Journal articles on the topic 'Placental oxidative stress'
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1
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.
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Arachidonic and docosahexaenoic acids (ARA and DHA) are important during pregnancy. However, the effects of dietary supplementation on fetal growth and oxidative stress are inconclusive. We aimed to assess the effect of high ARA and DHA diet during rat gestation on: (1) ARA and DHA availability in plasma and placenta, (2) fetal growth, and (3) placental oxidative stress, analyzing the influence of sex. Experimental diet (ED) was prepared by substituting soybean oil in the control diet (CD) by a fungi/algae-based oil containing ARA and DHA (2:1). Rats were fed with CD or ED during gestation; plasma, placenta, and fetuses were obtained at gestational day 20. DHA, ARA, and their precursors were analyzed in maternal plasma and placenta by gas chromatography/mass spectrophotometry. Fetuses and placentas were weighed, the proportion of fetuses with intrauterine growth restriction (IUGR) determined, and placental lipid and protein oxidation analyzed. ED fetuses exhibited lower body weight compared to CD, being >40% IUGR; fetal weight negatively correlated with maternal plasma ARA, but not DHA. Only ED female placenta exhibited higher lipid and protein oxidation compared to its CD counterparts; lipid peroxidation is negatively associated with fetal weight. In conclusion, high ARA during gestation associates with IUGR, through placental oxidative stress, with females being more susceptible.
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Trifunović, 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.
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As the mediator between the mother and fetus, the placenta allows the most appropriate environment and optimal fetal growth. The placenta of one sex sometimes has a greater ability over the other to respond to and protect against possible maternal insults. Here, we characterized sex differences in the placenta’s morphological features and antioxidant status following dexamethasone (Dx) exposure. Pregnant rats were exposed to Dx or saline. The placenta was histologically and stereologically analyzed. The activity of the antioxidant enzymes, lipid peroxides (TBARS), superoxide anion and nitric oxide (NO) was measured. The decrease in placental zone volumes was more pronounced (p < 0.05) in female placentas. The volume density of PCNA-immunopositive nuclei was reduced (p < 0.05) in both sexes. The reduced (p < 0.05) antioxidant enzyme activities, enhanced TBARS and NO concentration indicate that Dx exposure triggered oxidative stress in the placenta of both fetal sexes, albeit stronger in the placenta of female fetuses. In conclusion, maternal Dx treatment reduced the size and volume of placental zones, altered placental histomorphology, decreased cell proliferation and triggered oxidative stress; however, the placentas of female fetuses exerted more significant responses to the treatment effects. The reduced placental size most probably reduced the transport of nutrients and oxygen, thus resulting in the reduced weight of fetuses, similar in both sexes. The lesser ability of the male placenta to detect and react to maternal exposure to environmental challenges may lead to long-standing health effects.
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Thomas, 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.
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Placental fatty acid oxidation (FAO) is impaired and lipid storage is increased in pregnancy states associated with chronic oxidative stress. The effect of acute oxidative stress, as seen in pregnancies complicated with asthma, on placental lipid metabolism is unknown. We hypothesized that induction of acute oxidative stress would decrease FAO and increase esterification. We assessed [3H]-palmitate oxidation and esterification in term placental explants from lean women after exposure to hydrogen peroxide (H2O2) for 4 hours. Fatty acid oxidation decreased 16% and 24% in placental explants exposed to 200 ( P = .02) and 400 µM H2O2 ( P = .01), respectively. Esterification was not altered with H2O2 exposure. Neither messenger RNA nor protein expression of key genes involved in FAO (eg, peroxisome proliferator-activated receptor α, carnitine palmitoyl transferase 1b) were altered. Adenosine triphosphate (ATP) levels decreased with induction of oxidative stress, without increasing cytotoxicity. Acute oxidative stress decreased FAO and ATP production in the term placenta without altering fatty acid esterification. As decreases in placental FAO and ATP production are associated with impaired fetal growth, pregnancies exposed to acute oxidative stress may be at risk for fetal growth restriction.
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Natarajan, 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.
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Acute fatty liver of pregnancy (AFLP), characterized by hepatic microvesicular steatosis, is a sudden catastrophic illness occurring almost exclusively in the third trimester of pregnancy. Defective fatty acid oxidation in the fetus has been shown to be associated with this disease. Since the placenta has the same genetic makeup as the fetus and as AFLP patients generally recover following delivery, we hypothesized that the placenta might be involved in pathogenesis of this disease. In an animal model of hepatic microvesicular steatosis (using sodium valproate), we found that microvesicular steatosis results in mitochondrial structural alterations and oxidative stress in subcellular organelles of the liver. In placentas from patients with AFLP, we observed placental mitochondrial dysfunction and oxidative stress in subcellular organelles. In addition, defective placental fatty acid oxidation results in accumulation of toxic mediators such as arachidonic acid. Escape of these mediators into the maternal circulation might affect the maternal liver resulting in microvesicular steatosis.
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Chen, 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.
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The human placenta is key to pregnancy outcome, and the elevated oxidative stress present in many complicated pregnancies contributes to placental dysfunction and suboptimal pregnancy outcomes. We tested the hypothesis that pomegranate juice, which is rich in polyphenolic antioxidants, limits placental trophoblast injury in vivo and in vitro. Pregnant women with singleton pregnancies were randomized at 35∼38 wk gestation to 8 oz/day of pomegranate juice or apple juice (placebo) until the time of delivery. Placental tissues from 12 patients (4 in the pomegranate group and 8 in the control group) were collected for analysis of oxidative stress. The preliminary in vivo results were extended to oxidative stress and cell death assays in vitro. Placental explants and cultured primary human trophoblasts were exposed to pomegranate juice or glucose (control) under defined oxygen tensions and chemical stimuli. We found decreased oxidative stress in term human placentas from women who labored after prenatal ingestion of pomegranate juice compared with apple juice as control. Moreover, pomegranate juice reduced in vitro oxidative stress, apoptosis, and global cell death in term villous explants and primary trophoblast cultures exposed to hypoxia, the hypoxia mimetic cobalt chloride, and the kinase inhibitor staurosporine. Punicalagin, but not ellagic acid, both prominent polyphenols in pomegranate juice, reduced oxidative stress and stimulus-induced apoptosis in cultured syncytiotrophoblasts. We conclude that pomegranate juice reduces placental oxidative stress in vivo and in vitro while limiting stimulus-induced death of human trophoblasts in culture. The polyphenol punicalagin mimics this protective effect. We speculate that antenatal intake of pomegranate may limit placental injury and thereby may confer protection to the exposed fetus.
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Ruano, 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.
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Oxidative stress (OS) plays a pivotal role in placental development; however, abnormal loads in oxidative stress molecules may overwhelm the placental defense mechanisms and cause pathological situations. The environment in which the mother evolves triggers an exposure of the placental tissue to chemical, physical, and biological agents of OS, with potential pathological consequences. Here we shortly review the physiological and developmental functions of OS in the placenta, and present a series of environmental pollutants inducing placental oxidative stress, for which some insights regarding the underlying mechanisms have been proposed, leading to a recapitulation of the noxious effects of OS of environmental origin upon the human placenta.
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Jones, 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.
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Placental oxidative stress plays a key role in the pathophysiology of placenta-related disorders in humans, most notably in preeclampsia (PE) and intrauterine growth restriction (IUGR). Protection from oxidative stress is provided by antioxidant enzymes including superoxide dismutase-1 and 2 (SOD-1 and –2) and catalase (CAT), which convert reactive oxygen species (ROS) to inert products. It has also been proposed that uncoupling protein-2 (UCP2) may limit oxidative stress by reducing ROS production, but little is known of UCP2 expression in placenta. Here we measured placental UCP2, SOD-1, SOD-2 and CAT mRNA expression (by qRT–PCR) in normal gestation and after glucocorticoid-induced IUGR. The latter was included because glucocorticoids can increase oxidative stress in other tissues, and placental glucocorticoid exposure is elevated in both PE and IUGR. Placentas were collected on days 16 and 22 of normal pregnancy (term = day 23) and on day 22 after dexamethasone treatment (0.75 mg/mL in drinking water from day 13). The two morphologically-distinct regions of the placenta, the junctional (JZ) and labyrinth (LZ) zones, were analysed separately because effectively all growth occurs in the LZ over this period. Expression of UCP2 in LZ exceeded that in JZ (P < 0.001) and increased in both zones between days 16 and 22 (LZ: 2.0-fold; JZ: 3.2-fold). Dexamethasone treatment reduced UCP2 in LZ (44%; P < 0.05) but not in JZ. SOD1 and SOD2 increased with gestational age in LZ (P < 0.01) and JZ (P < 0.05), but neither were affected by dexamethasone. CAT expression was higher (2.4-fold, P < 0.001) in LZ compared with JZ but did not change with gestational age or dexamethasone. In summary, these data suggest that endogenous protection against oxidative stress increases in the rat placenta during late pregnancy. Moreover, this protection may be compromised by reduced placental UCP2 expression in a model of glucocorticoid-induced IUGR.
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Nakashima, 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.
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Placental homeostasis is directly linked to fetal well-being and normal fetal growth. Placentas are sensitive to various environmental stressors, including hypoxia, endoplasmic reticulum stress, and oxidative stress. Once placental homeostasis is disrupted, the placenta may rebel against the mother and fetus. Autophagy is an evolutionally conservative mechanism for the maintenance of cellular and organic homeostasis. Evidence suggests that autophagy plays a crucial role throughout pregnancy, including fertilization, placentation, and delivery in human and mouse models. This study reviews the available literature discussing the role of autophagy in preeclampsia.
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Ma, 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.
