Lipid and protein peroxidation process and catalase activity in pre-eclamptic placenta

There are some suggestions that free radicals are involved in some dysfunctions observed in preeclampsia. In this study we have examined the antioxidant status of preeclamptic placentas. We have used placentas obtained from normal pregnant women and women with preeclampsia. Lipoperoxidative process was measured by means of Okhawa method. Sedlak method was used to measured the total thiol groups. The catalase activity was measured by means of Pffeifer method. The results show that the catalase activity decreases, the amount of MDA increases and the total amount of thiol groups is smaller in preeclamptic placentas. The level of lipid peroxides in preeclamptic placentas is about 1.8 times higher in comparison with normal placentas. The decreased level of total thiol groups in preeclamptic placentas can be caused by a more intensive process of protein peroxidation. Catalase is less active in preeclamptic placentas. It can be due to lower activity of antioxidant systems or the destruction of antioxidant systems by reactive oxygen species. The results of our experiments confirm lower antioxidant status in preeclamptic placentas and suggest that peroxidative reaction may cause many dysfunctions associated with preeclampsia.     

PAF levels and PAF-AH activities in placentas from normal and preeclamptic pregnancies

OBJECTIVE: The aim of this study was to determine: (1) platelet-activating factor (PAF) levels and PAF-acetylhydrolase (PAF-AH) activities in normal and preeclamptic placentas; (2) lipid peroxide production by placental tissues stimulated with PAF. METHODS: Placentas were obtained immediately after delivery from normal and preeclamptic pregnancies. Tissue pieces were snap frozen in liquid nitrogen and stored at -70 degrees C. One gram of tissue from each placenta was used for PAF extraction and for total RNA isolation. PAF was measured by PAF [3H] scintillation proximity assay (SPA) system. Trophoblast PAF-AH activity was determined by enzyme-linked immunosorbent assay (ELISA). mRNA expression for PAF receptor was assessed by RNase protection assay (RPA). Normal placental explants were incubated with PAF at concentrations of 1 and 10 microg/ml for 48 h. Lipid peroxide productions of 8-isoprostane and malondialdehyde (MDA) were measured by ELISA and thiobarbituric acid reaction, respectively. Data were presented as mean+/-SE and analyzed by nonparametric Mann-Whitney U test and ANOVA. A p level less than 0.05 was considered statistically significant. RESULTS: (1) The mean tissue level for PAF was elevated, but not statistically different, in preeclamptic (n=7) than in normal (n=8) placentas, 6.45+/-1.05 versus 4.47+/-0.60 ng/g, p=0.42. (2) PAF-AH activity was higher in trophoblasts from preeclamptic (n=7) placentas than that in trophoblasts from normal (n=8) placentas, 0.69+/-0.16 versus 0.38+/-0.03 micromol/min/microg protein, p<0.05. (3) The relative mRNA expression for PAF receptor was not different between normal (0.70+/-0.08) and preeclamptic (0.76+/-0.13) placental tissues, p=0.60. (4) Productions of 8-isoprostane and MDA were not increased in tissues with PAF in culture, 8-isoprostane: 0.37+/-0.09 ng/mg (control) versus 0.32+/-0.09 ng/mg (1 microg/ml) and 0.37+/-0.07 ng/mg (10 microg/ml), p>0.5; MDA: 0.62+/-0.05 nmol/mg (control) versus 0.68+/-0.04 nmol/mg (1 microg/ml) and 0.69+/-0.03 nmol/mg (10 microg/ml), p>0.5. CONCLUSIONS: Increased PAF-AH activity in trophoblasts may be a compensatory effect to control PAF level in the preeclamptic placenta. The co-existence of PAF-AH and PAF receptor in trophoblasts suggests an autocrine regulation of PAF in these cells to limit PAF and its metabolites within the placenta.     

