Academic literature on the topic 'Placenta; transporter; transportér'
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Journal articles on the topic "Placenta; transporter; transportér"
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Shearman, Lauren P., Alison M. McReynolds, Feng C. Zhou, and Jerrold S. Meyer. "Relationship between [125I]RTI-55-labeled cocaine binding sites and the serotonin transporter in rat placenta." American Journal of Physiology-Cell Physiology 275, no. 6 (December 1, 1998): C1621—C1629. http://dx.doi.org/10.1152/ajpcell.1998.275.6.c1621.
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We investigated the characteristics of cocainelike binding sites in rat placenta using [125I]RTI-55. [3H]paroxetine binding and immunocytochemical staining for serotonin [5-hydroxytryptamine (5-HT)] and for the 5-HT transporter were also used to obtain evidence for rat placental 5-HT uptake. [125I]RTI-55 saturation analyses with membranes from normal gestational day 20 placentas yielded curvilinear Scatchard plots that were resolved into high- and low-affinity components (mean dissociation constants of 0.29 and 7.9 nM, respectively). Drug competition studies with various monoamine uptake inhibitors gave rise to complex multiphasic displacement curves, although the results obtained with the selective 5-HT uptake inhibitor citalopram suggest that the 5-HT transporter is an important component of placental high-affinity [125I]RTI-55 binding. The presence of a rat placental 5-HT uptake system was additionally supported by the [3H]paroxetine binding experiments and by the presence throughout the placenta of immunoreactivity for 5-HT and the 5-HT transporter. Immunostaining with both antibodies was most intense in the junctional zone, whereas the density of [125I]RTI-55 binding sites was greater in the placental labyrinth. This discrepancy may be due to the fact that [125I]RTI-55 appears to be labeling additional cellular components besides the 5-HT transporter. The presence of cocaine- and antidepressant-sensitive 5-HT transporters in the placenta has important implications for the possible effects of these compounds on pregnancy and fetal development.
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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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do Imperio, Guinever Eustaquio, Enrrico Bloise, Mohsen Javam, Phetcharawan Lye, Andrea Constantinof, Caroline Dunk, Fernando Marcos dos Reis, et al. "Chorioamnionitis Induces a Specific Signature of Placental ABC Transporters Associated with an Increase of miR-331-5p in the Human Preterm Placenta." Cellular Physiology and Biochemistry 45, no. 2 (2018): 591–604. http://dx.doi.org/10.1159/000487100.
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Background/Aims: The ATP-binding cassette (ABC) transporters mediate drug biodisposition and immunological responses in the placental barrier. In vitro infective challenges alter expression of specific placental ABC transporters. We hypothesized that chorioamnionitis induces a distinct pattern of ABC transporter expression. Methods: Gene expression of 50 ABC transporters was assessed using TaqMan® Human ABC Transporter Array, in preterm human placentas without (PTD; n=6) or with histological chorioamnionitis (PTDC; n=6). Validation was performed using qPCR, immunohistochemistry and Western blot. MicroRNAs known to regulate P-glycoprotein (P-gp) were examined by qPCR. Results: Up-regulation of ABCB9, ABCC2 and ABCF2 mRNA was detected in chorioamnionitis (p<0.05), whereas placental ABCB1 (P-gp; p=0.051) and ABCG2 (breast cancer resistance protein-BCRP) mRNA levels (p=0.055) approached near significant up-regulation. In most cases, the magnitude of the effect significantly correlated to the severity of inflammation. Upon validation, increased placental ABCB1 and ABCG2 mRNA levels (p<0.05) were observed. At the level of immunohistochemistry, while BCRP was increased (p<0.05), P-gp staining intensity was significantly decreased (p<0.05) in PTDC. miR-331-5p, involved in P-gp suppression, was upregulated in PTDC (p<0.01) and correlated to the grade of chorioamnionitis (p<0.01). Conclusions: Alterations in the expression of ABC transporters will likely lead to modified transport of clinically relevant compounds at the inflamed placenta. A better understanding of the potential role of these transporters in the events surrounding PTD may also enable new strategies to be developed for prevention and treatment of PTD.
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Xu, Jie, Jiao Wang, Yang Cao, Xiaotong Jia, Yujia Huang, Minghui Cai, Chunmei Lu, and Hui Zhu. "Downregulation of Placental Amino Acid Transporter Expression and mTORC1 Signaling Activity Contributes to Fetal Growth Retardation in Diabetic Rats." International Journal of Molecular Sciences 21, no. 5 (March 7, 2020): 1849. http://dx.doi.org/10.3390/ijms21051849.
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Alterations in placental transport may contribute to abnormal fetal intrauterine growth in pregnancies complicated by diabetes, but it is not clear whether the placental amino acid transport system is altered in diabetic pregnancies. We therefore studied the changes in the expressions of placental amino acid transporters in a rat model of diabetes induced by streptozotocin, and tested the effects of hyperglycemia on trophoblast amino acid transporter in vitro. Our results showed that the expressions for key isoforms of system L amino acid transporters were significantly reduced in the placentas of streptozotocin-induced diabetic pregnant rats, which was associated with the decreased birthweight in the rats. A decreased placental efficiency and decreased placental mammalian target of rapamycin (mTOR) complex 1 (mTORC1) activity were also found in the rat model. In addition, hyperglycemia in vitro could inhibit amino acid transporter expression and mTORC1 activity in human trophoblast. Inhibition of mTORC1 activity led to reduced amino acid transporter expression in placental trophoblast. We concluded that reduced placental mTORC1 activity during pregnancy resulted in decreased placental amino acid transporter expression and, subsequently, contributed to fetal intrauterine growth restriction in pregnancies complicated with diabetes.
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Roos, S., Y. Kanai, P. D. Prasad, T. L. Powell, and T. Jansson. "Regulation of placental amino acid transporter activity by mammalian target of rapamycin." American Journal of Physiology-Cell Physiology 296, no. 1 (January 2009): C142—C150. http://dx.doi.org/10.1152/ajpcell.00330.2008.