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Vitamin D insufficiency/deficiency during pregnancy has been linked to increased risk of preeclampsia. Placenta dysfunction plays an important role in the pathogenesis of this pregnancy disorder. In this study, we tested the hypothesis that disturbed vitamin D metabolism takes place in preeclamptic placentas. Protein expressions of vitamin D binding protein (VDBP), 25-hydroxylase (CYP2R1), 1α-hydroxylase (CYP27B1), 24-hydroxylase (CYP24A1), and vitamin D receptor (VDR) were examined in placentas from normotensive and preeclamptic pregnancies. By immunostaining we found that in normal placenta VDBP, CYP24A1, and VDR expressions are localized mainly in trophoblasts, whereas CYP2R1 and CYP27B1 expressions are localized mainly in villous core fetal vessel endothelium. Protein expressions of CYP2R1 and VDR are reduced, but CYP27B1 and CYP24A1 expressions are elevated, in preeclamptic compared with normotensive placentas. Because increased oxidative stress is an underlying pathophysiology in placental trophoblasts in preeclampsia, we further determined whether oxidative stress contributes to altered vitamin D metabolic system in placental trophoblasts. Trophoblasts isolated from normal-term placentas were treated with hypoxic-inducing agent CoCl2, and protein expressions of VDBP, CYP2R1, CYP27B1, CYP24A1, and VDR were determined. We found that hypoxia-induced downregulation of VDBP, CYP2R1, and VDR and upregulation of CYP27B1 and CYP24A1 expressions were consistent with that seen in preeclamptic placentas. CuZnSOD expression was also downregulated in trophoblasts treated with CoCl2. These results provide direct evidence of disrupted vitamin D metabolic homeostasis in the preeclamptic placenta and suggest that increased oxidative stress could be a causative factor of altered vitamin D metabolism in preeclamptic placentas.
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Wu, 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.
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During pregnancy, development of the placenta is interrelated with the oxygen concentration. Embryo development takes place in a low oxygen environment until the beginning of the second trimester when large amounts of oxygen are conveyed to meet the growth requirements. High metabolism and oxidative stress are common in the placenta. Reactive oxidative species sometimes harm placental development, but they are also reported to regulate gene transcription and downstream activities such as trophoblast proliferation, invasion, and angiogenesis. Autophagy and apoptosis are two crucial, interconnected processes in the placenta that are often influenced by oxidative stress. The proper interactions between them play an important role in placental homeostasis. However, an imbalance between the protective and destructive mechanisms of autophagy and apoptosis seems to be linked with pregnancy-related disorders such as miscarriage, preeclampsia, and intrauterine growth restriction. Thus, potential therapies to hold oxidative stress in leash, promote placentation, and avoid unwanted apoptosis are discussed.
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Pereira, Robyn D., Nicole E. De Long, Ruijun C. Wang, Fereshteh T. Yazdi, Alison C. Holloway, and Sandeep Raha. "Angiogenesis in the Placenta: The Role of Reactive Oxygen Species Signaling." BioMed Research International 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/814543.
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Proper placental development and function are central to the health of both the mother and the fetus during pregnancy. A critical component of healthy placental function is the proper development of its vascular network. Poor vascularization of the placenta can lead to fetal growth restriction, preeclampsia, and in some cases fetal death. Therefore, understanding the mechanisms by which uterine stressors influence the development of the placental vasculature and contribute to placental dysfunction is of central importance to ensuring a healthy pregnancy. In this review we discuss how oxidative stress observed in maternal smoking, maternal obesity, and preeclampsia has been associated with aberrant angiogenesis and placental dysfunction resulting in adverse pregnancy outcomes. We also highlight that oxidative stress can influence the expression of a number of transcription factors important in mediating angiogenesis. Therefore, understanding how oxidative stress affects redox-sensitive transcription factors within the placenta may elucidate potential therapeutic targets for correcting abnormal placental angiogenesis and function.
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Stark, Michael J., Vicki L. Clifton, and Nicolette A. Hodyl. "Differential effects of docosahexaenoic acid on preterm and term placental pro-oxidant/antioxidant balance." REPRODUCTION 146, no. 3 (September 2013): 243–51. http://dx.doi.org/10.1530/rep-13-0239.
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Docosahexaenoic acid (DHA) supplementation in pregnancy may confer some clinical benefits; however, this compound can exert pro-oxidant effects. In this study, we investigated the effects of DHA on pro-oxidant/antioxidant balance in term and preterm placental explants, assessing oxidative stress marker concentrations, antioxidant capacity and pro-inflammatory cytokine production. Term (n=8) and preterm (n=9) placental explants were exposed to lipopolysaccharide (LPS, 1 ng/ml), DHA (1, 10 and 100 μM), and DHA and LPS simultaneously or pre-treated with DHA for 24 h prior to LPS treatment. The production of malondialdehyde (MDA, lipid peroxidation), 8-hydroxy-2-deoxy guanosine (8-OHdG, oxidative DNA damage) and pro-inflammatory cytokines (tumour necrosis factor α (TNFα), interleukin 6 and interferon-γ) and total antioxidant capacity were measured. DHA at a concentration of 100 μM induced oxidative stress in term placentas, while at all the three concentrations, it induced oxidative stress in preterm placentas. DHA and LPS resulted in reduced MDA levels in term (P<0.005) and preterm (P=0.004) placentas and reduced 8-OHdG levels in preterm placentas (P=0.035). DHA pre-treatment, but not co-treatment with LPS, reduced 8-OHdG levels (P<0.001) in term placentas. DHA increased antioxidant capacity only in term placentas (P<0.001), with lower antioxidant capacity being observed overall in preterm placentas compared with term placentas (P≤0.001). In term placentas, but not in preterm ones, DHA co-treatment and pre-treatment reduced LPS-induced TNFα levels. The ability of DHA to alter placental pro-oxidant/antioxidant balance is dependent on the DHA concentration used and the gestational age of the placental tissue. DHA has a greater capacity to increase oxidative stress in preterm placentas, but it offers greater protection against inflammation-induced oxidative stress in term placentas. This appears to be a result of DHA altering placental antioxidant capacity. These data have implications for the timing and concentration of DHA supplementation in pregnancy.
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Vaka, Ramana, Evangeline Deer, Mark Cunningham, Kristen M. McMaster, Kedra Wallace, Denise C. Cornelius, Lorena M. Amaral, and Babbette LaMarca. "Characterization of Mitochondrial Bioenergetics in Preeclampsia." Journal of Clinical Medicine 10, no. 21 (October 29, 2021): 5063. http://dx.doi.org/10.3390/jcm10215063.
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Preeclampsia (PE) is characterized by new onset hypertension during pregnancy and is associated with oxidative stress, placental ischemia, and autoantibodies to the angiotensin II type I receptor (AT1-AA). Mitochondrial (mt) dysfunction in PE and various sources of oxidative stress, such as monocytes, neutrophils, and CD4 + T cells, have been identified as important players in the pathophysiology of PE. We have established the significance of AT1-AA, TNF-α, and CD4 + T cells in causing mitochondrial (mt) dysfunction in renal and placental tissues in pregnant rats. Although the role of mt dysfunction from freshly isolated intact placental mitochondria has been compared in human PE and normally pregnant (NP) controls, variations among preterm PE or term PE have not been compared and mechanisms contributing to mt ROS during PE are unclear. Therefore, we hypothesized PE placentas would exhibit impaired placental mt function, which would be worse in preterm PE patients than in those of later gestational ages. Immediately after delivery, PE and NP patient’s placentas were collected, mt were isolated and mt respiration and ROS were measured. PE patients at either < or >34 weeks gestational age (GA) exhibited elevated blood pressure and decreased placental mt respiration rates (state 3 and maximal). Patients delivering at >34 weeks exhibited decreased Complex IV activity and expression. Placental mtROS was significantly reduced in both PE groups, compared to NP placental mitochondria. Collectively, the study demonstrates that PE mt dysfunction occurs in the placenta, with mtROS being lower than that seen in NP controls. These data indicate why antioxidants, as a potential target or new therapeutic agent, may not be ideal in treating the oxidative stress associated with PE.
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Mandò, Chiara, Valeria M. Savasi, Gaia M. Anelli, Silvia Corti, Anaïs Serati, Fabrizia Lisso, Chiara Tasca, Chiara Novielli, and Irene Cetin. "Mitochondrial and Oxidative Unbalance in Placentas from Mothers with SARS-CoV-2 Infection." Antioxidants 10, no. 10 (September 24, 2021): 1517. http://dx.doi.org/10.3390/antiox10101517.
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SARS-CoV-2 infection has been related to adverse pregnancy outcomes. A placental role in protecting the fetus from SARS-CoV-2 infection has been documented. Nevertheless, it is still unclear how the placenta is affected in SARS-CoV-2 infection. Here we assessed placental mitochondrial (mt) and oxidative features in COVID-19 and healthy mothers. mtDNA levels, DNA oxidative damage, expression levels of genes involved in antioxidant defenses, mitochondrial dynamics and respiratory chain subunits were investigated in placentas from singleton pregnancies of 30 women with SARS-CoV-2 infection during the third trimester (12 asymptomatic, 18 symptomatic) and 16 controls. mtDNA levels decreased in COVID-19 placentas vs. controls and inversely correlated with DNA oxidative damage, which increased in the symptomatic group. Antioxidant gene expressions decreased in SARS-CoV-2 mothers (CAT, GSS). Symptomatic cases also showed a lower expression of respiratory chain (NDUFA9, SDHA, COX4I1) and mt dynamics (DNM1L, FIS1) genes. Alterations in placental mitochondrial features and oxidative balance in COVID-19-affected mothers might be due to the impaired intrauterine environment, generated by systemic viral effects, leading to a negative vicious circle that worsens placental oxidative stress and mitochondrial efficiency. This likely causes cell homeostasis dysregulations, raising the potential of possible long-term effects.
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Jones, Megan L., Peter J. Mark, and Brendan J. Waddell. "Maternal omega-3 fatty acid intake increases placental labyrinthine antioxidant capacity but does not protect against fetal growth restriction induced by placental ischaemia–reperfusion injury." REPRODUCTION 146, no. 6 (December 2013): 539–47. http://dx.doi.org/10.1530/rep-13-0282.
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Placental oxidative stress plays a key role in the pathophysiology of several placenta-related disorders. Oxidative stress occurs when excess reactive oxygen species (ROS) damages cellular components, an outcome limited by antioxidant enzymes; mitochondrial uncoupling protein 2 (UCP2) also limits ROS production. We recently reported that maternal dietary omega-3 polyunsaturated fatty acid (n-3 PUFA) supplementation reduced placental oxidative damage and enhanced fetal and placental growth in the rats. Here, we examined the effect of n-3 PUFAs on placental antioxidant defences and whether n-3 PUFA supplementation could prevent growth restriction induced by placental ischaemia–reperfusion (IR), a known inducer of oxidative stress. Rats were fed either standard or high-n-3 PUFA diets from day 1 of pregnancy. Placentas were collected on days 17 and 22 in untreated pregnancies (term=day 23) and at day 22 following IR treatment on day 17. Expression of several antioxidant enzyme genes (Sod1,Sod2,Sod3,Cat,Txn1andGpx3) andUcp2was measured by quantitative RT-PCR in the placental labyrinth zone (LZ) and junctional zone (JZ). Cytosolic superoxide dismutase (SOD), mitochondrial SOD and catalase (CAT) activities were also analyzed. Maternal n-3 PUFA supplementation increased LZ mRNA expression ofCatat both gestational days (2- and 1.5-fold respectively;P<0.01) and femaleSod2at day 22 (1.4-fold,P<0.01). Cytosolic SOD activity increased with n-3 PUFA supplementation at day 22 (1.3-fold,P<0.05).Sod1andTxn1expression decreased marginally (30 and 22%,P<0.05). JZ antioxidant defences were largely unaffected by diet. Despite increased LZ antioxidant defences, maternal n-3 PUFA supplementation did not protect against placental IR-induced growth restriction of the fetus and placental LZ.
