There are growing evidences suggesting a pivotal role of oxidative stress in the pathophysiology of preeclampsia. We investigated oxidative stress in the rat model of preeclampsia, and in clinical cases. Pregnant female rats were injected intraperitoneally with deoxycorticosterone acetate (DOCA) and given 0.9% saline as drinking water during their pregnancy. We assessed plasma $F_2-isoprostane(8-iso-PGF_{2{\alpha})$ and malondialdehyde (MDA) in a rat model, and the same markers in the plasma of maternal blood and fetal cord blood in pregnant women with preclampsia. Blood samples from the umbilical arteries and veins were collected separately. The concentrations of MDA were increased in the preeclampsia groups of animal and humans, compared with the control group; it was significantly increased in the umbilical artery and vein of the preeclampsia group. The concentrations of $F_2-isoprostane$ were elevated in the preeclampsia groups of animal and humans, compared with the control group, and the increase in $F_2-isoprostane$ concentration was prominent in the umbilical vein than umbilical artery of the preeclampsia group. Therefore, it appears that the placenta has an important role in the pathophysiology of preeclampsia, and the $F_2-isoprostane$ of the umbilical vein may serve as a relatively reliable marker for ischemic/hypoxic injury to the fetus during the perinatal period.
In vitro contractile response of the uterus in the pregnant rat to oxytocin increases with advancing gestation. This increase coincides with an increase in uterine oxytocin receptor number. However, in vitro the change in uterine contractile response of the pregnant uterus to oxytocin with advancing gestation is not clear. The purpose of the present study was to find out that the uterine response in vitro to oxytocin changes as delivery a, pp.oaches. Secondly, to determine if the incubation of uterine tissue in vitro altered the uterine oxytocin receptor number and affinity and thus explain the ambiguity between the in vitro and in vitro results. The studies were performed on rats at days 15, 20 and 21 or pregnancy. In vitro the uterine contractile response to oxytocin was sgreater (P<0.05) at day 21 compared to days 15 and 20 (Emax : 724.8 88.9, 130.0 81.5 and 133.4 53.4, respectively). This correlated with a significant increase (P<0.05) in uterine oxytocin receptor number at day 21 (days 21, 15 and 20 : 540 89, 53 24, 89 35 fmoles/mg protein, respectively). However, the kids at days 15, 20 and 21 did not differ (P>0.05). Finally no difference (P>0.05) in oxytocin receptor number or affinity was detected between incubated and non-incubated tissue. The results of these studies suggest that either pre-oxytocin or post-oxytocin receptor factors are important in determining the uterine myometrial responsiveness to oxytocin.
Insulin-like growth factors (IGFs) and their binding proteins (IGFBPs) are important regulators on the development of maternal tissues during pregnancy. This study was performed to examine the relationship between maternal IGFs/IGFBPs system (i.e: IGF-I, II, their receptors, and IGFBPs) in pre- and post-partum rats. The liver and kidney are important organs for the synthesis of IGFs and IGFBPs in adults. The levels of materanal IGFs and IGFBPs in serum, liver, and kidney were examined at 14 and 21 days of gestation and at 3, 7, 11, and 14 days after birth. The expression of IGFs and their receptors mRNA was also examined in fetal and maternal rat liver, kidney. IGF-I concentrations in maternal serum and liver were decreased during pregnancy. However, IGF-I concentration in maternal kidney was increased, having maximal effect at 14 days of gestation. IGF-I concentrations were decreased in serum, liver, and kidney of postpartum rat, compared to control (p < 0.05). On the other hand, IGF-II concentrations in serum, liver, and kidney were increased during pregnancy (p<0.05) and gradually decreased to control level in postpartum period. The levels of IGFBP-3 and IGFBP-2 are expressed in serum, liver, and kidney. However, IGFBP-3 is mainly expressed in serum and liver, and IGFBP-2 in kidney. The levels of IGFBP-3 and IGFBP-2 in maternal serum were markedly decreased during pregnancy and gradually recovered to control level during postpartum period by western ligand blotting. However, there was no change of IGFBP-3 and IGFBP-2 levels by western immunoblotting. The levels of IGFBP-3 and IGFBP-2 in maternal liver and kidney also showed the same pattern of serum, although the main IGFBP is different. In normal rat serum, IGF-I 150 kDa and 50 kDa carrier proteins were detected. The level of IGF-I 150 kDa carrier proteins in pregnant rat was decreased compared to normal rat, but that of 50 kDa carrier proteins was increased. IGFBP-3 protease activity was identified in pregnant rat serum and maternal placenta, and it was inhibited by EDTA ($Ca^{2+}$ chelating agent) and aprotinin (serine proteinase inhibitor). Taken together, these results suggest that the changes of IGFs and IGFBPs in maternal rats are regulated by liver and kidney IGFs and their receptors mRNA during the pregnancy.