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The activity of placental amino acid transporters is decreased in intrauterine growth restriction (IUGR), but the underlying regulatory mechanisms have not been established. Inhibition of the mammalian target of rapamycin (mTOR) signaling pathway has been shown to decrease the activity of the system L amino acid transporter in human placental villous fragments, and placental mTOR activity is decreased in IUGR. In the present study, we used cultured primary trophoblast cells to study mTOR regulation of placental amino acid transporters in more detail and to test the hypothesis that mTOR alters amino acid transport activity by changes in transporter expression. Inhibition of mTOR by rapamycin significantly reduced the activity of system A (−17%), system L (−28%), and taurine (−40%) amino acid transporters. mRNA expression of isoforms of the three amino acid transporter systems in response to mTOR inhibition was measured using quantitative real-time PCR. mRNA expression of l-type amino acid transporter 1 (LAT1; a system L isoform) and taurine transporter was reduced by 13% and 50%, respectively; however, mTOR inhibition did not alter the mRNA expression of system A isoforms (sodium-coupled neutral amino acid transporter-1, -2, and -4), LAT2, or 4F2hc. Rapamycin treatment did not significantly affect the protein expression of any of the transporter isoforms. We conclude that mTOR signaling regulates the activity of key placental amino acid transporters and that this effect is not due to a decrease in total protein expression. These data suggest that mTOR regulates placental amino acid transporters by posttranslational modifications or by affecting transporter translocation to the plasma membrane.
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Cleal, J. K., P. E. Day, C. L. Simner, S. J. Barton, P. A. Mahon, H. M. Inskip, K. M. Godfrey, et al. "Placental amino acid transport may be regulated by maternal vitamin D and vitamin D-binding protein: results from the Southampton Women's Survey." British Journal of Nutrition 113, no. 12 (May 5, 2015): 1903–10. http://dx.doi.org/10.1017/s0007114515001178.
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Both maternal 25-hydroxyvitamin D (25(OH)D) concentrations during pregnancy and placental amino acid transporter gene expression have been associated with development of the offspring in terms of body composition and bone structure. Several amino acid transporter genes have vitamin D response elements in their promoters suggesting the possible linkage of these two mechanisms. We aimed to establish whether maternal 25(OH)D and vitamin D-binding protein (VDBP) levels relate to expression of placental amino acid transporters. RNA was extracted from 102 placental samples collected in the Southampton Women's Survey, and gene expression was analysed using quantitative real-time PCR. Gene expression data were normalised to the geometric mean of three housekeeping genes, and related to maternal factors and childhood body composition. Maternal serum 25(OH)D and VDBP levels were measured by radioimmunoassay. Maternal 25(OH)D and VDBP levels were positively associated with placental expression of specific genes involved in amino acid transport. Maternal 25(OH)D and VDBP concentrations were correlated with the expression of specific placental amino acid transporters, and thus may be involved in the regulation of amino acid transfer to the fetus. The positive correlation of VDBP levels and placental transporter expression suggests that delivery of vitamin D to the placenta may be important. This exploratory study identifies placental amino acid transporters which may be altered in response to modifiable maternal factors and provides a basis for further studies.
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Ericsson, Anette, Bengt Hamark, Nina Jansson, Bengt R. Johansson, Theresa L. Powell, and Thomas Jansson. "Hormonal regulation of glucose and system A amino acid transport in first trimester placental villous fragments." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 288, no. 3 (March 2005): R656—R662. http://dx.doi.org/10.1152/ajpregu.00407.2004.
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Alterations in placental nutrient transfer have been implicated in fetal growth abnormalities. In pregnancies complicated by diabetes and accelerated fetal growth, upregulations of glucose transporter 1 (GLUT1) and amino acid transporter system A have been shown in the syncytiotrophoblast of term placenta. In contrast, intrauterine growth restriction is associated with a downregulation of placental system A transporters. However, underlying mechanisms of transporter regulation are poorly understood, particularly in early pregnancy. In this study, hormonal regulation of placental glucose and system A transporters was investigated. The uptake of 3-O-[methyl-14C]-d-glucose was studied in villous fragments isolated from first trimester (6–13 wk of gestation) and term human placenta. Villous fragments were incubated in buffer containing insulin, leptin, cortisol, growth hormone (GH), prolactin, IGF-I, or under hypo/hyperglycemic conditions for 1 h. Subsequently, 3-O-[methyl-14C]-d-glucose uptake was measured with and without phloretin for 70 s in first trimester tissue and 20 s in term tissue. Methylaminoisobutyric uptake was measured with and without Na+ for 20 min. Glucose uptake was unaltered by hormones or hypo/hyperglycemia. GH decreased system A activity by 31% in first trimester ( P < 0.05). The uptake of glucose was 50% higher in term compared with first trimester fragments and increased markedly between 6 and 13 wk of gestation ( P < 0.05). We conclude that placental glucose transporter activity is not regulated by short exposures to the hormones or glucose concentrations tested. In contrast to term placental villous fragments, system A activity was not regulated by insulin or leptin in first trimester but was downregulated by GH.
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Audette, Melanie C., John R. G. Challis, Rebecca L. Jones, Colin P. Sibley, and Stephen G. Matthews. "Synthetic Glucocorticoid Reduces Human Placental System A Transport in Women Treated With Antenatal Therapy." Journal of Clinical Endocrinology & Metabolism 99, no. 11 (November 1, 2014): E2226—E2233. http://dx.doi.org/10.1210/jc.2014-2157.
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Context: Synthetic glucocorticoids (sGCs) are routinely given to women with threatened preterm labor and have been linked to fetal growth restriction and developmental programming. Reductions in fetal growth are likely to be mediated by placental dysfunction, including altered nutrient transport. sGCs modify the system A neutral amino acid transporter in vitro, but there are no in vivo comparable data in human placenta. Objective: Because ∼30% of women who receive sGCs carry to term, our objective was to examine the short- and longer-term consequences of antenatal sGCs on placental system A transport. Methods and Patients: Placental tissue was collected from women treated with sGCs between 24 hours and 14 days before delivery (24h-14d), 14 days after treatment but before term (14d-term), or at term, compared with healthy term (control) deliveries to measure system A-mediated activity (Na+-dependent [14C]methylaminoisobutyric acid uptake per gram placenta) and mRNA expression. Results: After sGC treatment, system A activity was significantly reduced at term compared with both sGC placentas delivered 24h-14d and compared with controls. Placentae from women treated with sGCs who delivered between 14d-term also had significantly reduced system A activity compared with 24h-14d placentas. SLC38A1 and SLC38A2 mRNA expression was unaffected. However, SLC38A4 was significantly reduced by sGCs at term compared with placentas delivered between 14d-term. Conclusion: We conclude that women who are at risk of preterm labor and receive sGCs but deliver at term have significantly reduced placental system A amino acid transporter activity. Altered placental transporter function could affect fetal growth and may contribute to developmental programming reported in both animal and clinical studies.