Role of lipid peroxidation and enzymatic antioxidants in pregnancy-induced hypertension

AIMS AND OBJECTIVES: Preeclampsia remains a major cause of maternal mortality and morbidity. It is a leading indication for iatrogenic premature delivery. Oxidative stress is considered to be one of the factors in the disease process. The present study is centered on the concept that elevated levels of lipid peroxidation (malondialdehyde) due to a decline in the efficacy of antioxidant defenses may predispose an individual to preeclampsia. MATERIAL AND METHODS: In the present study we measured lipid peroxidation products (MDA) and the counteracting enzymatic antioxidants. The study comprises 25 healthy non-pregnant women as controls, 25 third trimester normal pregnant women and 25 preeclamptic patients of the same trimester. Estimation of lipid peroxidation by thiobarbituric acid (TBARS) and enzymatic antioxidants were carried out by standard methods. RESULTS: In the preeclamptic group malondialdehyde, a product of lipid peroxidation, was significantly increased while enzymatic antioxidants like superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase were reduced significantly as compared to normal pregnant and non-pregnant controls. CONCLUSION: Increased levels of lipid peroxides and reduced antioxidant activities clearly demonstrate the presence of oxidative stress in preeclampsia.     

Potential atherogenic roles of lipids, lipoprotein(a) and lipid peroxidation in preeclampsia.

AIMS: To evaluate changes in lipid profile, serum levels of malondialdehyde (MDA) and lipoprotein(a) (Lp(a)) and placental MDA in preeclamptic women, and to evaluate the atherogenic role of these changes in the pathophysiology of pre-eclampsia. METHOD: A cross-sectional study was performed in 20 normal pregnant women, 25 women with mild preeclampsia and 28 women with severe preeclampsia in the third trimester. MDA, which is the endproduct of lipid peroxidation, was measured in placental tissue by the thiobarbituric acid (TBA) method of Ohkawa and colleagues and in serum by the TBA method of Asakawa and Matsushita. Serum lipid levels were measured by with an autoanalyzer, serum apolipoprotein (Apo) A-I and Apo B were measured by nephelometric assay and serum Lp(a) level using a nephelometric agglutination assay method. In preeclamptic and normal pregnant women, multiple comparisons between groups were performed by one-way analysis of variance supplemented with Tukey's HSD post hoc test. The association between placental and serum concentrations among groups was analyzed using the Pearson correlation test. RESULTS: Serum levels of MDA, Lp(a), total cholesterol, triglycerides (TG), low-density lipoprotein cholesterol (LDL-C) and placental MDA were significantly higher, and high-density lipoprotein cholesterol (HDL-C) and Apo A-I levels were significantly lower, in severely preeclamptic and mildly preeclamptic women than in the normal pregnant women, but no difference was observed in Apo B among groups. Serum level of Lp(a) was positively correlated with body mass index in severely preeclamptic women (r=0.489, p=0.008). A significant positive correlation was also found between serum level of MDA and systolic blood pressure in women with severe preeclampsia (r=0.375, p=0.049). CONCLUSIONS: Our findings suggest that high Lp(a), lipid peroxidation, LDL-C and TG, and low HDL-C and Apo A-I levels, are important risk factors for atherosclerosis among preeclamptic women.     

Assessment of lipid peroxidation intensification in normal and preeclamptic placentas

