidativo.
Objective: To evaluate the oxidative stress in blood sample and placental of female rats that received streptozotocin in the neonatal period. Methods: The diabetes was induced in female offspring (diabetic group) in the day of the birth (day 0) for streptozotocin (100 mg/kg, subcutaneous route). Female control rat (control group) received only citrate buffer. In the adult life, the female rats were submitted to the mating and the day the positive diagnosis, was considered day 0 of pregnancy. The glycemia was measured in the 0, 7, 14 and 21 of pregnancy. At day 21 of pregnancy, the female rats were anesthetized and died by decapitation for collection of the blood for determination of the enzymatic activity of the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione reductase (GSH-Rd) and of the concentrations of thiols group and thiobarbituric acid reactive substances (TBARS). Afterwards, placental were removed and processed for determinations of the enzymatic activity of the SOD and catalase and of the concentrations of the TBARS, glutathione reduced (GSH) and thiols group (SH). Results: Diabetic rats presented blood glucose concentration greater than 120 mg/dL in the day 0 of pregnancy and hyperglycemia in 14 º day of pregnancy. The analysis of the oxidative stress in maternal blood sample showed increased in GSH-Px activity. In placental tissue catalase activity of diabetic group is found to be increase in homogenate tissue in diabetic group. Conclusion: The hyperglycemia in diabetic rats increased antioxidant system biomarkers, however, these alterations were enough to control oxidative stress.
Spada, Ana Paula Machado. "Avaliação do estresse oxidativo no sangue e na placenta de ratas com diabete de intensidade moderada /". Botucatu : [s.n.], 2009. http://hdl.handle.net/11449/99250.
Pełny tekst źródłaAbstract: Objective: To evaluate the oxidative stress in blood sample and placental of female rats that received streptozotocin in the neonatal period. Methods: The diabetes was induced in female offspring (diabetic group) in the day of the birth (day 0) for streptozotocin (100 mg/kg, subcutaneous route). Female control rat (control group) received only citrate buffer. In the adult life, the female rats were submitted to the mating and the day the positive diagnosis, was considered day 0 of pregnancy. The glycemia was measured in the 0, 7, 14 and 21 of pregnancy. At day 21 of pregnancy, the female rats were anesthetized and died by decapitation for collection of the blood for determination of the enzymatic activity of the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione reductase (GSH-Rd) and of the concentrations of thiols group and thiobarbituric acid reactive substances (TBARS). Afterwards, placental were removed and processed for determinations of the enzymatic activity of the SOD and catalase and of the concentrations of the TBARS, glutathione reduced (GSH) and thiols group (SH). Results: Diabetic rats presented blood glucose concentration greater than 120 mg/dL in the day 0 of pregnancy and hyperglycemia in 14 º day of pregnancy. The analysis of the oxidative stress in maternal blood sample showed increased in GSH-Px activity. In placental tissue catalase activity of diabetic group is found to be increase in homogenate tissue in diabetic group. Conclusion: The hyperglycemia in diabetic rats increased antioxidant system biomarkers, however, these alterations were enough to control oxidative stress.
Orientador: Débora Cristina Damasceno
Coorientador: Tiago Rodrigues
Mestre
Nash, Peppi. "Experimental and Clinical Studies of Oxidative Stress in Pre-Eclampsia". Doctoral thesis, Uppsala University, Department of Medical Cell Biology, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-7717.
Pełny tekst źródłaImpaired placentation and oxidative stress are proposed to play major roles in the pathogenesis of pre-eclampsia (PE). It has recently been pointed out that PE might be more than one disease and may have several different pathogeneses. This thesis describes a new animal model for PE and examines the role of oxidative stress in early respective late onset PE.
The effects of Suramin injections on day 10 and 11 of pregnancy were investigated in normal and diabetic rats of two strains (U and H), with or without additional vitamin E treatment. Suramin caused placental dysfunction in both rat strains: foetal growth restriction, increased resorption rate, reduced placental blood flow, and decreased maternal blood volume in the placenta. In the U strain Suramin also caused maternal hypertension and reduced renal blood flow. Oxidative stress in the Suramin treated rats was indicated by increased levels of isoprostane 8-iso-PGF2α in the placenta. Antioxidative treatment with vitamin E partly protected against the effects of Suramin. Streptozotocin-induced diabetes seemed to cause similar placental effects as Suramin, and in the diabetic rats the additional effects of Suramin were only moderate. In conclusion, Suramin-injected pregnant rats constitute a valid animal model for placental dysfunction (U and H rats) and PE (U rats).