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Han, Lyrialle W., Chunying Gao, Yuchen Zhang, Joanne Wang, and Qingcheng Mao. "Transport of Bupropion and its Metabolites by the Model CHO and HEK293 Cell Lines." Drug Metabolism Letters 13, no. 1 (April 30, 2019): 25–36. http://dx.doi.org/10.2174/1872312813666181129101507.
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<P>Background: Bupropion (BUP) is widely used as an antidepressant and smoking cessation aid. There are three major pharmacologically active metabolites of BUP, Erythrohydrobupropion (EB), Hydroxybupropion (OHB) and Threohydrobupropion (TB). At present, the mechanisms underlying the overall disposition and systemic clearance of BUP and its metabolites have not been well understood, and the role of transporters has not been studied. </P><P> Objective: The goal of this study was to investigate whether BUP and its active metabolites are substrates of the major hepatic uptake and efflux transporters. </P><P> Method: CHO or HEK293 cell lines or plasma membrane vesicles that overexpress OATP1B1, OATP1B3, OATP2B1, OATP4A1, OCT1, BCRP, MRP2 or P-gp were used in cellular or vesicle uptake and inhibition assays. Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS) was used to quantify transport activity. </P><P> Results: BUP and its major active metabolites were actively transported into the CHO or HEK293 cells overexpressing OATP1B1, OATP1B3 or OATP2B1; however, such cellular active uptake could not be inhibited at all by prototypical inhibitors of any of the OATP transporters. These compounds were not transported by OCT1, BCRP, MRP2 or P-gp either. These results suggest that the major known hepatic transporters likely play a minor role in the overall disposition and systemic clearance of BUP and its active metabolites in humans. We also demonstrated that BUP and its metabolites were not transported by OATP4A1, an uptake transporter on the apical membrane of placental syncytiotrophoblasts, suggesting that OATP4A1 is not responsible for the transfer of BUP and its metabolites from the maternal blood to the fetal compartment across the placental barrier in pregnant women. Conclusion: BUP and metabolites are not substrates of the major hepatic transporters tested and thus these hepatic transporters likely do not play a role in the overall disposition of the drug. Our results also suggest that caution should be taken when using the model CHO and HEK293 cell lines to evaluate potential roles of transporters in drug disposition.</P>
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Vinot, C., L. Gavard, J. M. Tréluyer, S. Manceau, E. Courbon, J. M. Scherrmann, X. Declèves, et al. "Placental Transfer of Maraviroc in anEx VivoHuman Cotyledon Perfusion Model and Influence of ABC Transporter Expression." Antimicrobial Agents and Chemotherapy 57, no. 3 (January 7, 2013): 1415–20. http://dx.doi.org/10.1128/aac.01821-12.
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ABSTRACTNowadays, antiretroviral therapy is recommended during pregnancy to prevent mother-to-child transmission of HIV. However, for many antiretroviral drugs, including maraviroc, a CCR5 antagonist, very little data exist regarding placental transfer. Besides, various factors may modulate this transfer, including efflux transporters belonging to the ATP-binding cassette (ABC) transporter superfamily. We investigated maraviroc placental transfer and the influence of ABC transporter expression on this transfer using the human cotyledon perfusion model. Term placentas were perfusedex vivofor 90 min with maraviroc (600 ng/ml) either in the maternal-to-fetal (n= 10 placentas) or fetal-to-maternal (n= 6 placentas) direction. Plasma concentrations were determined by ultra performance liquid chromatography coupled with tandem mass spectrometry (UPLC-MS/MS). Fetal transfer rates (FTR) and clearance indexes (CLI) were calculated as ratios of fetal to maternal concentrations at steady state (mean values between 30 and 90 min) and ratios of FTR of maraviroc to that of antipyrine, respectively. ABC transporter gene expression levels were determined by quantitative reverse transcription (RT)-PCR and ABCB1 protein expression by Western blotting. For the maternal-to-fetal direction, the mean FTR and CLI were 8.0% ± 3.0 and 0.26 ± 0.07, respectively, whereas the mean CLI was 0.52 ± 0.23 for the fetal-to-maternal direction. We showed a significant inverse correlation between maraviroc CLI andABCC2,ABCC10, andABCC11placental gene expression levels (P< 0.05). To conclude, we report a low maraviroc placental transfer probably involving ABC efflux transporters and thus in all likelihood associated with a limited fetal exposition. Nevertheless, these results would need to be supported byin vivodata obtained from paired maternal and cord blood samples.
Dissertations / Theses on the topic "Placenta; transporter; transportér"
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Russi, Rachel Mary. "The molecular regulation of placental zinc transporters." Thesis, University of Newcastle Upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402646.
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Peres, Kenya Costa [UNESP]. "Transporte placentário via cavéola na placenta de bovinos clonados e transgênicos." Universidade Estadual Paulista (UNESP), 2014. http://hdl.handle.net/11449/115903.