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Rolfo, Alessandro, Stefano Cosma, Anna Maria Nuzzo, Chiara Salio, Laura Moretti, Marco Sassoè-Pognetto, Andrea Roberto Carosso, Fulvio Borella, Juan Carlos Cutrin, and Chiara Benedetto. "Increased Placental Anti-Oxidant Response in Asymptomatic and Symptomatic COVID-19 Third-Trimester Pregnancies." Biomedicines 10, no. 3 (March 9, 2022): 634. http://dx.doi.org/10.3390/biomedicines10030634.
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Despite Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) -induced Oxidative Stress (OxS) being well documented in different organs, the molecular pathways underlying placental OxS in late-pregnancy women with SARS-CoV-2 infection are poorly understood. Herein, we performed an observational study to determine whether placentae of women testing positive for SARS-CoV-2 during the third trimester of pregnancy showed redox-related alterations involving Catalase (CAT) and Superoxide Dismutase (SOD) antioxidant enzymes as well as placenta morphological anomalies relative to a cohort of healthy pregnant women. Next, we evaluated if placental redox-related alterations and mitochondria pathological changes were correlated with the presence of maternal symptoms. We observed ultrastructural alterations of placental mitochondria accompanied by increased levels of oxidative stress markers Thiobarbituric Acid Reactive Substances (TBARS) and Hypoxia Inducible Factor-1 α (HIF-1α) in SARS-CoV-2 women during the third trimester of pregnancy. Importantly, we found an increase in placental CAT and SOD antioxidant enzymes accompanied by physiological neonatal outcomes. Our findings strongly suggest a placenta-mediated OxS inhibition in response to SARS-CoV-2 infection, thus contrasting the cytotoxic profile caused by Coronavirus Disease 2019 (COVID-19).
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Shahnawaz, Saira, Usman Shah Nawaz, Jonas Zaugg, Ghulam Hussain, Nadia Malik, Muhammad Zahoor-ul-Hassan Dogar, Shoaib Ahmad Malik, and Christiane Albrecht. "Dysregulated Autophagy Leads to Oxidative Stress and Aberrant Expression of ABC Transporters in Women with Early Miscarriage." Antioxidants 10, no. 11 (October 30, 2021): 1742. http://dx.doi.org/10.3390/antiox10111742.
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Early miscarriage (EMC) is a devastating obstetrical complication. ATP-binding cassette (ABC) transporters mediate cholesterol transfer across the placenta and enhance cell survival by effluxing substrates from target cells in the presence of stressors. Recent evidence reports an intricate interplay between autophagy and ABC transporters. We hypothesized that dysregulated autophagy and oxidative stress (OS) in the placenta leads to abnormal expression of membrane transporters contributing to poor pregnancy survival in EMC. We determined mRNA and protein expression of autophagy genes (Beclin-1/Bcl-2/LC3I/LC3II/p62) and ABC transporters (ABCA1/ABCG1/ABCG2) in placentae from EMC patients (n = 20), term controls (n = 19), first trimester (n = 6), and term controls (n = 5) controls. Oxidative/antioxidant status and biomarkers of oxidative damage were evaluated in maternal serum and placentae from EMC and healthy controls. In EMC, placental expression of LC3II/LC3I as well as of the key autophagy regulatory proteins Beclin-1 and Bcl-2 were reduced, whereas p62 was increased. Both in the serum and placentae of EMC patients, total OS was elevated reflected by increased oxidative damage markers (8-OHdG/malondialdehyde/carbonyl formation) accompanied by diminished levels of total antioxidant status, catalase, and total glutathione. Furthermore, we found reduced ABCG1 and increased ABCG2 expression. These findings suggest that a decreased autophagy status triggers Bcl-2-dependent OS leading to macromolecule damage in EMC placentae. The decreased expression of ABCG1 contributes to reduced cholesterol export to the growing fetus. Increasing ABCG2 expression could represent a protective feedback mechanism under inhibited autophagy conditions. In conclusion, dysregulated autophagy combined with increased oxidative toxicity and aberrant expression of placental ABC transporters affects materno-fetal health in EMC.
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Vangrieken, Philippe, Salwan Al-Nasiry, Aalt Bast, Pieter A. Leermakers, Christy B. M. Tulen, Ger M. J. Janssen, Iris Kaminski, et al. "Hypoxia-induced mitochondrial abnormalities in cells of the placenta." PLOS ONE 16, no. 1 (January 12, 2021): e0245155. http://dx.doi.org/10.1371/journal.pone.0245155.
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Introduction Impaired utero-placental perfusion is a well-known feature of early preeclampsia and is associated with placental hypoxia and oxidative stress. Although aberrations at the level of the mitochondrion have been implicated in PE pathophysiology, whether or not hypoxia-induced mitochondrial abnormalities contribute to placental oxidative stress is unknown. Methods We explored whether abnormalities in mitochondrial metabolism contribute to hypoxia-induced placental oxidative stress by using both healthy term placentae as well as a trophoblast cell line (BeWo cells) exposed to hypoxia. Furthermore, we explored the therapeutic potential of the antioxidants MitoQ and quercetin in preventing hypoxia-induced placental oxidative stress. Results Both in placental explants as well as BeWo cells, hypoxia resulted in reductions in mitochondrial content, decreased abundance of key molecules involved in the electron transport chain and increased expression and activity of glycolytic enzymes. Furthermore, expression levels of key regulators of mitochondrial biogenesis were decreased while the abundance of constituents of the mitophagy, autophagy and mitochondrial fission machinery was increased in response to hypoxia. In addition, placental hypoxia was associated with increased oxidative stress, inflammation, and apoptosis. Moreover, experiments with MitoQ revealed that hypoxia-induced reactive oxygen species originated from the mitochondria in the trophoblasts. Discussion This study is the first to demonstrate that placental hypoxia is associated with mitochondrial-generated reactive oxygen species and significant alterations in the molecular pathways controlling mitochondrial content and function. Furthermore, our data indicate that targeting mitochondrial oxidative stress may have therapeutic benefit in the management of pathologies related to placental hypoxia.
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Hu, Chengjun, Yunyu Yang, Ming Deng, Linfang Yang, Gang Shu, Qingyan Jiang, Shuo Zhang, et al. "Placentae for Low Birth Weight Piglets Are Vulnerable to Oxidative Stress, Mitochondrial Dysfunction, and Impaired Angiogenesis." Oxidative Medicine and Cellular Longevity 2020 (May 25, 2020): 1–12. http://dx.doi.org/10.1155/2020/8715412.
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Intrauterine growth restriction (IUGR) is associated with fetal mortality and morbidity. One of the most common causes of IUGR is placental insufficiency, including placental vascular defects, and mitochondrial dysfunction. In addition, a high level of oxidative stress induces placental vascular lesions. Here, we evaluated the oxidative stress status, mitochondrial function, angiogenesis, and nutrient transporters in placentae of piglets with different birth weights: <500 g (L), 500–600 g (LM), 600–700 g (M), and >700 g (H). Results showed that placentae from the L group had higher oxidative damage, lower adenosine triphosphate and citrate synthase levels, and lower vascular density, compared to those from the other groups. Protein expression of angiogenic markers, including vascular endothelial cadherin, vascular endothelial growth factor A, and platelet endothelial cell adhesion molecule-1, was the lowest in the L group placentae compared to the other groups. In addition, the protein levels of glucose transporters GLUT1 and GLUT3 were downregulated in the L group, compared to the other groups. Furthermore, oxidative stress induced by H2O2 inhibited tube formation and migration in porcine vascular endothelial cells. Collectively, placentae for lower birth weight neonates are vulnerable to oxidative damage, mitochondrial dysfunction, and impaired angiogenesis.
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Jones, M. L., P. J. Mark, T. A. Mori, and B. J. Waddell. "523. PLACENTAL ANTIOXIDANT ENZYMES IN RAT PREGNANCY SHOW ZONE- AND STAGE-DEPENDENT VARIATION." Reproduction, Fertility and Development 21, no. 9 (2009): 122. http://dx.doi.org/10.1071/srb09abs523.
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Placental oxidative stress plays a key role in the pathophysiology of placenta-related disorders including preeclampsia. Protection from oxidative stress is provided by antioxidant enzymes which inactivate reactive oxygen species (ROS). The rat placenta consists of two major zones, the junctional (JZ) and labyrinth (LZ), and because only the LZ grows in late gestation we hypothesized it generates more ROS and thus requires greater antioxidant protection. Our previous studies on expression of the antioxidants superoxide dismutase (SOD)-1, SOD-2 and catalase support this hypothesis. Here, we extend these observations to include mRNA expression of SOD-3 and thioredoxin reductases (Txnrd-1, -2, -3) and activities of SOD, hydrogen peroxide (H2O2) scavenging and xanthine oxidase (XO). Placental oxidative damage was assessed by measurement of F2-isoprostanes and TBARS concentrations. We also measured the effects of maternal dexamethasone treatment, since glucocorticoid excess is known to induce oxidative damage in other tissues. Placentas were collected from untreated mothers on days 16 and 22 (term=day 23) and on day 22 after dexamethasone treatment from day 13 (1 μg/ml drinking water). SOD-3, Txnrd-1, -2, and -3 mRNAs were measured in JZ and LZ by qRT-PCR. F2-isoprostanes were measured by GC-MS and kit assays were used to measure TBARS and the activities of SOD, H2O2 scavenging and XO. In both placental zones, expression of SOD-3 and Txnrd-1 mRNAs and H2O2 scavenging activity decreased from day 16 to 22, whereas XO activity increased. Dexamethasone treatment increased H2O2 scavenging in both zones, but had no effect on SOD or XO activities or antioxidant mRNA expression. Despite predicted increases in placental ROS generation in late pregnancy and after dexamethasone, neither F2-isoprostanes nor TBARS were increased. These and our previous data suggest that endogenous protection against oxidative stress is abundant in the rat placenta and provides protection against potential oxidative insults including glucocorticoid excess.