The present study was carried out to investigate morphologic changes in the corpus luteum of the pregnant rat by electron microscope after administration of prostaglandin F2$\alpha$(PGF2$\alpha$). Pregnant rates were treated with PGF2$\alpha$(1,500$\mu\textrm{g}$/rat) and their corpura lutea were observed morphologically. The results obtained in this study were summarized as follows ; 1. The weight of the ovaries and corpura lutea were decreased slightly at 8~24 hours after PGF2$\alpha$ administratin but no significant differences were observed. 2. The number of corpora lutea and luteal cells decreased slightly at 12~48 hours and 18~24 hours after PGF2$\alpha$ tretment but there were no signifciant differences between control and treatment. 3. The weight of uterus and the unmber of embryo decreased slightly at 96 hours and at 18~96 hours after PGF2$\alpha$ administration but no significant differences were obtained. 4. In the electron microscopic observatons, lipid droplets which are electron dense and appear in the cytoplasm moderately increased in number after PGF2$\alpha$ treatment. The lipid droplets were surrounded by mitochodria and appeared in the autophagic vacuoles. 5. Moderated and high electron dense mitochondria which are round or elongated in shape showed pleomorphism from 3 hours after PGF2$\alpha$ treatment. Destruction of tubular of vesicular cristae was observed at 6 hours after the treatment. Dense body and myelin figures in matrix of mitochondria were also appeared. 6. Well-developed smooth endoplasmic reticulum(sER) showed tubular or vesicular cisternae. A number of whorl membranes containing ribosomes, mitochondria and lipid droplets were observed at 1.5 hour after treatment. sER was abundant in luteal cells at 12 hours were treatment. 7. Well-developed Golgi pparatus appeared obviously 6 hours and more prominently at 12 hours. Those Golgi vesicles were remarkably dilated. 8. Generally, a few rough endoplasmic reticulum (rER) were appeared after treatment and cisternae showed slight dilatation. No differences among the treatments were observed. However, slight dilation of cisternae was observed at 1.5 hours after treatment. 9. Ribosomes composed of free and polyribosomes were abundant before treatment but polyribosomes were appeared at 12 to 24 hours after treatment. 10. Intercellular space were slightly extended at 3 hours and markedly extended at 12 hours. Numerous microvillous protrusions were observed at these times. Membranous multivesicular structures and autophagic vacuoles were also appeared in the intercellular space. 11. At 3 hours after the treatment, autophagic vacuoles appeared in the cytoplasm of the cell. They increased in number with time and were observed to transfer to the intercellular space. Lysosomal dense body appeared in the cytoplasm and the inclusion body was also observed in nucleus at 12 to 24 hours after treatment.
Silver nanoparticles (size: $7.9{\pm}0.95$ nm, dosage: 250 mg/kg) were orally administered to pregnant rats. At 4 days after parturition, four pups were randomly selected (one pup from one dam) and silver level in liver, kidney, lung and brain was determined by ICP-MS and electron microscope. As results, silver nanoparticles highly accumulated in the tissues of the pups. Silver level in the treated group was $132.4{\pm}43.9$ ng/g in the kidney (12.3 fold compared to control group), $37.3{\pm}11.3$ ng/g in the liver (7.9 fold), $42.0{\pm}8.6$ ng/g in the lung (5.9 fold), and $31.1{\pm}4.3$ ng/g in the brain (5.4 fold). This result suggested that the possible transfer of silver nanoparticles from pregnant dams to the fetus through mainly placenta.
Pregnant rats were treated at various stages of gestation with prostaglandin analogue, cloprostenol alone or concomitant with HCG to study effects on termination of gestation and plasma estrogen and progesterone. Cloprostenol (90 or 180 mg/kg) was administered alone on 1~3, 4~6, 7~9, 9~11 or 11~13 consecutive days of gestation twice a day and in combination with HCG (50 or 100 IU/day) on days of 1~3 or 7~9 once a day. Rats were autopsied on day 21 of gestation or at 6, 12 or 24 hours after treatment on day 6 or 9, respectively. Cloprostenol was found to be nearly 100% effective in preventing implantation, destroying viable fetuses and causing preimplantation losses, but in early gestation, on days 1-3, there was little effect. And when cloprostenol administered concomitant with HCG, corpora lutea were significantly increased, implantation sites and viable fetuses significantly decreased, and pre-and post-implantation losses significantly increased in most cases. Plasma concentrations of estradiol and progesterone were significantly decreased by administering cloprostenol, and estradiol concentration significantly decreased but progesterone significantly increased by administering of cloprostenol concomitant with HCG. It is suggested that cloprostenol was more effective in terminating pregnancy than a combination of cloprostenol and HCG in the rat.