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000809964.pdf: 1108463 bytes, checksum: 43fa89dc624ca99b382ecaa200b42518 (MD5)A utilização da transgenia com a proteína fluorescente verde (GFP) como marcador de células de origem fetal nas placentas de clones bovinos servirá de modelo inédito para estudo morfofisiológico e imunológico da interação materno-fetal, visto que possibilitará o seu mapeamento, diferenciando as células fetais das maternas. Tal modelo terá aplicação direta, principalmente porque estes são animais que apresentam problemas em relação ao seu desenvolvimento. Com o auxílio deste modelo, pretende- se verificar o transporte de substâncias entre a mãe e o feto via endocitose, pela imunolocalização das proteínas chamadas de caveolinas. Para tanto foram utilizados 06 bovinos clonados e 30 bovinos de inseminação artificial (IA) com idade até 90 dias de gestação, os quais tiveram seu desenvolvimento interrompido mediante abate humanitário das receptoras e ovariosalpingohisterectomia, com posterior recuperação do útero gestante. Foram coletados os placentônios e o cório. Uma parte das amostras foi recortada e fixada, por imersão, em solução de parafolmaldeído a 4% ou formoldeído a 10% em tampão fosfato de sódio (PBS) a 0,1M pH 7.4, solução de Zamboni (4% de paraformoldeído, 15% de ácido pícrico, em tampão fosfato de sódio a 0,1M pH 7.4), metacarn (60% de metanol, 30% de clorofórmio, e 10% de ácido acético glacial), para verificação da morfologia e realização de imuno-histoquímica para as proteínas caveolinas -1 e -2 (CAV -1 e CAV-2). As caveolinas -1 foram localizadas nos vilos fetais e maternos, mas sua marcação mais forte foi observada no estroma endometrial. As caveolinas -2 tiveram marcação positiva no trofoblasto e membrana corioalantoide, e, especificamente em célula trofoblástica gigante binucleada. Sendo assim, os resultados mostram que a proteína CAV-1 teve uma maior expressão em relação a proteína CAV-2 e que as proteínas CAV-1 e -2 são parte da composição das cavéolas, sendo .
The transgenic application of green fluorecent protein (GFP) as fetal cell marker on cattle cloned placenta could provide an exclusive model for studying the morphologic and immunologic maternal-fetal interactions, providing information about its mapping, distinguishing the fetal from maternal cells. This model will have direct application, mainly because these are animals that present problems during its development. With this model's support, we intend to verify the substances transport between mother and fetus during endocytocis, through the immunolocalization of protein named caveolae. For these, we used 06 cloned bovine and 30 cattle samples of artificial insemination (AI) with 90 days of pregnancy, which had been their development interrupted by humanitarian slaughter of the recipient and recovery of the pregnant uterus. We collected the placentome and the chorion. A part of the samples will be cutted and fixed, by immersion, on a solution containing 4% of parafomaldehyde or 10% of formaldehyde on a sodium phosphate buffer (PBS) at 0,1M pH 7.4, Zamboni solution (4% of paraformaldehyde, 15% of picric acid, on sodium phosphate buffer 0,1M pH 7.4), metacarn (60% of metanol, 30% of chloroform, and 10% glacial acetic acid), for morphologic and immunohistochemistry verification for caveolinas proteins -1 and -2 ( -1 CAV and CAV- 2). The caveolinas -1 were found in fetal and maternal villi , but its strongest staining was observed in the endometrial stroma . The caveolinas -2 had positive staining in trophoblast and chorioallantoic membrane , and specifically in giant trophoblastic binucleated cell . therefore the results were compared between cloned cattle and from AI or natural mating, for assisting on detection of the reason of many placental alterations, embryonic losses, spontaneous abortion, post-natal mortality and large offspring syndrome on laboratory-manipulated animals. The result suggests that the proteins caveolins -1 and ...
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Peres, Kenya Costa. "Transporte placentário via cavéola na placenta de bovinos clonados e transgênicos/." Dracena, 2014. http://hdl.handle.net/11449/115903.
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Orientador: Flavia Thomaz Verechia PereiraBanca: Cristiana Andrighetto
Banca: Vanessa Gomes Ueno
Resumo: A utilização da transgenia com a proteína fluorescente verde (GFP) como marcador de células de origem fetal nas placentas de clones bovinos servirá de modelo inédito para estudo morfofisiológico e imunológico da interação materno-fetal, visto que possibilitará o seu mapeamento, diferenciando as células fetais das maternas. Tal modelo terá aplicação direta, principalmente porque estes são animais que apresentam problemas em relação ao seu desenvolvimento. Com o auxílio deste modelo, pretende- se verificar o transporte de substâncias entre a mãe e o feto via endocitose, pela imunolocalização das proteínas chamadas de caveolinas. Para tanto foram utilizados 06 bovinos clonados e 30 bovinos de inseminação artificial (IA) com idade até 90 dias de gestação, os quais tiveram seu desenvolvimento interrompido mediante abate humanitário das receptoras e ovariosalpingohisterectomia, com posterior recuperação do útero gestante. Foram coletados os placentônios e o cório. Uma parte das amostras foi recortada e fixada, por imersão, em solução de parafolmaldeído a 4% ou formoldeído a 10% em tampão fosfato de sódio (PBS) a 0,1M pH 7.4, solução de Zamboni (4% de paraformoldeído, 15% de ácido pícrico, em tampão fosfato de sódio a 0,1M pH 7.4), metacarn (60% de metanol, 30% de clorofórmio, e 10% de ácido acético glacial), para verificação da morfologia e realização de imuno-histoquímica para as proteínas caveolinas -1 e -2 (CAV -1 e CAV-2). As caveolinas -1 foram localizadas nos vilos fetais e maternos, mas sua marcação mais forte foi observada no estroma endometrial. As caveolinas -2 tiveram marcação positiva no trofoblasto e membrana corioalantoide, e, especificamente em célula trofoblástica gigante binucleada. Sendo assim, os resultados mostram que a proteína CAV-1 teve uma maior expressão em relação a proteína CAV-2 e que as proteínas CAV-1 e -2 são parte da composição das cavéolas, sendo .
