Serum Of Pregnant Rats Research Articles

Mitochondrial Function and Resistance to Oxidative Stress in the Kidney during Pregnancy.

We demonstrated that the serum of pregnant rats increases viability of kidney epithelial cells and promotes their proliferation. The intensity of oxidative stress in the kidneys was also reduced during pregnancy, but only in rats that were not exposed to acute ischemic kidney injury. This decrease in oxidative stress was not associated with changes in transmembrane mitochondrial potential, the size of mitochondria, time of opening of mitochondrial permeability transition pore (mPTP), mitochondrial respiration rate, antioxidant activity, or nitric oxide level.

Biological impacts of the green synthesized silver nanoparticles on the pregnant albino rats and their fetuses.

With the increasing production and applications of silver nanoparticles (AgNPs), they can be released into the air, water, and soil environments leading to direct exposure to human beings. On this, the current study revealed the physiological, histological, and genotoxic effects of the green biosynthesized AgNPs using two methods; lemon juice or saponin reduction on the maternal and fetal tissues. Twenty-eight pregnant female rats were divided into four groups (seven/group) and orally administrated the corresponding treatment doses once daily from the first to the 19th gestational day. The first group was administered distilled water as a control. The second group was administrated saponin. The third was administrated AgNps. The fourth was administrated saponin-loaded silver nanoparticles (Sn-AgNPs). Compared with the control group, the serum of pregnant rats treated with saponin, AgNPs, and Sn-AgNPs exhibited significant alterations in liver and kidney function parameters. In addition, maternal hepatic and renal tissues showed elevated oxidative stress, with a significant increase in the comet parameters. Histologically, both mothers and fetuses showed changes in the liver and kidney tissues. Green synthesized AgNPs have toxic effects on maternal and fetal tissues. Sn-AgNPs revealed an increase in the transfer, accumulation, and toxicity.

Nigericin Abrogates Maternal and Embryonic Oxidative Stress in the Streptozotocin-Induced Diabetic Pregnant Rats.

Hyperglycemic exposure in diabetic pregnancy can lead to many developmental changes, such as delayed development, fetal malformations, and fetal/embryo death. These detrimental complications are collectively known as diabetic embryopathy or teratogenesis. The current study focuses to discover the therapeutic properties of the nigericin against the STZ-stimulated diabetic embryopathy via alleviation of maternal and embryonic oxidative stress. The male and female rats at a 1:1 ratio were permitted to mate overnight to establish the course of pregnancy. The pregnant rats were distributed into four groups control, diabetic pregnant (via administering 40mg/kg of STZ), and diabetic + 10 and 20mg/kg of nigericin-administered (via oral gavage from days 5 to 12) groups, respectively. The glucose level, urine output, diet intake, and body weight were determined carefully. The embryo and placenta weight and implantation rates were examined, and data were tabulated. The total protein and lipid profiles were assessed using respective kits. The oxidative stress markers and antioxidant enzymes were examined using respective assay kits. The 10 and 20mg/kg of nigericin treatment decreased the glucose level and urine output and improved the diet intake and body weight gain in diabetic pregnant rats. The nigericin also decreased the total protein, cholesterol, triglycerides, and very-low-density lipoprotein (VLDL) and improved the high-density lipoprotein (HDL) in the serum of pregnant rats. The levels of malondialdehyde (MDA), reactive oxygen species (ROS), and protein carbonyls were decreased by the nigericin in both liver and embryos of the pregnant rats. The levels of glutathione (GSH), total thiols, and activities of catalase (CAT), glutathione reductase (GR), superoxide dismutase (SOD), glutathione peroxidase (GPX), and glutathione S-transferase (GST) were improved by the nigericin in the diabetic pregnant rats. Altogether, these results provide evidence that nigericin treatment remarkably attenuates the diabetes-stimulated embryopathy in rats. The nigericin effectively decreased embryo lethality, reduced glucose and dyslipidemia, and relieves oxidative stress via upregulating the antioxidant enzyme activities. Hence, it can be a talented therapeutic agent to treat diabetic pregnancy-associated complications.