Komariah, Komariah;Manalu, Wasmen;Kiranadi, Bambang;Winarto, Adi;Handharyani, Ekowati;Roeslan, M. Orliando
Toxicological Research
/
제34권2호
/
pp.173-182
/
2018
Valproic acid (VPA) plays a role in histone modifications that eventually inhibit the activity of histone deacetylase (HDAC), and will affect the expressions of genes Pdx1, Nkx6.1, and Ngn3 during pancreatic organogenesis. This experiment was designed to study the effect of VPA exposure in pregnant rats on the activity of HDAC that controls the expression of genes regulating the development of beta cells in the pancreas to synthesize and secrete insulin. This study used 30 pregnant Sprague-Dawley rats, divided into 4 groups, as follows: (1) a control group of pregnant rats without VPA administration, (2) pregnant rats administered with 250 mg VPA on day 10 of pregnancy, (3) pregnant rats administered with 250 mg VPA on day 13 of pregnancy, and (4) pregnant rats administered with 250 mg VPA on day 16 of pregnancy. Eighty-four newborn rats born to control rats and rats administered with VPA on days 10, 13, and 16 of pregnancy were used to measure serum glucose, insulin, DNA, RNA, and ratio of RNA/DNA concentrations in the pancreas and to observe the microscopical condition of the pancreas at the ages of 4 to 32 weeks postpartum with 4-week intervals. The results showed that at the age of 32 weeks, the offspring of pregnant rats administered with 250 mg VPA on days 10, 13, and 16 of pregnancy had higher serum glucose concentrations and lower serum insulin concentrations, followed by decreased concentrations of RNA, and the ratio of RNA/DNA in the pancreas. Microscopical observations showed that the pancreas of the rats born to pregnant rats administered with VPA during pregnancy had low immunoreaction to insulin. The exposure of pregnant rats to VPA during pregnancy disturbs organogenesis of the pancreas of the embryos that eventually disturb the insulin production in the beta cells indicated by the decreased insulin secretion during postnatal life.
This study was to investigate the effects of maternal diabetes on the lung tissue of the fetal rat using lectin histochemistry and electron microscope technique. Maternal diabetes was induced by intraperitoneal injection of streptozotocin (75 mg/kg the body weight) into pregnant Sprague-Dawley rats on the 7th day of gestation. Fetuses of streptozotocin induced diabetic rats exhibited delayed lung maturation and reduced air space. In lectin histochemistry, the binding of Maclura pomifera (MPA) to fetal lungs from diabetic mothers was reduced, but no significant changes in the bindings of Concanavalin A (Con A), Wheat germ agglutinin (WGA), Ricinus communis I (RCA I) and Griffonia simplicifolia (GSI-$B_4$) were noted. Because the MPA has affinity to terminal N-acetyl-D-galactosamine residues constantly linked O-glycosidically to serine or threonine, the present findings may indicates that maternal diabetes interfere with the processes of O-linked glycosylation in fetal rat lung.
This study was investigated to determine whether nicotine causes the morphological changes and expression of heat shock protein(HSP) 70 in the central nervous system of rat embryo. The pregnant rats were injected s.c. twice daily with 3 mg nicotine per 100g body weight from day 0 to 14 of gestation and embryos were removed on gestation day 15. As morphological changes, retardation of cell proliferaton was observed in the telencephalon of nicotine-treated groups and no changes in the other region were found. Minimal HSP 70 was expressed over chole central nervous system was similar between control and nicotine-treated group, the expression of blood cells in the meinges and chroid plexus was significantly greater in nicotine-treated group than in control.
The present study was undertaken to evaluate the potential adverse effects of 2-BP on pregnant dams and embryo-fetal development after maternal exposure during the gestational days (GD) 6 through 19 in Sprague-Dawley rats. The test chemical was administered subcutaneously to pregnant rats at dose levels of 0, 375, 750 and 1250 mg/kg/day. During the test period, clinical signs, mortality, body weights and food consumption were examined. All dams were subjected to caesarean section on GD 20 and their fetuses were examined for external, visceral and skeletal abnormalities. At above 750 mg/kg, toxic effects including signs of toxicity, suppressed body weight, decreased gravid uterine weight and reduced food intake were observed in pregnant dams. An increase in the fetal deaths, a decrease in the litter size, a reduction in the fetal body weight and an increase in the incidence of fetal morphological alterations were also found. There were no adverse effects on either pregnant dams or embryo-fetal development at a dose level of 375 mg/kg. These results suggest that a 14-day subcutaneous dose of 2-BP is embryolethal and teratogenic at above 750 mg/kg/day in pregnant rats. In the present experimental condition, the no-observed-adverse-effect level of 2-BP is considered to be 375 mg/kg/day for dams and embryo-fetuses, respectively.
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