Abstract: The transgenic application of green fluorecent protein (GFP) as fetal cell marker on cattle cloned placenta could provide an exclusive model for studying the morphologic and immunologic maternal-fetal interactions, providing information about its mapping, distinguishing the fetal from maternal cells. This model will have direct application, mainly because these are animals that present problems during its development. With this model's support, we intend to verify the substances transport between mother and fetus during endocytocis, through the immunolocalization of protein named caveolae. For these, we used 06 cloned bovine and 30 cattle samples of artificial insemination (AI) with 90 days of pregnancy, which had been their development interrupted by humanitarian slaughter of the recipient and recovery of the pregnant uterus. We collected the placentome and the chorion. A part of the samples will be cutted and fixed, by immersion, on a solution containing 4% of parafomaldehyde or 10% of formaldehyde on a sodium phosphate buffer (PBS) at 0,1M pH 7.4, Zamboni solution (4% of paraformaldehyde, 15% of picric acid, on sodium phosphate buffer 0,1M pH 7.4), metacarn (60% of metanol, 30% of chloroform, and 10% glacial acetic acid), for morphologic and immunohistochemistry verification for caveolinas proteins -1 and -2 ( -1 CAV and CAV- 2). The caveolinas -1 were found in fetal and maternal villi , but its strongest staining was observed in the endometrial stroma . The caveolinas -2 had positive staining in trophoblast and chorioallantoic membrane , and specifically in giant trophoblastic binucleated cell . therefore the results were compared between cloned cattle and from AI or natural mating, for assisting on detection of the reason of many placental alterations, embryonic losses, spontaneous abortion, post-natal mortality and large offspring syndrome on laboratory-manipulated animals. The result suggests that the proteins caveolins -1 and ...
Mestre
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Evseenko, Denis. "Regulation and functional significance of ATP binding cassette transporters in human placenta." Thesis, University of Auckland, 2008. http://hdl.handle.net/2292/2348.
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The aim of this project was to study ATP binding cassette (ABC) transporters in the human placenta, in particular their regulation and role in trophoblast differentiation and survival. The presence and localisation of four major placental drug transporters, multidrug resistance gene product 1 and 3 (MDR1 and 3)/ABC subfamily B members 1 and 4 (ABCB1 and 4), multidrug resistance associated proteins 1 and 2 (MRP1 and 2)/ABCC1 and 2 and breast cancer resistance protein (BCRP)/ABCG2 was initially studied in term human placenta, cultured primary trophoblast and BeWo and Jar trophoblast-like cell lines. Jar cells were found to be more similar to nondifferentiated cytotrophoblast with respect to their ABC protein expression profile, whereas BeWo cells more closely reflected differentiated syncytiotrophoblast. Treatment of primary term trophoblasts in vitro with cytokines (TNF- or IL-1) decreased expression and activity of apical transporters ABCB1/MDR1 and ABCG2/BCRP. Growth factors, on the other hand, increased BCRP expression and activity, while estradiol stimulated BCRP, MDR1 and MDR3 expression MDR1/3 functional activity. The ability of BCRP/ABCG2 to abrogate the apoptotic effects of TNF- and ceramides was studied in primary trophoblast and BeWo cells using pharmacological and molecular (siRNA) approaches. The results suggest that BCRP/ABCG2 contributes to the resistance of trophoblast cells to cytokine-induced (extrinsic) apoptosis, whereas its effects on apoptosis activated via the intrinsic mitochondrial pathway is minimal. This altered resistance was associated with increased intracellular accumulation of ceramides and reduced ability to maintain phosphatidylserine in the inner leaflet of the plasma membrane. A role for BCRP/ABCG2 in cell protection from differentiation-induced stressors was also demonstrated during the process of cell fusion associated with transient loss of plasma membrane lipid asymmetry. Finally, expression of BCRP/ABCG2 (and 9 other genes) was studied in 50 placentas from normal pregnancy and pregnancies complicated with fetal growth restriction (FGR). A marked reduction of BCRP/ABCG2 and MDR1/ABCB1 expression was observed in FGR placentas, while other transporter genes were unaffected. Collectively these data suggest that BCRP/ABCG2 and probably other ABC transporters may play a hitherto unrecognised survival role in the placenta, conferring a “stress resistance” to trophoblast cells.
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Hirst, Chloe. "Placental taurine transport in pre-eclampsia." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/placental-taurine-transport-in-preeclampsia(85a6b6e1-f0be-46f4-bec4-22c03183ff19).html.
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Pre-eclampsia (PE) is a serious disease affecting approximately 5% of pregnancies per annum. The disease etiology is complex but its origin lies in abnormal placental development and function. PE is associated with inflammation, increased nitrative stress and abnormal renewal of syncytiotrophoblast (STB), the transporting epithelium of the placenta. STB is renewed by cytotrophoblasts (CTBs) that proliferate, differentiate and fuse with STB and this is balanced by apoptosis. The amino acid taurine facilitates proliferation, differentiation and apoptosis in non-placental tissues. Taurine is also cytoprotective, protecting cells from damage by inflammatory cytokines. Taurine is transported from maternal blood into STB by the amino acid transporter TauT. In isolated STB membranes, TauT activity is inhibited by agents that nitrate tyrosine residues. This thesis tested the hypothesis that STB TauT activity is down-regulated in PE due to post-translational modification of TauT through tyrosine nitration which lowers intracellular taurine and contributes to altered STB renewal. Placentas were collected from normal pregnancy (NP) and PE (blood pressure >140/90mmHg after 20 weeks gestation in previously normotensive women plus proteinuria >300 mg/L in a 24-hour collection). STB TauT activity, measured as Na+-dependent uptake of 3H-taurine into placental villous fragments, was significantly lower in PE (n=24) compared to NP (n=44). Western blotting of membrane enriched homogenates showed that TauT protein expression (normalised to β-actin) was significantly higher in placentas from PE (n=8) compared to NP (n=9). The presence of nitrotyrosine residues (marker of nitrative stress) in placentas of women with PE and NP was assessed by immunohistochemistry (IHC). The intensity of STB nitrotyrosine staining was greater in PE placentas that had reduced TauT activity (n=8) than in NP (n=7). To determine the effect of nitrative stress on TauT activity and STB renewal, placental villous explants from NP were cultured (7 days; n=6) and treated with SIN-1 (1mM; days 5,6) to induce nitrative stress. STB nitrotyrosine (IHC) and TauT activity (3H-taurine uptake) was determined on day 7 and STB renewal was assessed by IHC for apoptosis (M30), proliferation (dual staining for Ki67 and the CTB marker E-cadherin) and STB integrity (cytokeratin 7). SIN-1 increased STB nitrotyrosine staining intensity compared to controls, confirming induction of nitrative stress. SIN-1 reduced STB TauT activity, increased apoptosis, reduced CTB proliferation and altered STB regeneration compared to control. To determine the effect of reducing intracellular taurine on STB renewal, villous explants were cultured for 7 days with 2.5mM β-alanine to competitively inhibit taurine uptake (n=6). At day 7, intracellular taurine, measured as the steady-state accumulation of 3H-taurine, was 15% of normal. STB turnover was assessed at day 7 as described above. β-alanine significantly increased apoptosis and altered STB regeneration compared to controls. Following statistical analysis all p <0.05.In conclusion, STB TauT activity was lower, and protein expression higher, in PE compared to NP. STB nitrotyrosine was elevated in PE and nitrative stress inhibited STB TauT activity and disrupted STB renewal in vitro. Reducing intracellular taurine also disrupted STB renewal in vitro. Overall the data support the hypothesis that post-translational modification of TauT by nitration inhibits TauT activity in PE. This reduces intracellular taurine which contributes to abnormal renewal of STB. Further work is needed (a) to confirm that TauT is nitrated in PE and that reduced STB TauT activity lowers intracellular taurine and reduces taurine delivery to the fetus and (b) to determine the mechanism/s by which taurine regulates CTB apoptosis and facilitates renewal of STB.