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Aljunaidy, Mais M., Jude S. Morton, Christy-Lynn M. Cooke, and Sandra T. Davidge. "Prenatal hypoxia and placental oxidative stress: linkages to developmental origins of cardiovascular disease." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 313, no. 4 (October 1, 2017): R395—R399. http://dx.doi.org/10.1152/ajpregu.00245.2017.
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Intrauterine growth restriction (IUGR, a pregnancy complication where the fetus does not reach its genetic growth potential) is a leading cause of fetal morbidity and mortality with a significant impact on population health. IUGR is associated with gestational hypoxia; which can lead to placental oxidative stress and fetal programming of cardiovascular disease. Mitochondria are a major source of placental oxidative stress and may provide a therapeutic target to mitigate the detrimental effects of placental oxidative stress on pregnancy outcomes. A nanoparticle-mediated delivery of a mitochondrial antioxidant to the placenta is a potential novel approach that may avoid unwanted off-target effects on the developing offspring.
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Denkl, Barbara, Nada Cordasic, Hanna Huebner, Carlos Menendez-Castro, Marius Schmidt, Alexander Mocker, Joachim Woelfle, Andrea Hartner, and Fabian B. Fahlbusch. "No evidence of the unfolded protein response in the placenta of two rodent models of preeclampsia and intrauterine growth restriction." Biology of Reproduction 105, no. 2 (May 6, 2021): 449–63. http://dx.doi.org/10.1093/biolre/ioab087.
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Abstract In humans, intrauterine growth restriction (IUGR) and preeclampsia (PE) are associated with induction of the unfolded protein response (UPR) and increased placental endoplasmic reticulum (ER) stress. Especially in PE, oxidative stress occurs relative to the severity of maternal vascular underperfusion (MVU) of the placental bed. On the premise that understanding the mechanisms of placental dysfunction could lead to targeted therapeutic options for human IUGR and PE, we investigated the roles of the placental UPR and oxidative stress in two rodent models of these human gestational pathologies. We employed a rat IUGR model of gestational maternal protein restriction, as well as an endothelial nitric oxide synthase knockout mouse model (eNOS−/−) of PE/IUGR. Placental expression of UPR members was analyzed via qRT-PCR (Grp78, Calnexin, Perk, Chop, Atf6, and Ern1), immunohistochemistry, and Western blotting (Calnexin, ATF6, GRP78, CHOP, phospho-eIF2α, and phospho-IRE1). Oxidative stress was determined via Western blotting (3-nitrotyrosine and 4-hydroxy-2-nonenal). Both animal models showed a significant reduction of fetal and placental weight. These effects did not induce placental UPR. In contrast to human data, results from our rodent models suggest retention of placental plasticity in the setting of ER stress under an adverse gestational environment. Oxidative stress was significantly increased only in female IUGR rat placentas, suggesting a sexually dimorphic response to maternal malnutrition. Our study advances understanding of the involvement of the placental UPR in IUGR and PE. Moreover, it emphasizes the appropriate choice of animal models researching various aspects of these pregnancy complications.
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Prijanti, Ani Retno, Nelly Marissa, Reni Paramita, Sarah Humaira, Eldesta Nisa Nabila, Anthony Eka Wijaya, Asiyah Nurul Fadila, and Yuditiya Purwosunu. "ANALYSIS OF OXIDATIVE STRESS MARKERS MALONDIALDEHYDE, GLUTATHIONE, NITRIC OXIDE, AND PRORENIN LEVEL IN PREECLAMPSIA PLACENTAL TISSUES." Asian Journal of Pharmaceutical and Clinical Research 11, no. 1 (January 1, 2018): 158. http://dx.doi.org/10.22159/ajpcr.2017.v11i1.18330.
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Objective: Preeclampsia was a syndrome of hypertension proteinuria in pregnant women. In failure of pseudo vasculogenesis, there is persistency of endothelial and smooth muscle cell of vessel wall in spiral artery. Spiral artery could not be emphasis and lead to relative hypoxia, and oxidative stress in placental tissues. Endothelial cell has property to produce nitric oxide (NO) that can dilated vessel. Placenta also produces prorenin, to maintain vascular wall tonicity. Therefore, we want to uncover the property of placenta is there any capacity of prorenin, is that prorenin could overcome the NO level, or is there any depression of NO production, and any oxidative stress.Methods: This observational study was used case–control design. We search preeclampsia cases during September-December 2015. We used preeclampsia placentas from early and late onset. We collect preeclampsia placentas from Cipto Mangunkusumo and normal placentas from Budi Kemuliaan Hospital. We used 30 preeclampsia placentas and 30 normal placentas. Markers measured were NO and prorenin. NO was measured using colorimetric assay kit (K262-200/ BioVision), and prorenin was measured using human prorenin enzyme-linked immunosorbent assay kit (ab157525/ Abcam). Glutathione (GSH) was measured using Ellman method and malondialdehyde (MDA) using Wills method.Results: Prorenin concentration between normal and preeclampsia placenta was analyzed using Mann–Whitney and show that there had no significant difference between preeclampsia and normal placentas (p=0.23). Besides, NO data analyzed using independent t-test show significant differences between preeclampsia and normal placentas (p=0.001). The difference between normal and preeclampsia GSH concentration was not significant (p=0.757), besides the difference between normal and preeclampsia MDA concentration was significant (p=0.000).Conclusion: NO concentration in preeclampsia placenta was increase, higher than normal placenta. There was no effect of preeclampsia on prorenin concentration and GSH. There was marked decrease of MDA in preeclampsia placentas.
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Prijanti, Ani Retno, Nelly Marissa, Reni Paramita, Sarah Humaira, Eldesta Nisa Nabila, Anthony Eka Wijaya, Asiyah Nurul Fadila, and Yuditiya Purwosunu. "ANALYSIS OF OXIDATIVE STRESS MARKERS MALONDIALDEHYDE, GLUTATHIONE, NITRIC OXIDE, AND PRORENIN LEVEL IN PREECLAMPSIA PLACENTAL TISSUES." Asian Journal of Pharmaceutical and Clinical Research 11, no. 1 (January 1, 2018): 158. http://dx.doi.org/10.22159/ajpcr.2018.v11i1.18330.
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Objective: Preeclampsia was a syndrome of hypertension proteinuria in pregnant women. In failure of pseudo vasculogenesis, there is persistency of endothelial and smooth muscle cell of vessel wall in spiral artery. Spiral artery could not be emphasis and lead to relative hypoxia, and oxidative stress in placental tissues. Endothelial cell has property to produce nitric oxide (NO) that can dilated vessel. Placenta also produces prorenin, to maintain vascular wall tonicity. Therefore, we want to uncover the property of placenta is there any capacity of prorenin, is that prorenin could overcome the NO level, or is there any depression of NO production, and any oxidative stress.Methods: This observational study was used case–control design. We search preeclampsia cases during September-December 2015. We used preeclampsia placentas from early and late onset. We collect preeclampsia placentas from Cipto Mangunkusumo and normal placentas from Budi Kemuliaan Hospital. We used 30 preeclampsia placentas and 30 normal placentas. Markers measured were NO and prorenin. NO was measured using colorimetric assay kit (K262-200/ BioVision), and prorenin was measured using human prorenin enzyme-linked immunosorbent assay kit (ab157525/ Abcam). Glutathione (GSH) was measured using Ellman method and malondialdehyde (MDA) using Wills method.Results: Prorenin concentration between normal and preeclampsia placenta was analyzed using Mann–Whitney and show that there had no significant difference between preeclampsia and normal placentas (p=0.23). Besides, NO data analyzed using independent t-test show significant differences between preeclampsia and normal placentas (p=0.001). The difference between normal and preeclampsia GSH concentration was not significant (p=0.757), besides the difference between normal and preeclampsia MDA concentration was significant (p=0.000).Conclusion: NO concentration in preeclampsia placenta was increase, higher than normal placenta. There was no effect of preeclampsia on prorenin concentration and GSH. There was marked decrease of MDA in preeclampsia placentas.
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Hu, Chengjun, Yunyu Yang, Jiaying Li, Hao Wang, Chuanhui Cheng, Linfang Yang, Qiqi Li, et al. "Maternal Diet-Induced Obesity Compromises Oxidative Stress Status and Angiogenesis in the Porcine Placenta by Upregulating Nox2 Expression." Oxidative Medicine and Cellular Longevity 2019 (October 1, 2019): 1–13. http://dx.doi.org/10.1155/2019/2481592.
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Maternal obesity is associated with placental oxidative stress. However, the mechanism underlying this association remains poorly understood. In the present study, a gilt obesity model was developed by exposure to different energy diets and used to investigate the role of NADPH oxidase 2 (Nox2) in the placenta. Specifically, 99 gilts (Guangdong Small-ear Spotted pig) at day 60 of gestation were randomly assigned to one of the following three treatments: low-energy group (L, DE=11.50 MJ/kg), medium-energy group (M, DE=12.41 MJ/kg), and high-energy group (H, DE=13.42 MJ/kg), with 11 replicate pens per treatment and 3 gilts per pen. At the start of the study, maternal body weight and backfat thickness were not significantly different in the three treatments. After the study, data indicated that the H group had higher body weight and backfat thickness gain for gilts during gestation and lower piglet birth weight compared with the other two groups. Additionally, the H group showed glucolipid metabolic disorders and increased triglyceride and nonesterified fatty acid contents in the placenta of gilts. Compared with the L group, the H group exhibited lower mitochondrial biogenesis and increased oxidative damage in the placenta. Importantly, increased mRNA expression and protein abundance of Nox2 were observed for the first time in H group placentae. Furthermore, compared with the L group, the H group showed a decrease in the density of placental vessels and the protein levels of vascular endothelial cadherin (VE-cadherin), vascular endothelial growth factor A (VEGF-A), and phosphorylation of vascular endothelial growth factor receptor 2 (p-VEGFR2) as well as the immunostaining intensity of platelet endothelial cell adhesion molecule-1 (CD31). Our findings suggest that maternal high-energy diet-induced obesity increases placental oxidative stress and decreases placental angiogenesis possibly through the upregulation of Nox2.
