Academic literature on the topic 'Placental oxidative stress'
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Journal articles on the topic "Placental oxidative stress"
Reyes-Hernández, Cynthia, David Ramiro-Cortijo, Pilar Rodríguez-Rodríguez, Sonia Giambelluca, Manuela Simonato, Mª González, Angel López de Pablo, et al. "Effects of Arachidonic and Docosohexahenoic Acid Supplementation during Gestation in Rats. Implication of Placental Oxidative Stress." International Journal of Molecular Sciences 19, no. 12 (December 4, 2018): 3863. http://dx.doi.org/10.3390/ijms19123863.
Full textTrifunović, Svetlana, Branka Šošić Jurjević, Nataša Ristić, Nataša Nestorović, Branko Filipović, Ivana Stevanović, Vesna Begović-Kuprešanin, and Milica Manojlović-Stojanoski. "Maternal Dexamethasone Exposure Induces Sex-Specific Changes in Histomorphology and Redox Homeostasis of Rat Placenta." International Journal of Molecular Sciences 24, no. 1 (December 29, 2022): 540. http://dx.doi.org/10.3390/ijms24010540.
Full textThomas, Megan M., Maricela Haghiac, Catalin Grozav, Judi Minium, Virtu Calabuig-Navarro, and Perrie O’Tierney-Ginn. "Oxidative Stress Impairs Fatty Acid Oxidation and Mitochondrial Function in the Term Placenta." Reproductive Sciences 26, no. 7 (October 10, 2018): 972–78. http://dx.doi.org/10.1177/1933719118802054.
Full textNatarajan, Sathish Kumar, Kavitha R. Thangaraj, Ashish Goel, C. E. Eapen, K. A. Balasubramanian, and Anup Ramachandran. "Acute fatty liver of pregnancy: an update on mechanisms." Obstetric Medicine 4, no. 3 (July 4, 2011): 99–103. http://dx.doi.org/10.1258/om.2011.100071.
Full textChen, Baosheng, Methodius G. Tuuli, Mark S. Longtine, Joong Sik Shin, Russell Lawrence, Terrie Inder, and D. Michael Nelson. "Pomegranate juice and punicalagin attenuate oxidative stress and apoptosis in human placenta and in human placental trophoblasts." American Journal of Physiology-Endocrinology and Metabolism 302, no. 9 (May 1, 2012): E1142—E1152. http://dx.doi.org/10.1152/ajpendo.00003.2012.
Full textRuano, Camino San Martin, Francisco Miralles, Céline Méhats, and Daniel Vaiman. "The Impact of Oxidative Stress of Environmental Origin on the Onset of Placental Diseases." Antioxidants 11, no. 1 (January 1, 2022): 106. http://dx.doi.org/10.3390/antiox11010106.
Full textJones, M. L., P. J. Mark, and B. J. Waddell. "215. Placental expression of uncoupling protein-2 is reduced by glucocorticoid treatment in late pregnancy: implications for placental oxidative stress." Reproduction, Fertility and Development 20, no. 9 (2008): 15. http://dx.doi.org/10.1071/srb08abs215.
Full textNakashima, Akitoshi, Tomoko Shima, Sayaka Tsuda, Aiko Aoki, Mihoko Kawaguchi, Satoshi Yoneda, Akemi Yamaki-Ushijima, Shi-Bin Cheng, Surendra Sharma, and Shigeru Saito. "Disruption of Placental Homeostasis Leads to Preeclampsia." International Journal of Molecular Sciences 21, no. 9 (May 7, 2020): 3298. http://dx.doi.org/10.3390/ijms21093298.
Full textMa, Rong, Yang Gu, Shuang Zhao, Jingxia Sun, Lynn J. Groome, and Yuping Wang. "Expressions of vitamin D metabolic components VDBP, CYP2R1, CYP27B1, CYP24A1, and VDR in placentas from normal and preeclamptic pregnancies." American Journal of Physiology-Endocrinology and Metabolism 303, no. 7 (October 1, 2012): E928—E935. http://dx.doi.org/10.1152/ajpendo.00279.2012.
Full textWu, Fan, Fu-Ju Tian, and Yi Lin. "Oxidative Stress in Placenta: Health and Diseases." BioMed Research International 2015 (2015): 1–15. http://dx.doi.org/10.1155/2015/293271.
Full textDissertations / Theses on the topic "Placental oxidative stress"
Vanderlelie, Jessica, and 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.
Full textVanderlelie, Jessica. "Placental Oxidative Stress in Preeclampsia." Thesis, Griffith University, 2006. http://hdl.handle.net/10072/365679.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
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Khera, Alisha. "Selenium Supplementation Protects Placental Trophoblast Cells from Mitochondrial Oxidative Stress." Thesis, Griffith University, 2016. http://hdl.handle.net/10072/367348.
Full textThesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
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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.
Full textAnto, 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.
Full textBelhareth, Rym. "Tabac et grossesse." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5007/document.
Full textActive 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.
Full textContext: 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.
Full textNunes, Priscila Rezeck. "Efeito do estresse oxidativo sobre autofagia em tecido placentário." Botucatu, 2017. http://hdl.handle.net/11449/148980.
Full textResumo: 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
Book chapters on the topic "Placental oxidative stress"
Shaman, Amani, Beena J. Premkumar, and Ashok Agarwal. "Placental Vascular Morphogenesis and Oxidative Stress." In Studies on Women's Health, 95–113. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-041-0_5.
Full textDesforges, Michelle, Hannah Whittaker, Etaoin Farmer, Colin P. Sibley, and Susan L. Greenwood. "Effects of Taurine Depletion on Human Placental Syncytiotrophoblast Renewal and Susceptibility to Oxidative Stress." In Taurine 9, 63–73. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15126-7_6.
Full textGoda, Nobuhito, Michiya Natori, Makoto Suematsu, Kaoru Kiyokawa, Yuzuru Ishimura, Yasunori Yoshimura, and Shiro Nozawa. "An Antioxidant Role of Nitric Oxide in Modulation of Oxidative Stress in Human Placental Trophoblastic Cells." In Oxygen Homeostasis and Its Dynamics, 557–61. Tokyo: Springer Japan, 1998. http://dx.doi.org/10.1007/978-4-431-68476-3_70.
Full textGoldman, Rose H. "Health Effects of Arsenic." In Modern Occupational Diseases Diagnosis, Epidemiology, Management and Prevention, 244–55. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/9789815049138122010016.
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