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Taylor, Louise. "Comparative analyses of ABC transporters and metabolising enzymes in human and rat placental models." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/comparative-analyses-of-abc-transporters-and-metabolising-enzymes-in-human-and-rat-placental-models(3daff296-0364-4e4b-89f8-337dac6dbf10).html.
Full textAbstract:
The placenta provides a protective barrier for the developing foetus during gestation. Physiological barriers including the placenta, liver, kidney, intestine and blood-brain barrier are known to express ATP-Binding cassette transporters (ABC transporters) and metabolising enzymes. These specialised proteins have the ability to transport or metabolise xenobiotics. There is evidence to suggest that ABC transporters and metabolising enzymes are located at the interface between the maternal and foetal blood supplies (a cell layer referred to as the syncytiotrophoblast) and therefore may help protect the foetus from harmful xenobiotics. During new compound development prenatal developmental toxicity testing forms an important part of safety assessment. In order to predict potential toxicity of a new chemical entity to humans, rodent and non-rodent species are currently used. This thesis investigates the rat and human placental barrier properties in order to help facilitate our knowledge of species differences and contribute to our understanding of the limitations of these surrogate models. The approaches taken include: genomic analyses using microarray data to compare the overall expression of ABC transporters and metabolising enzymes throughout gestation in both species, immunohistochemical techniques to localise transporters and metabolising enzymes in the rat placenta, and in vitro functionality assays of selected transporters performed in rat and human placental cell line models. The main findings have shown a similar mRNA expression level of ABCG2/BCRP (breast cancer resistance protein) throughout gestation in the rat and human, however different mRNA expression levels of other transporters (slco4a1/oatp4a1 in particular) and metabolising enzymes were also highlighted. Immunohistochemistry localised selected transporters to the syncytiotrophoblast region of the rat placenta (the interface of maternal and foetal circulations). Functional in vitro assays were successfully utilised in rat and human placental cell lines which showed functional ABCB1/P-gp in both species. Overall, these findings provide a genomic characterisation of the rat and human protective placental barrier properties and show transporter functionality in in vitro cell-based assays which will prove useful in prenatal and developmental toxicity tests. Alternatives to using animals have been explored by using functional in vitro assays which could potentially be implored during the new compound discovery phase. This could help to make animal testing more selective for given compounds and ensures the new chemical entity is being tested in the model closest resembling the human.
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Wang, Meng. "Enhancement of the Placental Transmission of Lopinavir Using a Transporter Targeted Prodrug Strategy." VCU Scholars Compass, 2015. http://scholarscompass.vcu.edu/etd/3973.
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Lopinavir (LPV) is a potent protease inhibitor specific for HIV-1. However, LPV has poor placental penetration due to substrate activity for efflux transporter by P-glycoprotein (P-gp). Since fatty acid transporters are highly expressed in the placenta during pregnancy, we designed fatty acid ester prodrug of lopinavir as substrates of fatty acid transporter in order to improve their uptake into placenta. Seven dicarboxylic acid esters of lopinavir have been made in our lab. The structures were characterized by 1H-NMR, 13C-NMR, LC-MS/MS, HRMS, IR and melting points. After making the prodrugs, an LC-MS/MS method with high specificity and sensitivity, as well as simultaneous quantitative analyses of lopinavir and SLPV, GLPV and DLPV in the BeWo cells methanol extraction was established and validated. The uptake of prodrugs (SLPV, GLPV and DLPV) in the BeWo cells was then determined. GLPV has the highest uptake followed by SLPV and then DLPV. The results suggest that the carbon length of the promoiety may have a positive relationship with the uptake. Ideal prodrugs should be stable before they reach placenta and can be hydrolyzed in the placenta and/or in fetal plasma. We did a series of stability and hydrolysis studies in human tissue fractions. The results showed that GLPV and SLPV were very stable in HIC, HLC and human adult plasma. DLPV was stable in HIC, HLC, but can be hydrolyzed in human adult plasma. GLPV and SLPV cannot be hydrolyzed in either human placenta or fetal plasma, while DLPV can be hydrolyzed in both human placenta and fetal plasma. Anti-HIV activities study of prodrugs was also conducted. The results showed that the EC50 of three prodrugs (GLPV, SLPV and DLPV) are 0.86 μM, 0.84 μM and 0.05 μM, which are much lower than 50 μM (The active drug criteria for this assay). It suggests that prodrugs have apparently anti-HIV activity. DLPV has comparable apparent anti-HIV activity to LPV (<0.02 μM). After incubation with CEM-SS cells for 6 days, almost half of DLPV was hydrolyzed into LPV. Therefore, the high anti-HIV potent of DLPV may be due to the anti-HIV activity of generated LPV.
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Jobarteh, Modou Lamin. "The effect of prenatal nutritional intervention on placental nutrient transporter expression and feto-placental outcome in rural Gambian women." Thesis, University of Aberdeen, 2015. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=225784.