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Jeung, E. B., and H. Yang. "81 MEMBRANE AND CYTOSOLIC CALCIUM PROTEINS, TRPV6, PMCA1, NCKX3, NCX1 AND CaBP-28k, APPEAR TO BE DISTINCTLY REGULATED IN HUMAN CHORIOCARCINOMA AND PLACENTAL CELLS." Reproduction, Fertility and Development 24, no. 1 (2012): 153. http://dx.doi.org/10.1071/rdv24n1ab81.
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Preeclampsia is a pregnancy-specific disease characterised by de novo development of concurrent hypertension, proteinuria and oxidative stress in the placenta. In the placenta, intervillous blood flow increases after 10 weeks of gestation and results in exposure of trophoblast cells to oxygen. Hypoxia occurs during the development of placenta in the first trimester and is implicated in trophoblast differentiation. Ca2+ is a universal intracellular second messenger involved in many processes such as signal transduction, hormone secretion and programmed cell death. Human placental primary cell cultures were established from first-trimester human placentas (at 7 to 12 weeks of gestation). In this study, calcium-related proteins (CRPs; TRPV6, PMCA1, NCKX3 and CaBP-28k) were investigated at normoxia (5% CO2 in 95% air) or hypoxia (2% O2/93% N2/5%CO2) for 12 h in human placental cell line (BeWo) and human placental primary cell (hPC). We confirmed mRNA expression by real-time PCR and protein expression by Western blot analysis. The data were 2 or 3 individual experiments with triplicate samples and analysed by one-way ANOVA using Tukey's multiple comparison test. In hypoxia, the level of TRPV6 mRNA and protein was not changed, however, calcium transporters' (NCKX3, CaBP-28k) mRNA and protein expressions were significantly increased in hypoxic BeWo cell compared with control (normoxia). In addition, expression of PMCA1 mRNA and protein was decreased in hypoxic BeWo cells. In hPC, CRPs (TRPV6, PMCA1, NCKX3 and CaBP-28k) mRNA and protein expressions were significantly induced by hypoxic stress compared with control. These results, taken together, indicate that alterations of calcium transporters in hypoxic stress may be involved in calcium transport in the placenta and protection of the placental trophoblasts from the oxidative stress during the pregnancy.
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Basu, Jayasri, Bolek Bendek, Enyonam Agamasu, Carolyn M. Salafia, Aruna Mishra, Nerys Benfield, Ronak Patel, and Magdy Mikhail. "Placental Oxidative Status throughout Normal Gestation in Women with Uncomplicated Pregnancies." Obstetrics and Gynecology International 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/276095.
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The effects of gestational age on placental oxidative balance throughout gestation were investigated in women with uncomplicated pregnancies. Placental tissues were obtained from normal pregnant women who delivered at term or underwent elective pregnancy termination at 6 to 23 + 6 weeks of pregnancy. Placental tissues were analyzed for total antioxidant capacity (TAC) and lipid peroxide (malondialdehyde, MDA) levels using commercially available kits. Two hundred and one placental tissues were analyzed and the mean ± SD MDA (pmol/mg tissue) and TAC (µmol Trolox equivalent/mg tissue) levels for first, second, and third trimester groups were 277.01 ± 204.66, 202.66 ± 185.05, and 176.97 ± 141.61,P< 0.004 and 498.62 ± 400.74, 454.90 ± 374.44, and 912.19 ± 586.21,P< 0.0001 by ANOVA, respectively. Our data reflects an increased oxidative stress in the placenta in the early phase of normal pregnancy. As pregnancy progressed, placental antioxidant protective mechanisms increased and lipid peroxidation markers decreased resulting in diminution in oxidative stress. Our findings provide a biochemical support to the concept of a hypoxic environment in early pregnancy. A decrease in placental oxidative stress in the second and third trimesters appears to be a physiological phenomenon of normal pregnancy. Deviations from this physiological phenomenon may result in placental-mediated disorders.
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Schoots, Mirthe H., Sanne J. Gordijn, Sicco A. Scherjon, Harry van Goor, and Jan-Luuk Hillebrands. "Oxidative stress in placental pathology." Placenta 69 (September 2018): 153–61. http://dx.doi.org/10.1016/j.placenta.2018.03.003.
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Armistead, Brooke, Leena Kadam, Sascha Drewlo, and Hamid-Reza Kohan-Ghadr. "The Role of NFκB in Healthy and Preeclamptic Placenta: Trophoblasts in the Spotlight." International Journal of Molecular Sciences 21, no. 5 (March 5, 2020): 1775. http://dx.doi.org/10.3390/ijms21051775.
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The NFκB protein family regulates numerous pathways within the cell—including inflammation, hypoxia, angiogenesis and oxidative stress—all of which are implicated in placental development. The placenta is a critical organ that develops during pregnancy that primarily functions to supply and transport the nutrients required for fetal growth and development. Abnormal placental development can be observed in numerous disorders during pregnancy, including fetal growth restriction, miscarriage, and preeclampsia (PE). NFκB is highly expressed in the placentas of women with PE, however its contributions to the syndrome are not fully understood. In this review we discuss the molecular actions and related pathways of NFκB in the placenta and highlight areas of research that need attention
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Habibi, Nahal, Jessica A. Grieger, and Tina Bianco-Miotto. "A Review of the Potential Interaction of Selenium and Iodine on Placental and Child Health." Nutrients 12, no. 9 (September 2, 2020): 2678. http://dx.doi.org/10.3390/nu12092678.
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A healthy pregnancy is important for the growth and development of a baby. An adverse pregnancy outcome is associated with increased chronic disease risk for the mother and offspring. An optimal diet both before and during pregnancy is essential to support the health of the mother and offspring. A key mediator of the effect of maternal nutrition factors on pregnancy outcomes is the placenta. Complicated pregnancies are characterized by increased oxidative stress in the placenta. Selenium and iodine are micronutrients that are involved in oxidative stress in placental cells. To date, there has been no comprehensive review investigating the potential synergistic effect of iodine and selenium in the placenta and how maternal deficiencies may be associated with increased oxidative stress and hence adverse pregnancy outcomes. We undertook a hypothesis-generating review on selenium and iodine, to look at how they may relate to pregnancy complications through oxidative stress. We propose how they may work together to impact pregnancy and placental health and explore how deficiencies in these micronutrients during pregnancy may impact the future health of offspring.
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Rudov, Alexander, Walter Balduini, Silvia Carloni, Serafina Perrone, Giuseppe Buonocore, and Maria Cristina Albertini. "Involvement of miRNAs in Placental Alterations Mediated by Oxidative Stress." Oxidative Medicine and Cellular Longevity 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/103068.
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Oxidative stress (OS) is known to be strongly involved in a large number of fetal, neonatal, and adult diseases, including placental disorders, leading to pregnancy loss and stillbirths. A growing body of research links OS to preeclampsia, gestational diabetes, obesity, spontaneous abortion, recurrent pregnancy, preterm labor, and intrauterine growth restriction. While a considerable number of miRNAs have been related to physiological functions and pathological conditions of the placenta, a direct link among these miRNAs, placental functions, and OS is still lacking. This review summarizes data describing the role of miRNAs in placental pathophysiological processes and their possible impact on OS damaging responses. As miRNAs can be found in circulation, improving our understanding on their role in the pathogenesis of pregnancy related disorders could have an important impact on the diagnosis and prognosis of these diseases.
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Mandò, Chiara, Gaia Maria Anelli, Chiara Novielli, Paola Panina-Bordignon, Maddalena Massari, Martina Ilaria Mazzocco, and Irene Cetin. "Impact of Obesity and Hyperglycemia on Placental Mitochondria." Oxidative Medicine and Cellular Longevity 2018 (August 14, 2018): 1–10. http://dx.doi.org/10.1155/2018/2378189.
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A lipotoxic placental environment is recognized in maternal obesity, with increased inflammation and oxidative stress. These changes might alter mitochondrial function, with excessive production of reactive oxygen species, in a vicious cycle leading to placental dysfunction and impaired pregnancy outcomes. Here, we hypothesize that maternal pregestational body mass index (BMI) and glycemic levels can alter placental mitochondria. We measured mitochondrial DNA (mtDNA, real-time PCR) and morphology (electron microscopy) in placentas of forty-seven singleton pregnancies at elective cesarean section. Thirty-seven women were normoglycemic: twenty-one normal-weight women, NW, and sixteen obese women, OB/GDM(−). Ten obese women had gestational diabetes mellitus, OB/GDM(+). OB/GDM(−) presented higher mtDNA levels versus NW, suggesting increased mitochondrial biogenesis in the normoglycemic obese group. These mitochondria showed similar morphology to NW. On the contrary, in OB/GDM(+), mtDNA was not significantly increased versus NW. Nevertheless, mitochondria showed morphological abnormalities, indicating impaired functionality. The metabolic response of the placenta to impairment in obese pregnancies can possibly vary depending on several parameters, resulting in opposite strains acting when insulin resistance of GDM occurs in the obese environment, characterized by inflammation and oxidative stress. Therefore, mitochondrial alterations represent a feature of obese pregnancies with changes in placental energetics that possibly can affect pregnancy outcomes.
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Lappas, Martha, Sofianos Andrikopoulos, and Michael Permezel. "Hypoxanthine–xanthine oxidase down-regulates GLUT1 transcription via SIRT1 resulting in decreased glucose uptake in human placenta." Journal of Endocrinology 213, no. 1 (January 19, 2012): 49–57. http://dx.doi.org/10.1530/joe-11-0355.
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Appropriate foetal growth and development is dependent on adequate placental glucose uptake. Oxidative stress regulates glucose uptake in various tissues. The effect of oxidative stress on placental glucose transport is not known. Thus, the aim of this study was to determine the effect of oxidative stress on glucose uptake and glucose transporters (GLUTs) in human placenta. Human placenta was incubated in the absence or presence of 0.5 mM hypoxanthine+15 mU/ml xanthine oxidase (HX/XO) for 24 h. Gene and protein expressions of the GLUTs were analysed by quantitative RT-PCR and western blotting respectively. Glucose uptake was measured using radiolabelled (14C) glucose. HX/XO significantly decreased GLUT1 gene and protein expression and resultant glucose uptake. There was no effect of the antioxidants N-acetylcysteine, catalase and superoxide dismutase or the NF-κB inhibitor BAY 11-0782 on HX/XO-induced decrease in glucose uptake. However, HX/XO treatment significantly decreased both gene and protein expression of SIRT1. In the presence of the SIRT1 activator resveratrol, the decrease in GLUT1 expression and glucose uptake mediated by HX/XO was abolished. Collectively, the data presented here demonstrate that oxidative stress reduces placental glucose uptake and GLUT1 expression by a SIRT1-dependent mechanism.