OBJECTIVE: Free radical induced lipid peroxidation (LP) in the placenta has been suggested as a possible pathogenetic factor of preeclampsia (PE). DESIGN: The aim of the study was to assess LP intensification by the measurement of lipid peroxidation products (LPP) content in placentas from normal and preeclamptic pregnancies. MATERIALS AND METHODS: The investigations comprised placentas obtained immediately after delivery from 24 normal pregnancies [group K], 26 pregnancies complicated by severe PE without intrauterine growth restriction (IUGR) [group PE] and 23 pregnancies complicated by severe PE and IUGR [group PEI]. LPP content was measured by the quantitative determination of thiobarbituric acid reactive substances (TBA-RS) amounts in studied placentas. Used TBA test was calibrated with malondialdehyde (MDA) and results were expressed as MDA equivalent in nmol/mg protein. Comparative analysis was performed using U Mann-Whitney and median tests. RESULTS: Mean placental level of LPP (MLPP) in the group PE-2.45 +/- 0.39 (M +/- SD) was significantly higher (p < 0.001) as compared to MLPP in the group K (1.58 +/- 0.24). MLPP in the PEI group (2.81 +/- 0.65) was higher (p < 0.001) than MLPP in the group K as well as MLPP in the group PE but statistical significance of the latter difference was lower (p = 0.032). CONCLUSIONS: The intensification of LP in placentas from pregnancies complicated by severe PE is IUGR dependent and higher than in placentas from normal pregnancies. Obtained results may indicate that higher degree of LP intensification in preeclamptic placentas may be involved in PE pathogenesis.     

Lipid peroxidation, antioxidant defense, status of trace metals and leptin levels in preeclampsia

OBJECTIVE: To investigate the changes in enzyme activities of erythrocyte superoxide dismutase (SOD), catalase, and placental glutathione peroxidase (GSH-Px), and analyze the levels of serum malondialdehyde (MDA), copper (Cu), zinc (Zn), selenium (Se), leptin and placental MDA and glutathione (GSH). STUDY DESIGN: Cross-sectional prospective study consisting of 32 preeclamptic (PE) pregnant, 25 non-pregnant (NP) women, 28 healthy pregnant (HP) women. Levels of lipid peroxides in serum and placenta, and activities of SOD, catalase in erythrocyte and placental GSH level, placental GSH-Px activity were measured by spectrophotometric methods. Serum levels of Cu, Zn, Se measured by atomic absorption spectrophotometry. Serum levels of leptin was measured by enzyme immunoassay by using the Cayman chemical kit. One-way analysis of variance and post hoc Tukey-HSD test and Pearson correlation test were used for the statistical analyses. RESULTS: Serum levels of MDA, Cu, Leptin were markedly higher (P < 0.001); and serum level of Se was markedly lower (P < 0.001) in PE women compared with HP women and NP women. Also, placental MDA level was higher (P < 0.001) and placental GSH-Px activity was lower in PE women compared with HP women. In preeclamptic women erythrocyte catalase activity was markedly increased (P < 0.001), while erythrocyte SOD activity was markedly decreased (P < 0.001) compared to HP women and NP women. Placental GSH level was decreased compared to HP women (P < 0.001). Serum level of Zn was markedly decreased compared to NP women (P < 0.001) but no significant difference was observed in PE pregnant when compared with HP women (P > 0.05). Placental MDA level in PE women had significant negative correlation with serum Se level (r = -0.353, P < 0.05). A negative correlation was found between erythrocyte catalase activity with birth weight (r = -0.528, P < 0.001). Also, there were a significant negative correlation between serum levels of Cu and Se in the preeclamptic women (r = -0.407, P < 0.05). CONCLUSION: Our data demonstrate that elevation of lipid peroxides together with impaired antioxidant defense mechanisms and status of trace metals and the presence of possible interrelationship and crosstalk between those parameters may be related at least partly to the pathogenesis of preeclampsia. Additionally, lipid peroxides and blood oxidative imbalance could be part of the cytotoxic mechanisms leading to endothelial cell injury.     

Lipid peroxidation in pregnancy with preeclampsia and diabetes

We studied lipid peroxidation and vitamin E levels in 12 diabetic preeclamptic, 13 nondiabetic preeclamptic, 8 gestational diabetic, 25 normotensive pregnant women, and 25 healthy nonpregnant women. A significant increase in malonaldehyde (MDA) levels was observed in preeclamptic and diabetic preeclamptic women as compared to normotensive pregnant and healthy controls (p<0.001). An increase in MDA levels was observed in gestational diabetics, but the difference was not statistically significant. Likewise, a significant fall in vitamin E levels was noted in preeclamptic and diabetic preeclamptic groups as compared to controls (p<0.001). Gestational diabetics had a slight decrease in vitamin E levels relative to controls. These findings suggest that lipid peroxidation plays a role in the pathogenesis of preeclampsia.     