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Iron and zinc deficiency during pregnancy is common among women in low-income nations. In such settings, prenatal nutritional intervention is encouraged to improve pregnancy outcome. The impact of the intervention on transporter proteins involved in fetal nutrient supply is unexplored. This study investigated gene expression of some transporter proteins involved in fetal nutrient supply in the placenta. In a trial in rural Gambia, pregnant women at <20weeks of gestation were randomised to 4 nutritional intervention arms: i) Iron and folic acid (FeFol), representing the usual care ii) Multiple micronutrients (MMN) iii) Protein energy (PE) iv) MMN and PE (PE+MMN). All the intervention arms contained 60mg iron and 400μg of folic acid. FeFol and MMN interventions were given in tablet format, whereas PE and PE+MMN were in food format (lipid-based nutrient supplement- LNS). Maternal blood samples collected at booking, 20 and 30 weeks of gestation were assessed for iron levels, and zinc levels measured only the later samples. Gene expression of proteins involved in fetal iron, zinc, amino acid and glucose transport were measured on placental samples collected at birth. LNS (PE and PE+MMN) intervention was associated with low maternal iron status in late pregnancy and increased placental mRNA expression of the primary iron-uptake protein, transferrin receptor 1(TfR1). Intervention arms with no supplementary zinc (FeFol and PE) had lower maternal plasma zinc levels and increased placental mRNA expression of intracellular zinc-uptake proteins, ZIP1, ZIP4 and ZIP8. Different nutritional intervention strategies are associated with changes in maternal iron and zinc status during pregnancy and corresponding changes in the gene expression of placental iron and zinc uptake proteins. This might suggest differential fetal intrauterine response to the interventions. Understanding the role of the placenta in the delivery of nutrients to the fetus is important when considering intervention strategies.
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Sivaprasadarao, A. "Studies on the transport and uptake of vitamin A by placenta." Thesis, University of Leeds, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384722.
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Vasilopoulou, Elisavet. "The role of thyroid hormones in placental development and the importance of the thyroid hormone transporter MCT8." Thesis, University of Birmingham, 2010. http://etheses.bham.ac.uk//id/eprint/1146/.
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Thyroid hormones (THs) are important for fetoplacental development. Human intrauterine growth restriction (IUGR) is associated with malplacentation and reduced fetal circulating concentration of THs. The expression of the plasma membrane TH transporters MCT8, MCT10, LAT1, LAT2, OATP1A2 and OATP4A1 was characterised in human placental biopsies across gestation. The protein expression of MCT8 was increased in samples from severe IUGR compared with normal pregnancies. In vitro, triiodothyronine (T\(_3\)) decreased survival and increased apoptosis of IUGR compared with normal cytotrophoblasts, which was associated with increased MCT8 expression. In normal cytotrophoblasts, MCT8 upregulation decreased survival, whilst MCT8 silencing increased survival independently of T\(_3\). In the extravillous trophoblast-like cell line, SGHPL-4, T\(_3\) resulted in a significant increase in cell invasion when MCT8 was upregulated. Contrary to cytotrophoblasts, silencing MCT8 decreased apoptosis in SGHPL-4s independently of T\(_3\). In mice, fetal to placental weight ratio was decreased in male MCT8-null compared with wild-type embryos. These findings support the hypothesis that THs have an important role in fetoplacental development and that IUGR is associated with changes in TH transport and responsiveness of the placenta. Furthermore, they highlight the importance of MCT8, which impacts on placental cells via both T\(_3\)- dependent and independent mechanisms.
Books on the topic "Placenta; transporter; transportér"
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1932-, Battaglia Frederick C., Nestlé Nutrition Services, and Nestlé Nutrition Workshop (39th : 1996 : East Sussex, England), eds. Placental function & fetal nutrition. [Vevey, Switzerland]: Nestlé Nutrition Services, 1997.
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H, Schneider, Bischof P, and Leiser Rudolf 1941-, eds. Fetal growth and the placenta: From implantation to delivery. Rochester, NY: University of Rochester Press, 1993.
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(Editor), Paul Bischoff, Henning Schneider (Editor), and Rudolf Leiser (Editor), eds. Fetal Growth and the Placenta-From Implantation to Delivery: From Implantation to Delivery (Trophoblast Research, Vol 7). Univ of Rochester Pr, 1993.
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Moléculas que participan en el transporte de hierro materno-fetal : importancia del receptor 1 de transferrina y de la ferroportina en la placenta humana. Editorial Académica Española, 2012.
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Allegaert, Karel, and Kristel Van Calsteren. Maternal, fetal, and neonatal pharmacokinetics. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198713333.003.0005.
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Most drugs are not thoroughly evaluated for use during pregnancy, delivery, or postpartum (e.g. breastfeeding). The same holds true for early infancy, and results in extensive off-label, unlicensed pharmacotherapy in these specific subpopulations. At present, most drug labels do not contain any instructions for use during pregnancy, in infancy, or during breastfeeding, yet these are the main concerns of healthcare providers considering medical treatment. Anaesthetists commonly treat pregnant women with similar dosing regimens recommended for use in adults and subsequently titrate to effect. The (dis)continuation of breastfeeding in the postpartum period following anaesthesia is commonly based on opinions instead of scientific evidence. This chapter describes the alterations in pharmacokinetics (absorption, distribution, metabolism, elimination) in pregnant women with specific emphasis on placental drug transport, and in neonates, with additional emphasis on breastfeeding. Drugs commonly administered by anaesthetists to women in the peripartum period are discussed with particular reference to the changed pharmacodynamics in both mother and infant.
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Malyszko, Jolanta, and Iain C. Macdougall. Iron metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0125.