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Tissot van Patot, Martha C., Andrew J. Murray, Virginia Beckey, Tereza Cindrova-Davies, Jemma Johns, Lisa Zwerdlinger, Eric Jauniaux, Graham J. Burton, and Natalie J. Serkova. "Human placental metabolic adaptation to chronic hypoxia, high altitude: hypoxic preconditioning." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 1 (January 2010): R166—R172. http://dx.doi.org/10.1152/ajpregu.00383.2009.
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We have previously demonstrated placentas from laboring deliveries at high altitude have lower binding of hypoxia-inducible transcription factor (HIF) to DNA than those from low altitude. It has recently been reported that labor causes oxidative stress in placentas, likely due to ischemic hypoxic insult. We hypothesized that placentas of high-altitude residents acquired resistance, in the course of their development, to oxidative stress during labor. Full-thickness placental tissue biopsies were collected from laboring vaginal and nonlaboring cesarean-section term (37–41 wk) deliveries from healthy pregnancies at sea level and at 3,100 m. After freezing in liquid nitrogen within 5 min of delivery, we quantified hydrophilic and lipid metabolites using 31P and 1H NMR metabolomics. Metabolic markers of oxidative stress, increased glycolysis, and free amino acids were present in placentas following labor at sea level, but not at 3,100 m. In contrast, at 3,100 m, the placentas were characterized by the presence of concentrations of stored energy potential (phosphocreatine), antioxidants, and low free amino acid concentrations. Placentas from pregnancies at sea level subjected to labor display evidence of oxidative stress. However, laboring placentas at 3,100 m have little or no oxidative stress at the time of delivery, suggesting greater resistance to ischemia-reperfusion. We postulate that hypoxic preconditioning might occur in placentas that develop at high altitude.
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Tian, Liang, Jiahe Huang, Aiyou Wen, and Peishi Yan. "Impaired Mitochondrial Function Results from Oxidative Stress in the Full-Term Placenta of Sows with Excessive Back-Fat." Animals 10, no. 2 (February 23, 2020): 360. http://dx.doi.org/10.3390/ani10020360.
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The aim of this study was to determine the effect of excessive back-fat (BF) of sows on placental oxidative stress, ATP generation, mitochondrial alterations in content and structure, and mitochondrial function in isolated trophoblasts. Placental tissue was collected by vaginal delivery from BFI (15–20 mm, n = 10) and BFII (21–27 mm, n = 10) sows formed according to BF at mating. Our results demonstrated that excessive back-fat contributed to augmented oxidative stress in term placenta, as evidenced by excessive production of ROS, elevated protein carbonylation, and reduced SOD, GSH-PX, and CAT activities (p < 0.05). Indicative of mitochondrial dysfunction, reduced mitochondrial respiration in cultured trophoblasts was linked to decreased ATP generation, lower mitochondrial Complex I activity and reduced expression of electron transport chain subunits in placenta of BFII sows (p < 0.05). Meanwhile, we observed negative alterations in mitochondrial biogenesis and structure in the placenta from BFII group (p < 0.05). Finally, our in vitro studies showed lipid-induced ROS production resulted in mitochondrial alterations in trophoblasts, and these effects were blocked by antioxidant treatment. Together, these data reveal that excessive back-fat aggravates mitochondrial injury induced by increased oxidative stress in pig term placenta, which may have detrimental consequences on placental function and therefore impaired fetal growth and development.
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Manna, Samprikta, Cathal McCarthy, and Fergus P. McCarthy. "Placental Ageing in Adverse Pregnancy Outcomes: Telomere Shortening, Cell Senescence, and Mitochondrial Dysfunction." Oxidative Medicine and Cellular Longevity 2019 (May 22, 2019): 1–11. http://dx.doi.org/10.1155/2019/3095383.
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Preeclampsia is a multisystemic pregnancy disorder and a major cause of maternal and neonatal morbidity and mortality worldwide. The exact pathophysiology of preeclampsia remains unclear; however, it is speculated that the various pathologies can be attributed to impaired vascular remodelling and elevated oxidative stress within the placenta. Oxidative stress plays a key role in cell ageing, and the persistent presence of elevated oxidative stress precipitates cellular senescence and mitochondrial dysfunction, resulting in premature ageing of the placenta. Premature ageing of the placenta is associated with placental insufficiency, which reduces the functional capacity of this critical organ and leads to abnormal pregnancy outcomes. The changes brought about by oxidative insults are irreversible and often lead to deleterious modifications in macromolecules such as lipids and proteins, DNA mutations, and alteration of mitochondrial functioning and dynamics. In this review, we have summarized the current knowledge of placental ageing in the aetiology of adverse pregnancy outcomes and discussed the hallmarks of ageing which could be potential markers for preeclampsia and fetal growth restriction.
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Abdelghany Hassan Abdelghany, Ahmed Abdelghany Hassan, Sarah Abdelghany Hassan, and Rania Mohamed Fawzy. "Ultrastructural changes of the placenta in cases of preeclampsia." Magna Scientia Advanced Research and Reviews 3, no. 2 (November 30, 2021): 047–60. http://dx.doi.org/10.30574/msarr.2021.3.2.0080.
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The placenta plays vital roles during fetal development and growth. The ultrastructure of the placenta together with remodeling of the uterine spiral arteries are very important to maintain the utero-placental blood flow. Preeclampsia (PE) is a multifactorial disorder with abnormal placentation affecting the mother and fetus. The aim of this study was to study the ultrastructural abnormalities of the placenta in cases of PE. The placentas of 10 PE women and 10 controls were studied. Women of PE group were delivered by caesarian section while seven control women were delivered vaginally, and three by caesarian section. Placental samples were studied both morphologically and histologically by light and transmission electron microscopy. Light microscopic study of control placentas showed numerous microvilli, few syncytial knots, thin-walled blood vessels. PE placentas showed reduced number of microvilli with numerous syncytial knots, thick-walled vessels, edematous spaces, fibrotic areas and fibrinoid degeneration. Electron microscopic study of the control placentas showed a thick layer of syncytiotrophoblast (Sy), numerous microvilli and a thin layer of cytotrophoblast (Cy). PE placenta showed hypertrophy of Cy with atrophy of Sy and scarce microvilli. The trophoblast showed edematous vacuoles and glycogen storage areas. The villous core had congested capillaries, edematous spaces, glycogen storage areas and widespread areas of fibrosis. All the changes in PE placentas were attributed to hypoxia and oxidative stress and reduced utero-placental flow due to abnormal remodeling of the uterine spiral arteries that was aggravated by the thick placental barrier and the presence of edema, fibrosis and glycogen storage areas.
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Jones, Megan L., Peter J. Mark, and Brendan J. Waddell. "Maternal dietary omega-3 fatty acids and placental function." REPRODUCTION 147, no. 5 (May 2014): R143—R152. http://dx.doi.org/10.1530/rep-13-0376.
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The developing fetus requires substantial amounts of fatty acids to support rapid cellular growth and activity. Although the fatty acid composition delivered to the fetus is largely determined by maternal circulating levels, the placenta preferentially transfers physiologically important long-chain polyunsaturated fatty acids (LC-PUFAs), particularly omega-3 (n-3) PUFAs. Maternal dietary supplementation with n-3 PUFAs during pregnancy has been shown to increase gestation length, enhance fetal growth, and reduce the risk of pregnancy complications, although the precise mechanisms governing these effects remain uncertain. Omega-3 PUFAs are involved in several physiological pathways which could account for these effects, including anti-inflammatory, pro-resolving, and anti-oxidative pathways. Recent studies have shown that maternal dietary n-3 PUFA supplementation during rat pregnancy can reduce placental oxidative damage and increase placental levels of pro-resolving mediators, effects associated with enhanced fetal and placental growth. Because several placental disorders, such as intrauterine growth restriction, preeclampsia, and gestational diabetes mellitus, are associated with heightened placental inflammation and oxidative stress, there is considerable interest in the potential for dietary n-3 PUFAs as a therapeutic intervention for these disorders. In this study, we review the impact of dietary n-3 PUFAs on placental function, with particular focus on placental inflammation, inflammatory resolution, and oxidative stress.
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Scaife, Paula J., Amy Simpson, Lesia O. Kurlak, Louise V. Briggs, David S. Gardner, Fiona Broughton Pipkin, Carolyn J. P. Jones, and Hiten D. Mistry. "Increased Placental Cell Senescence and Oxidative Stress in Women with Pre-Eclampsia and Normotensive Post-Term Pregnancies." International Journal of Molecular Sciences 22, no. 14 (July 7, 2021): 7295. http://dx.doi.org/10.3390/ijms22147295.
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Up to 11% of pregnancies extend to post-term with adverse obstetric events linked to pregnancies over 42 weeks. Oxidative stress and senescence (cells stop growing and dividing by irreversibly arresting their cell cycle and gradually ageing) can result in diminished cell function. There are no detailed studies of placental cell senescence markers across a range of gestational ages, although increased levels have been linked to pre-eclampsia before full term. This study aimed to determine placental senescence and oxidative markers across a range of gestational ages in women with uncomplicated pregnancies and those with a diagnosis of pre-eclampsia. Placentae were obtained from 37 women with uncomplicated pregnancies of 37–42 weeks and from 13 cases of pre-eclampsia of 31+2–41+2 weeks. The expression of markers of senescence, oxidative stress, and antioxidant defence (tumour suppressor protein p16INK4a, kinase inhibitor p21, interleukin-6 (IL-6), NADPH oxidase 4 (NOX4), glutathione peroxidases 1, 3, and 4 (GPx1, GPx3, and GPx4), placental growth factor (PlGF), and soluble fms-like tyrosine kinase-1 (sFlt-1)) genes was measured (quantitative real-time PCR). Protein abundance of p16INK4a, IL-6, NOX4, 8-hydroxy-2′-deoxy-guanosine (8-OHdG), and PlGF was assessed by immunocytochemistry. Placental NOX4 protein was higher in post-term than term deliveries and further increased by pre-eclampsia (p < 0.05 for all). P21 expression was higher in post-term placentae (p = 0.012) and in pre-eclampsia (p = 0.04), compared to term. Placental P16INK4a protein expression was increased post-term, compared to term (p = 0.01). In normotensive women, gestational age at delivery was negatively associated with GPx4 and PlGF (mRNA and protein) (p < 0.05 for all), whereas a positive correlation was seen with placental P21, NOX4, and P16INK4a (p < 0.05 for all) expression. Markers of placental oxidative stress and senescence appear to increase as gestational age increases, with antioxidant defences diminishing concomitantly. These observations increase our understanding of placental health and may contribute to assessment of the optimal gestational age for delivery.