Oxidative stress was estimated in women with early onset (≤ 32 weeks) or late onset (≥ 35 weeks) PE, in normotensive pregnant women of respective gestational length, and in healthy non-pregnant women. The ratio of PAI-1/PAI-2 was measured in serum, and the amount of isoprostane 8-iso-PGF2α was measured in placenta, serum, and urine. The ratio of PAI-1/PAI-2 and placental isoprostane levels were higher in women with early onset PE compared with all other groups. Serum levels of isoprostane were similar between groups. Urinary levels of isoprostane were similar in all pregnant women, but lower in non-pregnant women. These data indicate that pregnancy increases general oxidative stress, and that early onset, but not late onset PE, causes increased oxidative stress also in placental tissue. The pathogeneses of early and late onset PE are, therefore, not likely to be identical.
Hedlund, Malin. "Exosomes and the NKG2D receptor-ligand system in pregnancy and cancer : using stress for survival". Doctoral thesis, Umeå universitet, Klinisk immunologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-37122.
Pełny tekst źródłaSILVA, Natalie Emanuelle Ribeiro e. "Efeitos de uma sobrecarga de sódio ou de antioxidantes sobre o estresse oxidativo e angiogênese placentária: repercussão sobre indicadores de estresse oxidativo no fígado fetal". Universidade Federal Rural de Pernambuco, 2013. http://www.tede2.ufrpe.br:8080/tede2/handle/tede2/5058.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Intrauterine programmed cardiovascular disease may be linked to placental oxidative stress. It was investigated whether NaCl supplement, during pregnancy, affects placental oxidative stress and angiogenesis and imprints increased levels of oxidative stress in fetal liver. Dams were treated with 1.8% NaCl in drinking water from 20 days before and along pregnancy. Along pregnancy α-tocopherol, tempol or both were administered. Angiogenesis was evaluated throughout the expression of flt-1, the type 1 receptor for VEGF, in the villous bundles/labirinth. NaCl diminished flt-1 expression, as well as, reduced malonyldialdehide and augmented reduced gluthatione in placenta and fetal liver. α-Tocopherol led to an additional reduction in MDA levels in these organs, but diminished GSH. Otherwise, tempol increased MDA and diminished GSH in both placenta and fetal liver. No antioxidant changed the expression of flt-1. The reduced levels of MDA in placenta and fetal liver of dams under NaCl supplement might be due to reduced angiogenesis, that reduced oxygen supply, and also to the increased GSH levels. However the paradoxical pro-oxidant action of tempol indicates that the antioxidant reservoir in dams under sodium overload is limited. Furthermore, the parallel between the pattern of placental and fetal liver oxidative stress suggests that superoxide anions transferred from mothers may be important in programming cardiovascular diseases.
Doenças cardiovaculares programadas intrauterinamente podem está ligadas ao estresse oxidativo placentário. Neste trabalho, investigamos se a sobrecarga de NaCl, durante a gravidez, afeta o estresse oxidativo e angiogênese placentária, bem como se afeta os níveis de estresse oxidativo no fígado do feto. Mães foram tratadas com NaCl, 1,8%, na água de beber, 20 dias antes e ao longo da gravidez. α-Tocoferol, tempol ou ambos foram administrados ao longo da gravidez. A angiogênese foi avaliada por meio da expressão do flt-1, o receptor tipo 1 para o VEGF, nos feixes vilosos do labrinto. A suplementação com NaCl diminuiu a expressão de flt-1, bem como, reduziu os níveis de malonildialdeido e aumentou os níveis de glutationa reduzida na placenta e no fígado fetal. O α-tocoferol levou a uma redução adicional nos níveis de MDA nesses órgãos, mas diminuiu os níveis de GSH. De maneira diferente, o tempol aumentou os níveis de MDA e diminuiu os níveis de na placenta e no fígado fetal. O tratamento com os antioxidantes não alterou a expressão do flt-1. Os níveis reduzidos de MDA na placenta e no fígado do feto de mães submetidas a sobrecarga de NaCl podem ser devidos à angiogênese diminuida, o que reduziu o suprimento de oxigênio, ou aos os níveis aumentados de GSH. Entretanto, a ação paradoxal, pro-oxidante, do tempol indica que a reserva antioxidante nas mães submetidas a sobrecarga de sódio é limitada. Além disso, o paralelo entre o padrão de estresse oxidativo placentário e do fígado fetal sugere que ânions superóxidos transferidos a partir das mães podem ser importantes na programação das doenças cardiovaculares.
Ribeiro, Lígia Raquel Pinto. "In vitro evaluation of the effect of oxidative stress in placental function". Master's thesis, 2020. https://hdl.handle.net/10216/131355.