脂代谢相关基因ADRP和LPL在子痫前期胎盘组织表达的改变

目的:研究子痫前期患者胎盘组织中脂代谢相关基因的表达,探讨子痫前期脂肪代谢紊乱的可能原因。方法:利用基因芯片检查4例子痫前期胎盘与4例正常胎盘之间的差异表达基因;采用半定量RT-PCR方法验证子痫前期胎盘组织(研究组)和正常孕妇胎盘组织(对照组)脂代谢相关基因脂肪分化相关蛋白(ADRP)基因和脂蛋白脂酶(LPL)基因mRNA的表达改变。结果:在4轮杂交过程中,共筛选出22条有差异表达的基因,其中表达增高的基因有脂肪分化相关蛋白基因(NM-001122)等13条;表达降低的基因有脂蛋白脂酶基因(NMM-000237)等9条。研究组ADRPmRNA相对表达水平为1·98±0·50,显著高于对照组的1·09±0·20(P<0·01);研究组LPLmRNA相对表达水平为0208±0·067,显著低于对照组的0·524±0·139(P<0·05)。结论:脂代谢相关基因ADRP和LPL在子痫前期胎盘组织的异常表达可能是导致子痫前期发病的原因之一。     

Maternal circulating nitrite levels are decreased in both normal normotensive pregnancies and pregnancies with preeclampsia.

OBJECTIVE: To evaluate whether maternal nitric oxide synthesis in pregnancies with preeclampsia is different from that in normal normotensive pregnancies. MATERIALS: Maternal circulating combined nitrate and nitrite levels or nitrite level were compared between 10 normotensive nonpregnant women, 30 normotensive pregnant women (10 first-trimester, 10 second-trimester, and 10 third-trimester pregnancies), 20 normotensive postpartum women (10 at 1 week after delivery, and 10 at 4 weeks after delivery), and 13 preeclamptic women (32 to 40 weeks' gestation). End-products of nitric oxide synthesis were measured from maternal venous blood samples using a fluorometric assay. RESULTS: Maternal circulating nitrite levels in nonpregnant women (1.13 +/- 0.22 microM) were significantly higher than those in the first-trimester pregnant women (0.68 +/- 0.13 microM), second-trimester pregnant women (0.65 +/- 0.13 microM), third-trimester pregnant women (0.48 +/- 0.17 microM), first puerperal week women (0.36 +/- 0.16 microM), and fourth puerperal week women (0.67 +/- 0.17 microM), respectively (p < 0.05). Maternal circulating nitrite level was decreased with advancing gestation, still remained low just after delivery, and was increased 4 weeks later. There was no significant difference in maternal circulating nitrite level between preeclamptic women (0.40 +/- 0.17 microM) and third-trimester pregnant women (0.48 +/- 0.17 microM). However, there were no significant differences in maternal circulating combined nitrate and nitrite levels among the groups. CONCLUSION: These results suggest that the maternal nitric oxide synthesis is not changed in normal normotensive pregnancies and pregnancies with preeclampsia. However, plasma nitrite level, which has stronger spasmolytic activity than the activity of the nitrate, was decreased in both normal normotensive pregnancies and pregnancies with preeclampsia.     