Prenatal hypothyroidism diminished exogenous NO-mediated diastolic effects in fetal rat thoracic aorta smooth muscle via increased oxidative stress

Maternal hypothyroidism is an important problem of modern healthcare and is reported to increase the risk of cardiovascular diseases in the offspring later in life. However, it is unclear whether hypothyroidism during pregnancy causes vascular damage in the fetal period. We established the prenatal hypothyroidism rat model and collected the fetuses at the 21th day of gestation (GD21). Thyroid hormone concentrations in maternal and offspring blood serum were assessed by enzyme-linked immunosorbent assay (ELISA). The thoracic aortas of the fetuses were isolated for microvessel functional testing and histochemical stainings. qPCR and Western blot were performed to access mRNA and protein expression. We found that the concentrations of thyroid hormones in the serum of pregnant rats and fetuses were significantly suppressed at GD21. The responses of the fetal thoracic aortas to SNP were significantly attenuated in the PTU group. However, no statistical difference was found between the two groups when treated with either inhibitor (ODQ) or activator (BAY58–2667) of sGC. The production of O2−• in the arterial wall was significantly increased in hypothyroid fetuses. Moreover, the level of NADPH oxidase (NOX) was increased, while superoxide dismutase 2 (SOD2) was down-regulated in the PTU group, ultimately contributing to the increased production of superoxide. Additionally, decreased SNP-mediated vasodilation found in fetal vessels was improved by either NOX inhibitor (Apocynin) or SOD mimic (Tempol). These results indicate that increased oxidative stress is probably the cause of the diminished diastolic effect of exogenous NO in the thoracic artery of prenatal hypothyroidism exposed fetuses.

Study of the effect of fluoxetine on liver enzymes in the blood serum of pregnant albino rats

The current study examined the effect of fluoxetine on liver enzymes in pregnant female rats. 42 rats, including ten males, were used for inoculation only, while the number of females was 32 rats. Female rats were divided into two groups, the control group consisted of 8 rats. The fluoxetine-treated group of 24 females was divided into three groups. The first group included 8 pregnant female rats injected with fluoxetine at a concentration of 20 mg/kg of body weight from day 0 of gestation until day 7 or 18, and the second group also included 8 pregnant females injected with fluoxetine at a concentration of 40 mg/kg. of body weight from day day 0 of gestation until day 7 or 18, and the third group included 8 pregnant females injected with fluoxetine at a concentration of 60 mg/kg of body weight from day 0 of gestation until day 7 or 18, blood samples were collected on the 7 or 18 days From pregnancy from all animal groups to measure the following parameters: ALT, alkaline phosphatase, ALP, and aspartate aminotransferase (AST).

Effects of S-adenosyl methionine and essential phospholipids on serum biochemical parameters in simulated acute liver disease in late pregnancy

AIM: Liver diseases, developing in late pregnancy, remains a very important problem in obstetrics. In present study, the aim was to evaluate the effectiveness of monotherapy by essential phospholipids and by S-adenosyl methionine for simulated acute liver pathology during pregnancy using the biochemical parameters of blood serum.
 STUDY DESIGN AND METHODS: Acute liver injury was simulated in rats from 15th to 18th day of pregnancy using tyloxapol (300 mg / kg daily). As drugs for monotherapy, Essentiale (Sanofi-Aventis, France) and Heptral (Abbott srl, Italy) were used separately and were administered to rats daily from the 16th to the 18th day of pregnancy (50 mg / kg and 35 mg / kg, respectively). On the 19th day of pregnancy, blood serum biochemical parameters were analyzed.
 RESULTS: In the model, the concentrations of triglycerides and cholesterol were sharply increased, which can be caused not only by the inhibitory effect of tyloxapol on the lipoprotein lipase of the lumen of blood vessels, but also by damage to liver cells with the accumulation of lipids in them. The activities of aminotransferases (ALT, AST), glutamate dehydrogenase and lactate dehydrogenase were statistically significantly increased. In healthy pregnant rats, the activity of alkaline phosphatase (ALP) decreased from 15th to 19th day of gestation, but under the treatment by tyloxapol in some cases the increase of ALP activity was observed. After using essential phospholipids in the model of acute liver injury, normal values of ALT and ALP activities were observed, and a significant decrease in triglycerides was revealed, which did not reach the normal values. After using S-adenosyl methionine in this model, the significant changes in blood serum parameters were not observed. By themselves, the drugs change several biochemical parameters in the serum of healthy pregnant rats. Heptral increases urea levels and Essentiale appears to increase AST activity.
 CONCLUSION: The use of essential phospholipids or S-adenosyl methionine as monotherapy in a model of acute liver damage in late pregnancy has demonstrated their low efficiency. It is possible that the combined use of drugs is necessary to increase the effectiveness. The use of S-adenosyl methionine should be carried out under the control of the urea level and glutamate dehydrogenase activity in serum. While using essential phospholipids, it is advisable to control the AST activity.