Pełny tekst źródłaRibeiro, Lígia Raquel Pinto. "In vitro evaluation of the effect of oxidative stress in placental function". Dissertação, 2020. https://hdl.handle.net/10216/131355.
Pełny tekst źródłaSultana, Zakia. "Increased oxidative damage and premature placental aging contribute to the aetiology of stillbirth". Thesis, 2018. http://hdl.handle.net/1959.13/1391445.
Pełny tekst źródłaStillbirth is a neglected public health problem affecting more than two million women and families globally each year with devastating and long-lasting psychosocial and financial impact. Rates of stillbirth, even in high-income countries with access to optimal obstetric care, have remained static in the past two decades. The causes of, or associations with, stillbirth that have been identified clinically include fetal factors such as genetic/structural abnormalities and growth restriction, maternal factors such as preeclampsia and infections and placental factors such as abruption and placenta previa. However, no specific cause has been established for the majority of stillbirths at term, and the rate of this category of death rises drammatically as gestation progresses beyond 38 weeks. Taking into account the functional definition of aging that is an increase in the risk of death with time, and the existence of placental pathologies in the unexplained stillbirth pregnancies resembling aging in other organs, we hypothesise that premature placental aging may be the primary factor in the aetiology of unexplained stillbirth. Premature aging may occur when cells experience increased oxidative stress that causes damage to cellular macromolecules, including DNA, RNA and lipids, and alters protein expression patterns, especially those that are crucial for cellular survival and function. Therefore, the primary aim of this thesis was to investigate evidence that the placenta from late-gestation shows biochemical signs of oxidative damage and aging that would also be present in placentas associated with stillbirths. A further aim was to investigate the pathways that mediate the oxidative damage and aging in the placenta in pathologic pregnancies. We have shown that placentas from both late-term and stillbirth pregnancies show biochemical signs of aging in the form of increased DNA and lipid oxidation. Also, the expression of aldehyde oxidase 1 (AOX1), which is known to be involved in reactive oxygen species (ROS) generation and oxidative stress, is increased in placental tissues obtained from both late-gestation and stillbirth pregnancies. We tested the association of AOX1 in stillbirth pregnancy as an RNA sequencing study performed in our laboratory identified a significant increase in AOX1 mRNA in late-term placentas compared to term healthy placentas (unpublished). The demonstration of G-protein coupled estrogen receptor 1 (GPER1), a cell surface estrogen receptor, localisation on the apical surface of the normal placental syncytiotrophoblast and its role in the reduction of ROS generation and oxidative damage indicate that this receptor may be a critical step in the pathway of placental ROS induced oxidative damage. Using a placental explant and a cell line culture model, we then tested the pathways that regulate placental oxidative damage and aging. Results presented in this thesis revealed that growth factor removal resulted in placental oxidative damage, with impaired mitochondrial function, decreased expression of sirtuins (proteins that control aging), alteration of nutrient sensing mammalianTORC1, and energy sensing AMP activated protein kinase pathways, all the changes are known to be associated with oxidative damage and aging in other tissues. Inhibition of AOX1 or stimulation of estrogen activation at GPER1 resulted in the blocking of all the changes observed after removal of growth factors. Together, these findings support the hypothesis that placental oxidation is regulated by estrogen activation at the GPER1 and inhibition of AOX1 leading to the inhibition of ROS generation and oxidative stress. Our study identifies potential biomarkers of oxidative damage and aging in stillbirth placentas that raise the possibility that these biomarkers of placental oxidative damage and aging may be released into the maternal blood where they may have diagnostic value in predicting the fetus at risk for stillbirth. Treatment targeting AOX1 and/or GPER1 may arrest the oxidative damage in the placenta in pregnancies identified at risk and may lead to novel therapeutic strategies for delaying placental aging, as well as preventing stillbirth and other age-related adverse pregnancy outcomes.
Sperou, Arissa. "Heightened maternal inflammation is linked to placental oxidative and nitrosative stress associated with fetal growth restriction in the rat". Thesis, 2013. http://hdl.handle.net/1974/8105.
Pełny tekst źródłaThesis (Master, Anatomy & Cell Biology) -- Queen's University, 2013-07-05 14:37:05.15
Kalkat, Manpreet. "Regulation of Placental Autophagy by the Bcl-2 Family Proteins Myeloid Cell Leukemia Factor 1 (Mcl-1) and Matador/Bcl-2 Related Ovarian Killer (Mtd/Bok)". Thesis, 2012. http://hdl.handle.net/1807/33718.