DNA adducts level in normal and preeclamptic placentas

OBJECTIVE: An increase in lipid peroxidation intensification in preeclamptic placentas leads to an increased level of lipid peroxidation products and increased reactive oxygen species activity which can be associated with increased activation of chemicals to electrophilic species that bind covalently to DNA and form adducts. DESIGN: The aim of the study was the determination of DNA adducts (A-DNA) in placentas from normal and preeclamptic pregnancies. MATERIALS AND METHODS: The investigations comprised placentas obtained immediately after delivery from 21 normal pregnancies [group K], 24 pregnancies complicated by severe preeclampsia-PE without intrauterine growth restriction (IUGR [group PE] and 21 pregnancies complicated by severe PE and IUGR [group PEI]. DNA adducts were determined using nuclease P1 digestion enhancement version of the 32P-postlabeling method. The results were expressed in numbers of DNA adducts per 10(8) nucleotides. Comparative analysis was performed using ANO-VA and median tests. RESULTS: Mean level of A-DNA (MA-DNA) in the group PE--1.39 +/- 1.21 (M +/- SD) was similar (p = 0.57) to MA-DNA in group K (1.16 +/- 1.03). However MA-DNA in the PEI group (1.93 +/- 1.28) was significantly higher (p = 0.045) than MA-DNA in the group K as well as MA-DNA in the group PE (p = 0.025). MA-DNA level in all studied preeclamptic placentas (groups PE + PEI) was 1.65 +/- 1.26 and was similar (p = 0.152) to revealed in group K. CONCLUSIONS: The level of DNA adducts in placentas from pregnancies complicated by severe preeclampsia and IUGR is higher than in placentas from pregnancies complicated by severe preeclampsia without IUGR and higher than in placentas from normal pregnancies.     

DNA microarrays detect the expression of apoptosis-related genes in preeclamptic placentas

AIMS: To investigate the expression of apoptosis-related genes in preeclamptic placentas and the possible mechanism of the regulation process. METHODS: Complementary DNA microarrays were employed to compare gene expression profiles of five preeclamptic and five normal placentas. RESULTS: Among the 368 genes detected over 35% showed an over 2-fold difference of expression between preeclamptic placentas and normal placentas. Many genes involved in cell cycle or apoptosis were more highly expressed in preeclamptic placentas than in normal placentas. The expression of many immune-activation genes in preeclamptic placentas was also higher than that in normal placentas. Additionally, many cytokine receptor/kinase genes were also induced in preeclamptic placentas. CONCLUSIONS: The change in expression of cell apoptosis-related genes in placentas might be involved in the pathogenesis of preeclampsia, while the activation of the immune system might be one cause of this change.     

Expression of Human Leukocyte Antigen-G during Normal Placentation and in Preeclamptic Pregnancies

Objectives. This study was undertaken to investigate the expression pattern of human leukocyte antigen-G (HLA-G) during normal placentation and determine whether altered expression of HLA-G is associated with severe preeclampsia. Methods. We investigated HLA-G protein levels in first (n = 27), second (n = 7), and third trimester placentas (n = 10) from normal pregnancies, and determined HLA-G levels in term placentas from normal (n = 15) and severe preeclamptic pregnancies (n = 14) using real-time RT-PCR and western blot analysis. Results. In normal placentas, HLA-G protein expression reached a peak level at gestational weeks 6 and 7, then gradually decreased from week 8 to third trimester (p < 0.05). In preeclamptic placentas, both HLA-G mRNA and protein levels were decreased significantly in comparison with normal term placentas (p < 0.05). Conclusion. HLA-G may contribute to placentation during early and mid-term pregnancy, and participate in maintaining gestation during term pregnancy. The reduced level of HLA-G may be associated with pathogenesis of preeclampsia.     