Transthyretin increases migration and invasion of rat placental trophoblast cells.

Preeclampsia (PE) is a hypertensive disorder of pregnancy. Early diagnosis of PE is currently contingent on regular prenatal physical examinations and may be facilitated by identification of novel diagnostic markers. Transthyretin (TTR), also known as prealbumin, is primarily responsible for maintaining the normal levels of thyroxine and retinol binding protein. The expression of TTR is lower in patients with severe PE as compared with healthy controls. Here, we examined the suitability of TTR as a diagnostic marker in pregnant hypertensive rats. N′‐nitro‐l‐arginine‐methylesterhydrochloride (l‐NAME) was used to generate a rat model of hypertension during pregnancy. Rat placental trophoblast cells were divided into control and TTR groups for in vitro experiments. Systolic blood pressure, diastolic blood pressure, mean blood pressure and urinary protein of hypertensive pregnant rats were higher than those of healthy pregnant rats, but these effects could be reversed by TTR treatment. There were no significant changes in blood pressure and urinary protein in healthy pregnant rats before or after TTR treatment. TTR levels in the serum and placental tissues of pregnant hypertensive rats were significantly reduced compared with those of healthy pregnant rats. Changes in placental and fetal weights in the hypertensive model could also be rescued by TTR treatment. TTR treatment significantly increased the level of matrix metalloproteinase‐2/9 in hypertensive rats. Finally, in vivo and in vitro experiments demonstrated that TTR effectively increased the migration and invasion of rat placental trophoblast cells, as well as matrix metalloproteinase‐2/9 levels in these cells. In conclusion, our data from a rat model suggest that TTR may have potential as a novel marker for PE diagnosis.

Hormonal and Immunological Study in Serum of Pregnant albino rats Treated with Nickel Oxide Nanoparticles

The present study was aimed to elucidate the effect of Nickel oxide nanoparticle (100mg /kg b.wt) on some parameters in pregnant Albino rats which including serum reproductive hormonal level, Leutinlizing Hormone (LH), Follicle stimulating Hormone ( FSH) and Testosterone (Test), and some Immunoglobulin levels (IgA, IgG, IgM) for different period of pregnancy ( 12 and 14 days ). The hormonal results showed significant (P?0.05) increased of treatment groups as compared with control groups. Immunological results showed significant decreases in treated groups as compared with control groups, It could be concluded that increasing concentrations of NIO- NPs and durations of exposure leads to negative effects on the pregnant albino rat.

Long non-coding RNA CRNDE deteriorates intrauterine infection-induced neonatal brain injury

