scholarly journals Expression of cytochrome CYP2B1/2 in nonpregnant, pregnant and fetal rats exposed to tobacco smoke.

2000 ◽  
Vol 47 (4) ◽  
pp. 1115-1127 ◽  
Author(s):  
P Czekaj ◽  
A Wiaderkiewicz ◽  
E Florek ◽  
R Wiaderkiewicz
Keyword(s):  
Tobacco Smoke ◽  
Adult Liver ◽  
Pregnant Rats ◽  
Protein Levels ◽  
Pregnant Females ◽  
Fetal Rat ◽  
Fetal Rats ◽  
Brain Microsomes ◽  
Female Wistar Rats ◽  
Fetal Rat Liver

Four-month-old female Wistar rats were exposed for 20 days to tobacco smoke obtained from non-filter cigarettes. During the exposure, concentration of tobacco smoke was monitored indirectly by measuring the CO level (1500 mg/m3 air). The efficacy of exposure was assessed by measuring urine nicotine and cotinine levels. Cigarette smoke did not change total cytochrome P450 and b5 protein levels in any of the organs studied, and most of these organs did not show any changes in the activity of reductases associated with these cytochromes. Following exposure to tobacco smoke, fetal rat liver expressed CYP2B1/2 protein; in newborns (day 1) both liver and lung showed CYP2B1/2 protein expression and very low pentoxyresorufin O-dealkylase activity. Western blot analysis of adult liver, lung, heart, but not of brain microsomes, showed that tobacco smoke induced CYP2B1/2 in both nonpregnant and pregnant rats, though its expression was lower in the livers and hearts of pregnant females. In the rat and human placenta, neither rat CYP2B1/2 nor human CYP2B6 showed basal or tobacco smoke-induced expression at the protein level. This study shows clearly that the expression of CYP2B1/2, which metabolizes nicotine and some drugs and activates carcinogens, is controlled in rats by age-, pregnancy-, and tissue-specific regulatory mechanisms.

Endogenous Peroxidase Localization in Kupffer Cells of the Fetal Rat Liver

1977 ◽  
Vol 35 ◽  
pp. 424-425
Author(s):  
Richard M. Pino
Keyword(s):  
Rat Liver ◽  
Kupffer Cells ◽  
Wistar Rat ◽  
Adult Liver ◽  
Ether Anesthesia ◽  
Fetal Rat ◽  
Endogenous Peroxidase ◽  
Sinusoidal Endothelium ◽  
Fetal Rat Liver ◽  
Adult Bone

This study confirms the presence of endogenous peroxidase in fetal Kupffer cells. In adult hepatic sinusoids Kupffer cells are peroxidase positive; endothelial cells are not.1 The fetal rat liver sinusoidal endothelium during development changes from a lining similar to that found in adult bone marrow to an adult liver type.2 Cells that resemble adult Kupffer cells are evident at 13 days gestation and can endocytize carbon beginning at 14 days.Sixteen day Wistar rat fetuses were exposed in utero after ether anesthesia of their mothers. Colloidal carbon (Pelikan, Gunther Wagner) diluted 1:1 with double strength Tyrode1s solution, or as a control, single strength Tyrode's solution without carbon, was injected (0.01-0,03ml) into the fetal umbilical veins with a 30 gauge needle.2 After allowing one minute for the injected material to circulate, the fetuses were decapitated and the livers were removed and diced into small pieces.

scholarly journals Effect of maternal hypothyroidism during pregnancy on insulin resistance, lipid accumulation, and mitochondrial dysfunction in skeletal muscle of fetal rats

2018 ◽  
Vol 38 (4) ◽  
Author(s):  
Tongjia Xia ◽  
Xue Zhang ◽  
Youmin Wang ◽  
Datong Deng
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Signal Transduction ◽  
Drinking Water ◽  
Thyroid Hormone ◽  
Related Protein ◽  
Pregnant Rats ◽  
Insulin Signal Transduction ◽  
Fetal Rat ◽  
Fetal Rats