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Tang, Yunhui, Katie Groom, Larry Chamley, and Qi Chen. "Melatonin, a Potential Therapeutic Agent for Preeclampsia, Reduces the Extrusion of Toxic Extracellular Vesicles from Preeclamptic Placentae." Cells 10, no. 8 (July 27, 2021): 1904. http://dx.doi.org/10.3390/cells10081904.
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Preeclampsia, characterised by maternal endothelial cell activation, is triggered by toxic factors, such as placental extracellular vesicles (EVs) from a dysfunctional placenta. The increased oxidative stress seen in the preeclamptic placenta links to endoplasmic reticulum (ER) stress. The ER regulates protein folding and trafficking. When the ER is stressed, proteins are misfolded, and misfolded proteins are toxic. Misfolded proteins can be exported from cells, via EVs which target to other cells where the misfolded proteins may also be toxic. Melatonin is a hormone and antioxidant produced by the pineal gland and placenta. Levels of melatonin are reduced in preeclampsia. In this study we investigated whether melatonin treatment can change the nature of placental EVs that are released from a preeclamptic placenta. EVs were collected from preeclamptic (n = 6) and normotensive (n = 6) placental explants cultured in the presence or absence of melatonin for 18 h. Misfolded proteins were measured using a fluorescent compound, Thioflavin-T (ThT). Endothelial cells were exposed to placental EVs overnight. Endothelial cell activation was measured by the quantification of cell-surface ICAM-1 using a cell-based ELISA. EVs from preeclamptic placentae carried significantly (p < 0.001) more misfolded proteins than normotensive controls. Incubating preeclamptic placental explants in the presence of melatonin (1 µM and 10 µM) significantly (p < 0.001) reduced the misfolded proteins carried by EVs. Culturing endothelial cells in the presence of preeclamptic EVs significantly increased the expression of ICAM-1. This increased ICAM-1 expression was significantly reduced when the endothelial cells were exposed to preeclamptic EVs cultured in the presence of melatonin. This study demonstrates that melatonin reduces the amount of misfolded proteins carried by EVs from preeclamptic placentae and reduces the ability of these EVs to activate endothelial cells. Our study provides further preclinical support for the use of melatonin as a treatment for preeclampsia.
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Saroyo, Yudianto Budi, Noroyono Wibowo, Rima Irwinda, Ani Retno Prijanti, Evy Yunihastuti, Saptawati Bardosono, Sofie Rifayani Krisnadi, Putri Indah Permata, Stephanie Wijaya, and Victor Prana Andika Santawi. "Oxidative Stress Induced Damage and Early Senescence in Preterm Placenta." Journal of Pregnancy 2021 (June 24, 2021): 1–6. http://dx.doi.org/10.1155/2021/9923761.
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Introduction. Senescent cells have been demonstrated to release High Mobility Group Box 1 (HMGB1) which induces labor through an inflammatory pathway. This research is aimed at demonstrating whether telomere shortening, proinflammatory HMGB1, and oxidative damage marker 8-OHdG play a role in the placenta of preterm birth in comparison to term birth. Method. A cross-sectional study on 67 full thickness of the placenta obtained from mothers with term and preterm birth. Mothers with clinical signs of infection ( fever > 38 ° C , leukocytosis > 18000 / μ L , or abnormal vaginal discharge) and other pregnancy complications were excluded. Real-time polymerase chain reaction was performed to measure T/S ratio and ELISA quantification to measure the amount of HMGB1 and 8-OHdG. Result. A total of 34 placentas from preterm and 33 placentas from term birth were examined. Maternal characteristics were comparable between the two groups. There were no statistical difference of T/S ratio ( p = 0.181 ), HMGB1 ( p = 0.119 ), and 8-OHdG ( p = 0.144 ) between the preterm and term groups. HMGB1 was moderately correlated with 8-OHdG ( r = 0.314 ). Telomere T/S ratio of the placenta did not differ between preterm and term labor despite difference in gestational age, suggesting earlier shortening in the preterm group. It is possible that critical telomere length has been achieved in both term and preterm placenta that warrants labor through senescence process. The result of our study also showed that HMGB1 was not correlated to telomere length, due to the fact that HMGB1 is not upregulated until the critical length of telomere for senescence is exhibited. Conclusion. Similar telomere length might be exhibited due to early telomere shortening in preterm birth that mimics the term placenta. The relationship between placental telomere shortening and HMGB1 release remains to be uncovered. Further research is needed to discover the factors leading to early telomere shortening in the placenta of preterm birth.
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Balogun, Kayode, and Lena Serghides. "Comparison of the Effects of Three Dual-Nucleos(t)ide Reverse Transcriptase Inhibitor Backbones on Placenta Mitochondria Toxicity and Oxidative Stress Using a Mouse Pregnancy Model." Pharmaceutics 14, no. 5 (May 15, 2022): 1063. http://dx.doi.org/10.3390/pharmaceutics14051063.
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Nucleos(t)ide reverse transcriptase inhibitors (NRTIs) are the backbone of HIV antiretroviral therapy (ART). ART use in pregnancy has been associated with adverse birth outcomes, in part due to NRTI-induced mitochondrial toxicity. Direct comparison on the effects of commonly used dual-NRTI regimens on placental mitochondria toxicity in pregnancy is lacking. We compared zidovudine/lamivudine, abacavir/lamivudine, and tenofovir/emtricitabine using a mouse model and examined markers of placental mitochondrial function and oxidative stress. Zidovudine/lamivudine and abacavir/lamivudine were associated with lower fetal and placental weights compared to controls, whereas tenofovir/emtricitabine was associated with the least fetal and placental weight reduction, as well as lower resorption rates. Placental mitochondrial DNA content, as well as placental expression of cytochrome c-oxidase subunit-II, DNA polymerase gamma, and citrate synthase, was higher in tenofovir/emtricitabine-treated mice compared to other groups. Zidovudine/lamivudine-treated mice had elevated malondialdehyde levels (oxidative stress marker) compared to other groups and lower mRNA levels of manganese superoxide dismutase and peroxisome proliferator-activated receptor gamma coactivator 1-alpha in the placenta compared to tenofovir/emtricitabine-treated mice. We observed differences in effects between NRTI regimens on placental mitochondrial function and birth outcomes. Tenofovir/emtricitabine was associated with larger fetuses, increased mtDNA content, and higher expression of mitochondrial-specific antioxidant enzymes and mitochondrial biogenesis enzymes, whereas zidovudine/lamivudine was associated with markers of placental oxidative stress.
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Perkins, Anthony V. "Placental oxidative stress, selenium and preeclampsia." Pregnancy Hypertension: An International Journal of Women's Cardiovascular Health 1, no. 1 (January 2011): 95–99. http://dx.doi.org/10.1016/j.preghy.2010.10.008.
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Vangrieken, Philippe, Salwan Al-Nasiry, Aalt Bast, Pieter A. Leermakers, Christy B. M. Tulen, Paul M. H. Schiffers, Frederik J. van Schooten, and Alex H. V. Remels. "Placental Mitochondrial Abnormalities in Preeclampsia." Reproductive Sciences 28, no. 8 (February 1, 2021): 2186–99. http://dx.doi.org/10.1007/s43032-021-00464-y.
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AbstractPreeclampsia complicates 5–8% of all pregnancies worldwide, and although its pathophysiology remains obscure, placental oxidative stress and mitochondrial abnormalities are considered to play a key role. Mitochondrial abnormalities in preeclamptic placentae have been described, but the extent to which mitochondrial content and the molecular pathways controlling this (mitochondrial biogenesis and mitophagy) are affected in preeclamptic placentae is unknown. Therefore, in preeclamptic (n = 12) and control (n = 11) placentae, we comprehensively assessed multiple indices of placental antioxidant status, mitochondrial content, mitochondrial biogenesis, mitophagy, and mitochondrial fusion and fission. In addition, we also explored gene expression profiles related to inflammation and apoptosis. Preeclamptic placentae were characterized by higher levels of oxidized glutathione, a higher total antioxidant capacity, and higher mRNA levels of the mitochondrial-located antioxidant enzyme manganese-dependent superoxide dismutase 2 compared to controls. Furthermore, mitochondrial content was significantly lower in preeclamptic placentae, which was accompanied by an increased abundance of key constituents of glycolysis. Moreover, mRNA and protein levels of key molecules involved in the regulation of mitochondrial biogenesis were lower in preeclamptic placentae, while the abundance of constituents of the mitophagy, autophagy, and mitochondrial fission machinery was higher compared to controls. In addition, we found evidence for activation of apoptosis and inflammation in preeclamptic placentae. This study is the first to comprehensively demonstrate abnormalities at the level of the mitochondrion and the molecular pathways controlling mitochondrial content/function in preeclamptic placentae. These aberrations may well contribute to the pathophysiology of preeclampsia by upregulating placental inflammation, oxidative stress, and apoptosis.
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Wilson, Rebecca L., Weston Troja, Emily K. Sumser, Alec Maupin, Kristin Lampe, and Helen N. Jones. "Insulin-like growth factor 1 signaling in the placenta requires endothelial nitric oxide synthase to support trophoblast function and normal fetal growth." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 320, no. 5 (May 1, 2021): R653—R662. http://dx.doi.org/10.1152/ajpregu.00250.2020.