BackgroundThis study aimed to test the hypothesis that long non-coding RNA (lncRNA) colorectal neoplasia differentially expressed (CRNDE) could exacerbate brain injury caused by intrauterine infection in neonatal rats. MethodsIntrauterine infection was induced in pregnant rats by lipopolysaccharide (LPS). After delivery, newborn rats with brain injury caused by intrauterine infection were randomly divided into control, control shRNA, and CRNDE shRNA groups. CRNDE expression in serum and amniotic fluid of pregnant rats and neonatal brain tissues were determined by quantitative real-time PCR (qRT-PCR). Morris water maze (MWM) task was used to test the spatial learning and memory ability. Histological examination and apoptosis detection were performed by hematoxylin and eosin (H&E) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining, respectively. Immunohistochemistry was conducted to evaluate the activation of astrocytes and microglia. ResultsLncRNA CRNDE was highly expressed in serum and amniotic fluid of maternal rats and in brain tissues of offspring rats. Furthermore, shRNA-mediated CRNDE downregulation could rescue the spatial learning and memory ability, improve brain histopathological changes and cell death, and inhibit the activation of astrocytes and microglia caused by LPS. ConclusionCRNDE silencing possessed a cerebral protective effect in neonatal rats with brain injury caused by interauterine infection.

Hormonal and Immunological Study in Serum of Pregnant albino rats Treated with Nickel Oxide Nanoparticles

The present study was aimed to elucidate the effect of Nickel oxide nanoparticle (100mg /kg b.wt) on some parameters in pregnant Albino rats which including serum reproductive hormonal level, Leutinlizing Hormone (LH), Follicle stimulating Hormone ( FSH) and Testosterone (Test), and some Immunoglobulin levels (IgA, IgG, IgM) for different period of pregnancy ( 12 and 14 days). The hormonal results showed significant (P?0.05) increased of treatment groups as compared with control groups. Immunological results showed significant decreases in treated groups as compared with control groups, It could be concluded that increasing concentrations of NIO- NPs and durations of exposure leads to negative effects on the pregnant albino rat.

Neurotrophic factors and inflammatory cytokines in the mother-placenta-fetus system in experimental hyperhomocysteinemia

An essential aspect of metabolic imbalance of L-homocysteine and its accumulation in blood (hyperhomocysteinemia) is its aggravating effect in pregnancy. However, little is known about the effects of maternal increased L-homocysteine levels on brain development of fetuses. In the development of the fetus, accompanied by changes in metabolism in the placenta, an important role belongs to neurotrophic factors and apoptosis. This study investigated the effects of chronic L-methionine administration on some parameters of inflammation and on neurotrophic factor levels in the brain of embryos, as well as in the placenta and serum of pregnant rats. The observed disturbances can be resulted from both a direct impact of L-homocysteine and its metabolites on the fetal CNS, and hyperhomocysteinemia-caused changes in normal state of the placenta.

Ozone Exposure During Implantation Increases Serum Bioactivity in HTR-8/SVneo Trophoblasts.

Implantation is a sensitive window in reproductive development during which disruptions may increase the risk of adverse pregnancy outcomes including intrauterine growth restriction. Ozone exposure during implantation in rats reduces fetal weight near the end of gestation, potentially though impaired trophoblast migration and invasion and altered implantation. The current study characterized changes in ventilation, pulmonary injury, and circulating factors including hormonal, inflammatory, and metabolic markers related to exposure to ozone (0.4-1.2 ppm) for 4-h on gestation days 5 and 6 (window of implantation) in Long-Evans dams. To determine the effects of this exposure on trophoblast function, placental-derived, first trimester, HTR-8/SVneo cells were exposed to serum from air- or ozone (0.8 ppm×4 h)-exposed dams and examined for impacts on metabolic capacity, wound-closure, and invasion. Peri-implantation exposure to ozone induced ventilatory dysfunction and lung vascular leakage in pregnant rats, with little effect on most of the circulating markers measured. However, ozone inhalation induced a significant reduction in several serum cytokines (interferon-γ, interleukin-6, and interleukin-13). Treatment of HTR-8/SVneo trophoblasts with serum from ozone-exposed dams for 16-h downregulated metabolic capacity, wound-closure, and invasion through a Matrigel membrane compared with both air-serum and fetal bovine serum-treated cells. Ozone-serum treated cells increased the release of a critical inhibitor of invasion and angiogenesis (soluble fms-like receptor 1; sFlt1) compared with air-serum treatment. Together, our data suggest that circulating factors in the serum of pregnant rats exposed to ozone during implantation receptivity can hinder critical processes of implantation (eg, invasion and migration) and impair trophoblast metabolic capacity.