The present study aimed to investigate the effect of maternal hypothyroidism during pregnancy on thyroid function of the fetal rat. Female Sprague–Dawley rats were randomized into two groups. Propylthiouracil (PTU) group received PTU in drinking water for 6 weeks (n=90), normal group received normal drinking water (n=50). The pregnant rats were obtained and had a cesarean-section to get at gestational ages of 8.5, 13, and 21 days, following blood samples and skeletal muscle were obtained from fetal rats. Levels of thyroid hormone, insulin, mitochondrial protein, and adipokines were detected using ELISA. Western blotting was performed to analyze mitochondria and insulin signal transduction-related protein in fetal rat skeletal muscle. Immunostaining of Periodic Acid-Schiff (PAS) and Oil Red O was used to observe the accumulation of muscle glycogen and lipid in the fetal rat. The results showed that the levels of thyroid hormone, insulin, insulin signal transduction-related protein, mitochondrial, and adipokines increased with the fetus developed, but had no statistical differences in the PTU group compared with the normal group. In conclusion, pregnant rats with hypothyroidism had no influence on insulin resistance (IR), lipid accumulation, and mitochondrial dysfunction in skeletal muscle of the fetal rats.

Multiple forms of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase are expressed in perinatal rat liver

1996 ◽  
Vol 270 (2) ◽  
pp. E244-E250 ◽  
Author(s):  
M. Casado ◽  
L. Bosca ◽  
P. Martin-Sanz
Keyword(s):  
Liver Enzyme ◽  
Rat Liver ◽  
Fetal Liver ◽  
Ribonuclease Protection Assay ◽  
Adult Liver ◽  
Transcription Analysis ◽  
Fetal Rat ◽  
Protected Fragment ◽  
Fetal Rat Liver ◽  
Ribonuclease Protection

Fetal rat liver expresses a 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFK-2/Fru-2,6-Pase2) form that differs from the adult liver enzyme in the inhibition by phosphorylation by the adenosine 3',5'-cyclic monophosphate-dependent protein kinase and in the recognition by an antibody specific for the NH2-terminal domain of the adult liver enzyme. Northern blot analysis shows that fetal hepatocytes contain a species of mRNA that is 2.2 kb in size and that exhibits the maximal levels after delivery. PFK-2/Fru-2,6-Pase2 mRNA analysis using a sensitive ribonuclease protection assay reveals the presence of nearly similar amounts of adult liver-specific and skeletal muscle-specific mRNA in fetal liver and hepatocytes during the last days of gestation, as well as a 233-bp protected fragment present in fetal liver. These results were confirmed by polymerase chain reaction using specific oligonucleotide pairs. Primer extension of fetal liver cDNA suggests the presence of two initiation sites of transcription. Analysis of the adult liver PFK-2/Fru-2,6-Pase2 protein during the perinatal transition using a specific antibody shows a marked accumulation of this form immediately after birth.

Enzyme Activities During Culturing of Fetal Rat Liver

1973 ◽  
Vol 51 (4) ◽  
pp. 476-481 ◽  
Author(s):  
Lorne Kirby ◽  
Peter Hahn
Keyword(s):  
Oleic Acid ◽  
Culture Medium ◽  
Fetal Liver ◽  
Fetal Rat ◽  
Fetal Rats ◽  
Tyrosine Transaminase ◽  
Simple Medium ◽  
Fetal Rat Liver ◽  
Early Rise ◽  
Carnitine Palmitoyltransferases

Liver from fetal rats was cultured in a simple medium. In such cultures tyrosine transaminase (TTA) activity had increased after 20 min and reached twice the initial value within 2 h. Phosphoenolpyruvate earboxykinase (PEPCK) activity decreased during culturing. Incubation of microsomes from fresh fetal liver with dibutyryl cyclic AMP (DcAMP), oleic acid, or acetyl-CoA led to an increase in their TTA activity. It is suggested that the early rise in TTA during culturing is due to release of the enzyme from the microsomal fraction. In contrast to human fetal liver, oleic acid did not induce PEPCK in rat fetal liver cultures. In neither species was there an effect of DcAMP on the amount of fatty acids in the culture medium or on the activities of carnitine acetyl- and carnitine palmitoyltransferases.