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Currently, there is no effective treatment for placental dysfunction in utero. In a ligated mouse model of fetal growth restriction (FGR), nanoparticle-mediated human insulin-like 1 growth factor ( hIGF1) gene delivery (NP-Plac1-hIGF1) increased hIGF1 expression and maintained fetal growth. However, whether it can restore fetal growth remains to be determined. Using the endothelial nitric oxide synthase knockout (eNOS−/−) mouse model, a genetic model of FGR, we found that despite inducing expression of hIGF1 in the placentas treated with NP-Plac1-hIGF1 ( P = 0.0425), FGR did not resolve. This was associated with no change to the number of fetal capillaries in the placental labyrinth; an outcome which was increased with NP-Plac1-hIGF1 treatment in the ligated mouse model, despite increased expression of angiopoietin 1 ( P = 0.05), and suggested IGF1 signaling in the placenta requires eNOS to modulate placenta angiogenesis. To further assess this hypothesis, BeWo choriocarcinoma cell line and human placental explant cultures were treated with NP-Plac1-hIGF1, oxidative stress was induced with hydrogen peroxide (H2O2), and NOS activity was inhibited using the inhibitor NG-monomethyl-l-arginine (l-NMMA). In both BeWo cells and explants, the protective effect of NP-Plac1-hIGF1 treatment against H2O2-induced cell death/lactate dehydrogenase release was prevented by eNOS inhibition ( P = 0.003 and P < 0.0001, respectively). This was associated with an increase in mRNA expression of oxidative stress markers hypoxia inducing factor 1α ( HIF1α; P < 0.0001) and ADAM10 ( P = 0.0002) in the NP-Plac1-hIGF1 + H2O2 + l-NMMA-treated BeWo cells. These findings show for the first time the requirement of eNOS/NOS in IGF1 signaling in placenta cells that may have implications for placental angiogenesis and fetal growth.
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Granitzer, Sebastian, Isabella Ellinger, Rumsha Khan, Katharina Gelles, Raimund Widhalm, Markus Hengstschläger, Harald Zeisler, et al. "In vitro function and in situ localization of Multidrug Resistance-associated Protein (MRP)1 (ABCC1) suggest a protective role against methyl mercury-induced oxidative stress in the human placenta." Archives of Toxicology 94, no. 11 (September 11, 2020): 3799–817. http://dx.doi.org/10.1007/s00204-020-02900-5.
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Abstract Methyl mercury (MeHg) is an organic highly toxic compound that is transported efficiently via the human placenta. Our previous data suggest that MeHg is taken up into placental cells by amino acid transporters while mercury export from placental cells mainly involves ATP binding cassette (ABC) transporters. We hypothesized that the ABC transporter multidrug resistance-associated protein (MRP)1 (ABCC1) plays an essential role in mercury export from the human placenta. Transwell transport studies with MRP1-overexpressing Madin-Darby Canine Kidney (MDCK)II cells confirmed the function of MRP1 in polarized mercury efflux. Consistent with this, siRNA-mediated MRP1 gene knockdown in the human placental cell line HTR-8/SVneo resulted in intracellular mercury accumulation, which was associated with reduced cell viability, accompanied by increased cytotoxicity, apoptosis, and oxidative stress as determined via the glutathione (GSH) status. In addition, the many sources claiming different localization of MRP1 in the placenta required a re-evaluation of its localization in placental tissue sections by immunofluorescence microscopy using an MRP1-specific antibody that was validated in-house. Taken together, our results show that (1) MRP1 preferentially mediates apical-to-basolateral mercury transport in epithelial cells, (2) MRP1 regulates the GSH status of placental cells, (3) MRP1 function has a decisive influence on the viability of placental cells exposed to low MeHg concentrations, and (4) the in situ localization of MRP1 corresponds to mercury transport from maternal circulation to the placenta and fetus. We conclude that MRP1 protects placental cells from MeHg-induced oxidative stress by exporting the toxic metal and by maintaining the placental cells' GSH status in equilibrium.
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Akilla, Martin Awe. "Placental Oxidative Stress in the pathogenesis of Hypertensive Disorders of Pregnancy." Annals of Medical Laboratory Science 1, no. 2 (June 20, 2021): 39–49. http://dx.doi.org/10.51374/annalsmls.2021.1.2.0041.
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Background: Hypertensive disorders of pregnancy are a major complication of pregnancies and can lead to fetal growth retardation, premature delivery and maternal morbidity and mortality. The study aimed at assessing the potential role of the placenta in the pathogenesis of hypertensive disorders of pregnancy. Methods: This study was a case-control study conducted at the Upper East Regional Hospital, Ghana from September, 2016 to March 2017. Twenty (20) pregnant women with hypertensive disorders of pregnancy (i.e., Pregnancy induced hypertension, preeclampsia and eclampsia) as cases and 30 normotensive pregnancies as controls, were included in the study. The placenta was excised after delivery, homogenized and assayed for malondialdehyde, catalase, total peroxide, oxidative stress index, total antioxidant capacity and placental lipid profile. Results: The ages of the two groups were similar, with malondialdehyde (p = 0.001) and Oxidative Stress Index (p < 0.001) being significantly higher in the hypertensive group compared to the control group whereas Total Antioxidant Capacity (p < 0.001) and Catalase (p = 0.011) were significantly higher in the control group compared to the hypertensive group. The proportion of normal, term and livebirth deliveries were significantly higher among controls compared to the hypertensive disorders of pregnancy group. Among the estimated oxidative stress markers, total antioxidant capacity turned out to be the best predictor of the hypertensive disorders of pregnancy. Conclusion: Our findings suggest oxidative stress in women with hypertensive disorders of pregnancy and that placental oxidative stress could be the driving factor for the pathogenesis and severity of these hypertensive disorders of pregnancy.
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Zhou, Ling, Ruixue Zhang, Shuangyan Yang, Yaguang Zhang, and Dandan Shi. "Astragaloside IV alleviates placental oxidative stress and inflammation in GDM mice." Endocrine Connections 9, no. 9 (September 2020): 939–45. http://dx.doi.org/10.1530/ec-20-0295.
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Background: Our previous study revealed that astragaloside IV (AS-IV) effectively improved gestational diabetes mellitus (GDM) by reducing hepatic gluconeogenesis. Due to the importance of placental oxidative stress, we further explored the protective role of AS-IV on placental oxidative stress in GDM. Methods: First, non-pregnant mice were orally administrated with AS-IV to evaluate its safety and effect. Then GDM mice were orally administered with AS-IV for 20 days and its effect on the symptoms of GDM, placental oxidative stress, secretions of inflammatory cytokines, as well as toll-like receptor 4 (TLR4)/NF-κB signaling pathway, were evaluated. Results: AS-IV had no adverse effect on non-pregnant mice. On the other hand, AS-IV significantly attenuated the GDM-induced hyperglycemia, glucose intolerance, insulin resistance, placental oxidative stress, productions of inflammatory cytokines and the activation of TLR4/NF-κB pathway. Conclusion: AS-IV effectively protected against GDM by alleviating placental oxidative stress and inflammation, in which TLR4/NF-κB might be involved.
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Mark, P. J., J. L. Lewis, M. L. Jones, and B. J. Waddell. "158. THE UNFOLDED PROTEIN RESPONSE MAY CONTRIBUTE TO GLUCOCORTICOID-INDUCED PLACENTAL GROWTH RESTRICTION IN THE RAT VIA INCREASED PLACENTAL EXPRESSION OF HEAT SHOCK PROTEIN 70." Reproduction, Fertility and Development 22, no. 9 (2010): 76. http://dx.doi.org/10.1071/srb10abs158.
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Perturbations of normal endoplasmic reticulum (ER) physiology occur in a number of pathological conditions, including diabetes and preeclampsia. These pathologies are associated with elevated levels of inappropriately folded proteins and induction of ER stress. Accumulation of misfolded proteins induces the unfolded protein response which increases ER protein folding capacity and promotes ER-associated degradation of unfolded proteins. Glucocorticoids are essential for maturation of fetal organs, however excess exposure during pregnancy retards fetal and placental growth. Glucocorticoids also induce ER stress within macrophages, which reside within the placenta, and activate immune responses which can lead to oxidative stress and subsequent placental dysfunction. We hypothesised that excess glucocorticoid exposure would induce ER stress within the placenta and contribute to restriction of fetal and placental growth. This study compared placentas (n = 6/group) for control (Con) and dexamethasone-exposed pregnancies (Dex; 0.75 μg/mL drinking water from day 13 of gestation) at days 16 and 22 of gestation in the rat (term = 23 days). Placentas were dissected into junctional (JZ) and labyrinth (LZ) zones for separate analysis. Quantitative PCR was used to determine expression of mRNA for markers of ER stress, including heat shock factors (HSF-1 and HSF-2), heat shock proteins (HSP-70 and HSP-90) and C/EBP homologous protein (CHOP10). HSF-1 expression increased 2- to 4-fold from day 16 to 22 in both placental zones, but was not increased by glucocorticoids. Dex-exposure increased HSP-70 expression 2- to 3-fold in the LZ at both days of gestation, indicative of an ER stress response. Similar patterns for JZ expression of HSP-70 were observed. JZ expression of HSP-90 was also upregulated by Dex at day 22 but not day 16. CHOP10 was not induced by Dex-administration in either zone at either gestational time, which suggests that rather than activation of the ATF6/PERK pathway, the activation of ER stress is likely to be via XBP1 induction.
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Rodríguez-González, Guadalupe L., Lilia Vargas-Hernández, Luis A. Reyes-Castro, Carlos A. Ibáñez, Claudia J. Bautista, Consuelo Lomas-Soria, Nozomi Itani, et al. "Resveratrol Supplementation in Obese Pregnant Rats Improves Maternal Metabolism and Prevents Increased Placental Oxidative Stress." Antioxidants 11, no. 10 (September 21, 2022): 1871. http://dx.doi.org/10.3390/antiox11101871.
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Maternal obesity (MO) causes maternal and fetal oxidative stress (OS) and metabolic dysfunction. We investigated whether supplementing obese mothers with resveratrol improves maternal metabolic alterations and reduces OS in the placenta and maternal and fetal liver. From weaning through pregnancy female Wistar rats ate chow (C) or a high-fat diet (MO). One month before mating until 19 days’ gestation (dG), half the rats received 20 mg resveratrol/kg/d orally (Cres and MOres). At 19dG, maternal body weight, retroperitoneal fat adipocyte size, metabolic parameters, and OS biomarkers in the placenta and liver were determined. MO mothers showed higher body weight, triglycerides and leptin serum concentrations, insulin resistance (IR), decreased small and increased large adipocytes, liver fat accumulation, and hepatic upregulation of genes related to IR and inflammatory processes. Placenta, maternal and fetal liver OS biomarkers were augmented in MO. MOres mothers showed more small and fewer large adipocytes, lower triglycerides serum concentrations, IR and liver fat accumulation, downregulation of genes related to IR and inflammatory processes, and lowered OS in mothers, placentas, and female fetal liver. Maternal resveratrol supplementation in obese rats improves maternal metabolism and reduces placental and liver OS of mothers and fetuses in a sex-dependent manner.