Protective effect of sRAGE on fetal development in pregnant rats with gestational diabetes mellitus.

To investigate the protective effect of secretory receptor for advanced glycation endproducts (sRAGE) on the fetal development using rat model of gestational diabetes mellitus (GDM). The model of pregnant rats with intrauterine hyperglycemia was established by intraperitoneal injection of 25mg/kg streptozotocin (STZ). Rats with established GDM were randomly grouped, and the pregnant rats in the experimental group were subsequently injected with recombinant sRAGE protein (5mg/kg, in 0.2mL PBS) at tail vein every 24h, while the rats in control group were injected with the same dosage of albumin solution. Blood glucose, serum levels of advanced glycation endproducts (AGEs), and levels of RAGE protein in brain and heart tissues of pregnant rats were measured at 3, 13, and 19days postconception. At 19days fetuses were delivered by cesarean section, number of fetuses, their weight and placental weights were recorded, and fetal malformations and defects were analyzed visually and pathologically. The expression level of RAGE, NOX2, MCP-1, p65, VCAM-1, and VEGF mRNA in placenta was evaluated by real-time PCR. p65 protein localization was detected by immunohistochemistry in fetal brain and heart tissue sections. We analyzed the correlation between AGEs and RAGE level and the development of fetal rats, and the protective effect of blocking AGEs-RAGE pathway on the fetal development in the rat model of GDM was investigated. (1) The concentration of blood glucose and AGEs in serum of pregnant rats with GDM was significantly higher than in control group (p<0.05), with strong correlation between blood glucose and levels of AGEs (r=0.693, p<0.05). (2) While both the number of fetuses and placental wet weight in pregnant rat model of GDM were similar to control group, pups from GDM group exhibited higher incidence of developmental abnormalities and higher average weight (p<0.05). sRAGE treatment slightly but not significantly reduced the probability of the fetal developmental defects, as compared to GDM group. (3) p65, a part of the NF-kB heterodimeric complex, was localized to cell nuclei in the fetal tissues of pups delivered by GDM rats, while sRAGE treatment partially restored cytoplasmic localization of p65, similarly to control tissues. Increased incidence of fetal developmental defects observed in offsprings of pregnant rats with GDM had significant correlation with the level of AGEs in serum of pregnant rats and expression levels of RAGE protein in tissues. GDM resulted in upregulation of mRNA expression of several pro-inflammatory and ROS-inducing genes in placental tissues of pregnant rats. Elevated blood glucose, serum AGEs levels, and increased gene expression are attenuated by intravenous sRAGE treatment. sRAGE appears to reduce the activity of NF-κB in fetal tissues, thus potentially having a protective effect on fetal development.

Thermal stress conditions endothelial cells and improves cellular function (1084.10)

It is well established that temporary exposure to a stressor, such as heat, can induce the production of proteins that confer cellular protection (heat shock proteins ‐ HSP). Our lab has shown that exercise training (a stressor) in pregnant rats increases production of HSP 27, 60, and 90 in the placenta. The aim of this study is to determine whether heat shock, resulting in the up‐regulation of HSPs, improves endothelial function in human umbilical vascular endothelium (HUVEC) treated with normal pregnant rat serum or serum from rats with placental ischemia induced hypertension (RUPP). HUVECs were heat shocked at 42.5° C for 4hrs followed by 2hr recovery at 37° C. Extracts from shocked cells had 4x HSP 70 (p&lt;0.01) and 3x HSP 27 (p&lt;0.01) protein levels over the control. Shocked cells and 37° C control cells were treated with NP or RUPP serum and function was assessed with angiogenesis and wound healing assays. Tubule length counts in heat treated cells were at three times the level of no shock controls (p &lt;0.01), without any effect from serum. In the wound assay RUPP/heat shocked cells tended toward greater mitogenesis and motility. These benefits may involve endothelin 1, which has been shown to promote HUVEC proliferation and migration and was elevated by 20% (p&lt;0.05) in the media of RUPP/heat shock HUVECS in our study. These results suggest that human endothelial cells may improve function with conditioning by low level stressors. Such conditioning, as would be conferred by exercise, may improve the outcome for women with preeclampsia.Grant Funding Source: Supported by NIH RO1HL114096 and AHA 10SDG2600040