Chronic villitis of unknown etiology and maternal arterial lesions in preeclamptic pregnancies

Placental lesions from 361 singleton full-term pregnancies were studied. These placentas were divided into two major groups: the study group consisting of 146 placentas from mothers with pregnancy-induced hypertension and a normotensive control group, which included 215 placentas from mothers with normal pregnancies. Each group was divided into three subgroups according to the allocation of infant's birthweight in the normal ponderal curve. A statistically significant higher incidence and severity of villous lesions was observed in placentas of mothers with pregnancy-induced hypertension when infants were over the 25th centile of the ponderal curve. Vascular lesions, i.e., absence of physiological changes in spiral arteries of the placental bed, acute atherosis and chronic vasculitis-like lesions were also more frequently observed in the hypertensive group than in controls. These placental lesions have been described in placentas of small for gestational age infants with or without maternal hypertension and in those of preeclamptic women with appropriate for gestational age infants. Since acute atherosis-like lesions have been reported in placentas of pregnant women with systemic lupus erythematosus and in rejected renal transplants, a possible maternal immunological reaction against fetal tissues could be responsible for the pathogenesis of these entities.     

Reduced amount of cytochrome c oxidase subunit I messenger RNA in placentas from pregnancies complicated by preeclampsia

BACKGROUND: Cytochrome c oxidase is a marker enzyme of the mitochondrial inner membrane. A change in the structure and activity of cytochrome c oxidase may alter the electron transport in the inner membrane, leading to insufficient adenosine triphosphate (ATP) production. ATP is essential for maintaining the function of cells. The aim of this study was to compare the expression of cytochrome c oxidase subunit I mRNA in placentas from normal and preeclamptic pregnancies. METHODS: By means of in situ hybridization, frozen sections of placentas from 23 women with preeclampsia and 29 women with uneventful pregnancies were examined. Digoxigenin (DIG)-labeled probes were used to detect the expression of cytochrome c oxidase subunit I mRNA in the placentas. The expression density was assessed by using an image disposal and analysis system. RESULTS: Positive expression of cytochrome c oxidase subunit I mRNA was found in the cytoplasm of villous syncytiotrophoblasts. The mean light density of cytochrome c oxidase subunit I mRNA in placental villi of normal pregnant women was 0.2638, and 0.1763 in women with preeclampsia, a statistically significant difference (P < 0.05). The number density of cytochrome c oxidase subunit I mRNA in placental villi was also significantly reduced in preeclamptic women compared with the control group (P < 0.05). CONCLUSIONS: Our study demonstrates a reduced amount of cytochrome c oxidase subunit I mRNA in preeclamptic placentas compared to control placentas. We hypothesize that a reduced expression may play a role in the pathophysiology of preeclampsia.     

Expression of the proliferation marker Ki-67 and of p53 tumor protein in trophoblastic tissue of preeclamptic, HELLP, and intrauterine growth-restricted pregnancies.

The human placenta owns the biochemical machinery to proliferate throughout gestation. The aim of this study was to investigate the expression of the proliferation marker Ki-67 in trophoblastic tissue of intrauterine growth retarded (IUGR) placentas, preeclamptic, HELLP, and in normal trophoblastic tissue. Slides of paraffin-embedded trophoblastic tissue of patients with IUGR, preeclamptic patients, HELLP patients, and normal term placentas were incubated with monoclonal antibodies against Ki-67 and p53. Staining reaction was performed with the ABC reagent. Intensity of immunohistochemical reaction on the slides was analyzed using a semiquantitative score. Identification of Ki-67-expressing cells was done by immunofluorescence double staining with Ki-67 and cytokeratin antibodies. Expression of Ki-67 and p53 are significantly elevated in cytotrophoblastic cells of placentas with HELLP as investigated by immunohistochemistry and double immunofluorescence. However, preeclamptic cytotrophoblastic tissue on the other hand showed no significantly different expression intensity of Ki-67 compared with normal placental tissue controls and no changes in p53 expression compared with controls. In IUGR cytotrophoblastic cells, we found no statistically significant change in Ki-67 expression but a statistically significant down-regulation of p53. An elevated proliferation of cytotrophoblastic cells seems to be related to HELLP, and this enhanced proliferation seems to be controlled by p53.     