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While whole-body (‘absolute’) iron deficiency is common and probably increased in frequency in chronic kidney disease (CKD), functional iron deficiency is a particular problem in CKD. Absolute iron deficiency is likely to be present in advanced CKD when the ferritin falls below 100 ng/mL and the TSAT falls below 20%. Functional iron deficiency is characterized by the presence of adequate iron stores (as defined by conventional criteria), but with an inability to mobilize this iron rapidly enough to adequately support erythropoiesis with the administration of erythropoietin. Among such patients, the serum ferritin level is either normal or elevated (usually between 100 and 800 ng/mL), with a TSAT typically ≤20%. Hepcidin, a novel peptide discovered at the turn of the twenty-first century, is an iron gatekeeper that plays a key role in functional iron deficiency, and the ‘anaemia of chronic disease’. The main function of hepcidin is homeostatic regulation of iron metabolism and mediation of host defence and inflammation. Hepcidin is the predominant negative regulator of iron absorption in the small intestine, iron transport across the placenta, and iron release from the macrophages. Novel strategies that modulate hepcidin and its target ferroportin for the treatment of anaemia of chronic diseases are currently undergoing extensive research.
Book chapters on the topic "Placenta; transporter; transportér"
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Mason, Clifford W., and Carl P. Weiner. "Placental Drug Transport." In The Placenta, 310–17. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444393927.ch40.
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Mao, Qingcheng, Vadivel Ganapathy, and Jashvant D. Unadkat. "Drug Transport in the Placenta." In Drug Transporters, 341–53. Hoboken, NJ: John Wiley & Sons, Inc., 2014. http://dx.doi.org/10.1002/9781118705308.ch17.
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Dubé, Evemie, Guillaume Desparois, and Julie Lafond. "Placental Lipid Transport." In Preeclampsia, 305–16. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7498-6_24.
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Bendon, Robert W. "Amnion Transport: Histologic Features." In Pathology of the Placenta, 277–80. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-97214-5_40.
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Dicke, Jeffrey M. "Placental transport and metabolism." In Clinical Maternal-Fetal Medicine Online, 72.1–72.6. 2nd ed. London: CRC Press, 2021. http://dx.doi.org/10.1201/9781003222590-63.
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Cetin, Irene, and Chiara Mandò. "Stable Isotope Methodologies for the Study of Transport and Metabolism In Vivo." In The Placenta, 207–12. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444393927.ch27.
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Xia, Qinglan, Carolyn Salafia, and Simon Morgan. "Optimal Transport and Placental Function." In Springer Proceedings in Mathematics & Statistics, 509–15. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-12307-3_73.
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Maguire, D. J., R. Blums, R. Morgan, J. Collie, and G. R. Cannell. "A Placental Perfusion pO2 Logger." In Oxygen Transport to Tissue XIV, 649–52. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3428-0_77.
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Brunette, Michèle G., Sylvie Letendre, and Serge Allard. "Phosphate Transport Through Placenta Brush Border Membrane." In Phosphate and Mineral Homeostasis, 543–48. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5206-8_68.
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Faithfull, N. S., and H. W. Marshall. "The Effect of Fluorocarbon Emulsion on Placental Insufficiency." In Oxygen Transport to Tissue XI, 357–64. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5643-1_39.
Full textConference papers on the topic "Placenta; transporter; transportér"
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Perazzolo, S., B. Hirschmugl, C. Wadsack, G. Desoye, R. M. Lewis, and B. G. Sengers. "Computational modelling of fatty acid transport in the human placenta." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7320262.
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Lüscher, B., D. Surbek, P. Schneider, and M. Baumann. "Placental uric acid transport system and its impact on fetal development." In 62. Kongress der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe – DGGG'18. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1671120.
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Martin, John T., and Virginia L. Ferguson. "Regional Similarities in the Mechanical Properties of the Human Umbilical Artery." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206800.
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The human umbilical cord (UC) bridges the blood flow gap between baby and mother, protecting the blood supply in a way that allows the fetus freedom to move within the amniotic sac. Once the blood supply has been oxygenated by the maternal blood pool via the placenta, the umbilical vein (UV) provides a transport pathway to the fetus. Two umbilical arteries (UA) return the blood supply to the pool to eliminate CO2 and other metabolic wastes [1]. The walls of the UA’s and UV are made up of an intima composed a single layer of large, elongated endothelial cells [2], and a media composed of randomly distributed smooth muscles cells, collagen, elastin, and ground substance. These vessels are unique in that their adventitia is absent and substituted by Wharton’s jelly, a mucoid connective tissue.
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McCarthy, P., G. Gau, and M. Shearer. "PLASMA AND LIVER LEVELS OF VITAMIN K IN THE NEWBORN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643607.
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Few measurements have been made of vitamin K in neonatal tissues. Using an assay based on HPLC with dual-electrode electrochemical detection we have investigated the vitamin K status of the newborn from analyses of paired cord-maternal plasma samples and liver samples obtained at post-mortem. For vitamin K1 (K1) the median value in cord plasma (16 pg/ml, range 4-45 pg/ml) in 20 babies was some 30 fold lower than that in maternal plasma (median 0.47 ng/ml , range 0.14-2.42 ng/ml). This is the highest maternal-cord gradient of all the fat-soluble vitamins and together with the lack of correlation between cord and maternal values suggests that K1 does not rapidly equilibrate across the placenta. Hepatic neonatal-adult differences in K1 levels were less marked being about 5 fold lower at birth (median 1.2 ng/g, range 0.1-8.8 ng/g, n = 22) than in adults (median 5.4 ng/g, range 1.1-21.3 ng/g, n = 32). No relationship was found between hepatic K1 and gestational age and relatively high levels (1-2 ng/g) were detected at 10-12 weeks gestation. Post mortem livers obtained after intramuscular K1 prophylaxis at birth (0.5-1.0 mg) had K1 levels which were raised dramatically (1000 to 5000 fold after 24-48 h) and which remained raised for at least one week. A preliminary assessment of the contribution of vitamins K1 (menaquinones, MKs) to vitamin K1 status revealed undetectable levels in fetal or neonatal livers until about 14 days post-partum. This was in marked contrast to adults in whom MKs 7-10 accounted for the majority of liver vitamin K (75-97% on a molar basis). In adult plasma MKs were present at much lower levels than K1; the low circulating levels and poor1placental transport would explain our inability to detect MKs in newborn livers. When expressed as total vitamin K (K1 and MKs) we concluded that the newborn may have only about 2% of adult hepatic concentrations; this relative deficit of MKs may be responsible for the high susceptibility of the newborn to vitamin K deficiency.