Maternal endotoxin-induced fetal growth restriction in rats: Fetal responses in toll-like receptor

Background: Porphyromonas gingivalis as a major etiology of periodontal disease can produce virulence factor, lipopolysaccharide/LPS, which is expected to play a role in the intrauterine fetal growth. Trophoblast at the maternal-fetal interface actively participates in response to infection through the expression of a family of natural immune receptors, toll-like receptor (TLR). Purpose: the aims of study were to identify endotoxin concentration in maternal blood serum of Porphyromonas gingivalis-infected pregnant rats, to characterize the TLR-4 expression in trophoblast cells, and to determine its effect on fetal growth. Methods: Female rats were infected with live-Porphyromonas gingivalis at concentration of 2 x 10 9 cells/ml into subgingival sulcus area of the maxillary first molar before and/or during pregnancy. They were sacrified on 14 th and 20 th gestational day. Fetuses were evaluated for weight and length. Endotoxin was detected by limulus amebocyte lysate assay in the maternal blood serum. The TLR-4 expression in trophoblast cells was detected by immunohistochemistry. <span style=font-family: Tribune-Bold; font-size:

Specific Binding of Human Chorionic Somatomammotropin in Rat Liver and Mammary Gland

The binding of 125I-labeled hCS was examined in cell membrane fraction obtained from rat liver and mammary gland. The specific binding of 125I-labeled hCS was determined in pregnant rat liver (binding capacity: 1.4 times 10-12 mol/mg protein), nonpregnant liver (0.4 times 10-12) and lactating mammary gland on the 7th post-partum day (0.06 times 10-12). These bindings were displaced from liver or mammary gland by hormones capable of stimulating lactation (i.e., prolactins and human growth hormone). “Lactogenic activity” was investigated in pregnant rat serum by heterologous radioreceptor assay using 125I-labeled hCS and cell membranes of the rat liver. Two peaks of “lactogenic activity” were seen in rat serum throughout pregnancy. The first peak (1321 + 503 ng hCS equivalents/ml) was at mid-pregnancy and the second peak (1232 + 819 ng) was near term. It appears that this activity in serum is mainly due to a placental lactogenic hormone in rats.

Effects of chemical species of selenium on maternal transfer during pregnancy and lactation

Aims This study compares the transfer from mother to fetuses and pups of selenium (Se) in the form of selenite, selenate, and selenomethionine (SeMet) labeled with different homo-elemental isotopes. Main methods To completely substitute endogenous Se with natural abundance with Se enriched with a single stable isotope ( 82Se), female Wistar rats delivered by mother fed 82Se-selenite were fed Se-deficient diet and drinking water containing 82Se-selenite immediately after weaning, and then mated with male Wistar rat at the age of 15–17 weeks. The pregnant rats were divided into two groups. One group was fed Se-deficient diet and drinking water containing 76Se-selenite, 78Se-selenate, and 77Se-SeMet from gestation days 11 to 20. The other group was fed the same diet and drinking water containing the three Se species after delivery for 10 days of lactation. Non-pregnant rats were also fed Se mixture and Se-deficient diet for 10 days. Key finding Tissue and plasma Se concentrations showed significant changes among non-pregnant, pregnant, and lactating rats. The peak corresponding to selenoprotein P (Sel P) in serum of pregnant rats was reduced. The concentration of 77Se originating from SeMet was higher than those of 76Se from selenite and 78Se from selenate in the stomach content of pups. Significance Inorganic Se species are more preferably transformed into Sel P than SeMet, and Sel P is effectively incorporated into placenta during pregnancy. On the other hand, SeMet is a more efficient Se source than inorganic Se species during lactation.