Expression of galectin-1, -3 (gal-1, gal-3) and the Thomsen-Friedenreich (TF) antigen in normal, IUGR, preeclamptic and HELLP placentas

BACKGROUND: Galectin-1 (gal-1) and galectin-3 (gal-3), which are members of the mammalian beta-galactoside-binding proteins, recognise preferentially (Galbeta1-4GlcNAc) sequences of several cell surface oligosaccharides. In addition, gal-1 also binds to the Thomsen-Friedenreich (TF) antigen (Galbeta1-3GalNAc-). MATERIALS AND METHODS: Slides of frozen and paraffin-embedded placental tissue of patients with fetal intrauterine growth retardation (IUGR), preeclampsia, haemolysis, elevated liver enzymes, low platelets (HELLP) and normal term placentas were incubated with monoclonal and polyclonal antibodies against gal-1, gal-3 and TF. Staining reaction was performed with the avidin-biotinylated peroxidase complex (ABC) reagent. The intensity of the immunohistochemical reaction on the slides was analysed using a semi-quantitative score. The identity of galectin-expressing cells was analysed by using a double immunofluorescence method. RESULTS: We demonstrated immunohistochemically that the expression of gal-1 and gal-3 on the extravillous trophoblast (EVT) is significantly up-regulated in preeclamptic and HELLP placentas and unchanged compared with normal controls in IUGR placentas. The expression of the TF antigen is significantly up-regulated in IUGR and preeclamptic extravillous trophoblast cells and unchanged in HELLP placentas compared with normal controls. In addition, the expression of gal-1 is significantly up-regulated in the decidual tissue of preeclamptic placentas and in the villous trophoblast tissue of HELLP placentas. CONCLUSION: Our data showed that gal-1, gal-3 and TF were up-regulated on the membrane of EVT in preeclamptic placentas. In addition, the expression of gal-1 is significantly up-regulated in decidual tissue of preeclamptic placentas and villous trophoblast tissue of HELLP placentas. Taking into consideration the results of this study, we speculate that expression of both galectins and TF on the membrane of preeclamptic EVT and up-regulation of gal-1 in preeclamptic decidual cells may at least in part compensate for the apoptotic effects of maternal immune cells.     

Atherogenic profile in preeclampsia

Atherosis is accepted to underlie the pathogenesis of preeclampsia, therefore we aimed to determine malonyldialdehyde (MDA) levels as a marker of lipid peroxidation, and lipoprotein(a) (Lp(a)), apolipoprotein A-1 (Apo A-1) and apolipoprotein B (Apo B) levels as a marker of atherogenic profile in preeclamptic and normal pregnant women. Twenty preeclamptic and 20 gestational-age matched normal pregnant patients were enrolled in the study, mean gestational ages for the preeclamptic and the control group were 33.9+/-1.4 and 35.5+/-0.7 weeks, respectively. Blood was withdrawn from the patients soon after diagnosis, and from the controls at their routine prenatal visits. MDA levels was significantly higher in preeclamptic patients (P=0.0003), but no difference was observed in Apo A-1 and Apo B and Lp(a) levels between the 2 groups. We consider that higher MDA was due to oxidative stress seen in preeclampsia, and similar Apo A-1 and Apo B and Lp(a) levels were due to lack of systemic atherosis.     

Proliferation of villous trophoblast and stroma in normal and pathologic pregnancies (preeclampsia)

Pregnancies, complicated with preeclampsia, present with intrauterine growth retardation of the fetus and small (in size and weight) placentas. The present study aims at establishing the expression of proliferative nuclear antigen Ki-67 in the villous trophoblast and stroma, and to compare the results between study (preeclamptic cases n = 30) and control (normal n = 30) groups. The number of Ki-67 positive nuclei both in the preeclamptic trophoblast and stroma significantly increases those of the controls. Our results show that the defect in the development of the placenta in preeclampsia is not associated with low proliferative potential.