Pełny tekst źródłaHabibi, Nahal. "The effect of micronutrients in oxidative stress, proliferation and apoptosis in placenta". Thesis, 2020. http://hdl.handle.net/2440/129620.
Pełny tekst źródłaThesis (Ph.D.) -- University of Adelaide, School of Agriculture, Food and Wine, 2020
Hausermann, Leslie. "Les prostanoïdes contrôlent la circulation placentaire : implication dans la prééclampsie". Thèse, 2012. http://hdl.handle.net/1866/9012.
Pełny tekst źródłaThroughout pregnancy, appropriate placental perfusion is essential for the fœtus to grow properly. In disease such as preeclampsia, placental perfusion is impaired, compromising the fœtus and mother’s lives. Placenta delivery leads to a complete disappearance of the clinical symptoms of preeclampsia. This suggests that the placenta plays a central role in the disease. Placenta being devoid of autonomous innervation, placental vascular tone needs to be under the control of humoral and tissular factors; placental arteries are very reactive to prostanoids. The thromboxane A2 (TXA2)/prostacyclin (PGI2) ratio is increased in placenta from preeclamptic women. Furthermore, in placenta from preeclamptic pregnancies, isoprostane rate is increased, which is a marker of oxidative stress. Finally, preeclampsia is characterised by an important oxidative stress. Reactive oxygen species are known to form isoprostane through the oxidation of arachidonic acid (AA) and to increase TXA2 production in various tissues following an activation of the cyclooxygenases (COXs). We postulate that: 1. prostanoids are among the endogenous molecules that control placental vascular tone. 2. preeclampsia alters responses to isoprostanes in placental vessels. 3. induced placental oxidative stress leads to vasoactive responses through the activation of the AA metabolism. We first showed in placentas from normotensive pregnancies that the TXA2 mimetic U-46619 and the isoprostane 8-isoprostaglandin E2 (8-isoPGE2) markedly increased perfusion pressure in in vitro perfused cotyledons, as well as tension in isolated chorionic arteries. However, in placentas obtained from women with preeclampsia, those responses were altered in chorionic arteries. Indeed, maximal response to U-46619 was raised by preeclampsia, while the one to 8-isoPGE2 was decreased. We then showed that preterm delivery increased maximal responses to both prostanoids compared to term delivery. This observation suggests that placental arteries reactivity evolves along the 3rd trimester of pregnancy. Nevertheless, it appeared that delivery mode had no effect on vascular responses to prostanoids, suggesting that placental prostanoids are not involved in the delivery process. The use of specific blockers of the TXA2 TP receptors, SQ29,548 and ICI192,605, and of the prostaglandin E2 EP receptors, AH6809, revealed that U-46619 and 8-isoPGE2 could mediate their effects by acting on both receptors in a non-selective manner. Therefore, these results support our two first postulates: prostanoids could be the endogenous substances controlling the placental vascular tone and preeclampsia alters responses to isoprostanes in chorionic artery rings in a way compatible with the increased production of these substances possibly through the associated oxidative stress. Moreover, we were unable to identify any vasodilator substances capable of counteracting the effects of vasoconstrictors in the placental circulation. Indeed, blocker of nitric oxide synthases, L-NAME, as well as blockers of COXs, ibuprofen, indometacin and N-2PIA, did not reveal any effect of nitric oxide and vasodilator prostanoids at this level. Finally, we showed that induction of oxidative stress in in vitro perfused cotyledons and in isolated chorionic artery rings led to marked vasoconstriction. This would result from the action of prostanoids since a blockade of TP receptors or COXs significantly decreased maximal response to hydrogen peroxide. Prostanoids involved in this response would essentially come from COX activation. Indeed, the present results did not show any concrete involvement of isoprostane substances in the response to oxidative stress. Consequently, these observations confirm our hypothesis that, in the placenta, oxidative stress presents some vasoactive properties through the activation of the AA metabolism. In summary, results obtained in placentas from normotensive and preeclamptic pregnancies suggest that prostanoids are important in the regulation of the placental vascular tone. Furthermore, responses to prostanoids in chorionic arteries are altered by preeclampsia, which could explain why the placental perfusion is impaired in the disease. Moreover, it seems clear that there is a close relationship between oxidative stress and synthesis of placental prostanoids. However, more investigations are needed to better understand the nature of this relationship, which, in some way, could play an important role in the development of preeclampsia.
Zakiyanov, Oskar. "Nové biomarkery u pacientů s onemocněním ledvin". Doctoral thesis, 2014. http://www.nusl.cz/ntk/nusl-338466.
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