Enhanced Endothelin Synthesis by Endothelial Cells Exposed to Sera From Pregnant Rats With Decreased Uterine Perfusion

The initiating event in preeclampsia is thought be to reduced uteroplacental perfusion. Although we have reported previously that chronic reductions in uterine perfusion pressure (RUPP) in pregnant rats results in hypertension and enhanced endothelin production, the factors linking placental ischemia and endothelial cell activation remain unclear. The purpose of this study was to determine the role of angiotensin II type-1 (AT1) receptor activation on endothelin production induced by serum from pregnant rats exposed to reductions in uterine perfusion. To achieve this goal, human umbilical vein endothelial cells were exposed to sera collected from RUPP rats or normal pregnant rats. Arterial pressure was significantly higher in RUPP rats (135+/-2 mm Hg) than in pregnant rats (106+/-1 mm Hg). Six hours after exposure to RUPP serum (n=17), cell media endothelin concentration was 18.4+/-2.7 pg/mL as compared with 9.22+/-1.3 pg/mL from cells exposed to serum from normal pregnant rats (n=9). Eighteen hours after exposure to RUPP serum (n=7), endothelin concentration was 30.5+/-3.8 pg/mL as compared with 12.8+/-5.3 pg/mL from cells exposed to normal pregnant rat serum (n=6). In contrast, serum from RUPP rats did not increase endothelin production in human umbilical vein endothelial cells pretreated with an AT1 receptor antagonist, losartan (15 micromol/L). Eighteen hours after exposure to RUPP serum and losartan (n=14), endothelin concentration was 21.3+/-2.2 pg/mL as compared with 16.4+/-3.3 pg/mL from cells exposed to normal pregnant rat serum and losartan (n=10). These data indicate that serum from pregnant rats exposed to reductions in uterine perfusion enhances endothelin production by endothelial cells via by AT1 receptor activation.

Effects of oral androstenedione on phospholipid fatty acids, ATP, caspase-3, prostaglandin E 2 and C-reactive protein in serum and livers of pregnant and non-pregnant female rats

Androstenedione, a steroidal dietary supplement taken to enhance athletic performance, could affect serum and liver lipid metabolism, induce liver toxicity or alter inflammatory response depending on dose and duration of exposure. Pregnancy could further exaggerate these effects. To examine this, mature female rats were gavaged with 0, 5, 30 or 60 mg/kg/day androstenedione beginning two weeks prior to mating and continuing through gestation day 19. Non-pregnant female rats were gavaged over the same time frame with 0 or 60 mg/kg/day androstenedione. Serum was collected and livers were removed from dams on gestation day 20 and from non-pregnant rats after 5 weeks of treatment. Androstenedione had no effect on serum total cholesterol, triglycerides or HDL-cholesterol, but significantly decreased C-reactive protein in pregnant rats and prostaglandin E 2 in serum of both pregnant and non-pregnant rats. There were treatment related decreases in liver ATP and, to a lesser degree, caspase-3 and no change in alkaline phosphatase of pregnant female rats. Androstenedione decreased docosahexaenoic acid in both serum and liver phospholipids of pregnant female rats. In conclusion, oral androstenedione did not result in overt hepatotoxicity in pregnant female rats, but produced modest changes in lipid metabolism and may impair regeneration of injured hepatic cells or tissue.

Effect of the herbicide glyphosate on liver lipoperoxidation in pregnant rats and their fetuses

Glyphosate is a post-emergence herbicide that acts on the synthesis of amino acids and other endogenous metabolites in plants. It is commonly used in agriculture, forestry, and nurseries for the control or destruction of herbaceous plants. Metabolic processes during development and pregnancy could be sensitive to changes induced by glyphosate such as lipid peroxidation. The present study has investigated the effects that 1% glyphosate oral exposure has on lipoperoxidation and antioxidant enzyme systems in the maternal serum and liver of pregnant rats and their term fetuses at 21 days of gestation. The results suggest that excessive lipid peroxidation induced with glyphosate ingestion leads to an overload of maternal and fetal antioxidant defense systems.