The experimental investigations of the toxic influence of tobacco smoke affecting progeny during pregnancy

1999 ◽  
Vol 18 (4) ◽  
pp. 245-251 ◽  
Author(s):  
Ewa Florek ◽  
Andrzej Marszalek ◽  
Wieslawa Biczysko ◽  
Krzysztof Szymanowski
Keyword(s):  
Body Weight ◽  
Tobacco Smoke ◽  
Distress Syndrome ◽  
Experimental Investigations ◽  
Lung Maturation ◽  
Pregnant Rats ◽  
Pregnant Females ◽  
Morphological Studies ◽  
Passive Exposure ◽  
Different Doses

1 Tobacco smoke contains around 4000 substances, most of which are described as toxic, and they may have an influence on the development of progeny. 2 The present studies concentrate on the measurement and calculation of indices describing the new-born' survival, rearing of pups, weight of foetuses, young animals, placenta and females in relation to different doses of tobacco smoke (carbon monoxide levels). The morphological studies of placenta, foetal and newborn lungs were done as a supplement. Biochemical placenta study was also done. 3 The results of the experiment proved that some indices for animals in groups which were passively exposed to the highest concentrations of tobacco smoke were lower, others fluctuated (4 day, 12 day and total survival) and some did not reveal any changes (rearing). Direct correlation between maternal passive exposure to tobacco smoke and the presence of acute respiratory distress syndrome symptoms in new-boms was observed. A decrease of body weight of pregnant females passively exposed to tobacco smoke was also observed. An increase of placenta-foetal factor was found. A decrease of rat weight was observed after passive exposure to tobacco smoke. 4 We concluded that there is correlation between passive exposition to tobacco smoke during pregnancy and delayed lung maturation in the offspring. Exposure of the pregnant rats to cigarette smoke increases the activity of isocitric and glucose-6-phosphate dehydrogenases in placenta.

Effect of maternal chronic hypoxic exposure during gestation on apoptosis in fetal rat heart

2003 ◽  
Vol 285 (3) ◽  
pp. H983-H990 ◽  
Author(s):  
Soochan Bae ◽  
Yuhui Xiao ◽  
Guohu Li ◽  
Carlos A. Casiano ◽  
Lubo Zhang
Keyword(s):  
Heat Shock ◽  
Rat Heart ◽  
Caspase 3 ◽  
Chronic Hypoxia ◽  
Fetal Heart ◽  
Hypoxic Exposure ◽  
Protein Levels ◽  
Fetal Rat ◽  
Fetal Rats ◽  
Maternal Hypoxia

Chronic hypoxia during pregnancy is one of the most common insults to fetal development. We tested the hypothesis that maternal hypoxia induced apoptosis in the hearts of near-term fetal rats. Pregnant rats were divided into two groups, normoxic control and continuous hypoxic exposure (10.5% O2) from day 15 to 21 of gestation. Hearts were isolated from fetal rats of 21-day gestational age. Maternal hypoxia increased hypoxia-inducible factor-1α protein in fetal hearts. Chronic hypoxia significantly increased the percentage and size of binucleated myocytes and increased apoptotic cells from 1.4 ± 0.14% to 2.7 ± 0.3% in the fetal heart. In addition, the active cleaved form of caspase 3 was significantly increased in the hypoxic heart, which was associated with an increase in caspase 3 activity. There was a significant increase in Fas protein levels in the hypoxic heart. Chronic hypoxia did not change Bax protein levels but significantly decreased Bcl-2 proteins. In addition, chronic hypoxia significantly suppressed expression of heat shock protein 70. However, chronic hypoxia significantly increased expression of the anti-apoptotic protein 14–3-3 θ, among other 14–3-3 isoforms. Chronic hypoxia differentially regulated β-adrenoreceptor (β-AR) subtypes with an increase in β1-AR levels but no changes in β2-AR. The results demonstrate that maternal hypoxia increases apoptosis in fetal rat heart, which may be mediated by an increase in Fas and a decrease in Bcl-2 proteins. Chronic hypoxia-mediated increase in β1-AR and decrease in heat shock proteins may also play an important role in apoptosis in the fetal heart.

scholarly journals Glucocorticoids increase the fluidity of the fetal-rat liver microsomal membrane in the perinatal period

1986 ◽  
Vol 239 (1) ◽  
pp. 41-45 ◽  
Author(s):  
J Kapitulnik ◽  
E Weil ◽  
R Rabinowitz
Keyword(s):  
Fatty Acids ◽  
Rat Liver ◽  
Perinatal Period ◽  
Fatty Acyl ◽  
Microsomal Membrane ◽  
Fatty Acyl Moiety ◽  
Pregnant Rats ◽  
Fetal Rat ◽  
Fetal Rat Liver ◽  
Membrane Fluidization

Dexamethasone, a synthetic glucocorticoid, was administered to pregnant rats during the last week of pregnancy in order to examine its effects on the fluidity of the developing fetal-rat liver microsomal membrane. This early prenatal exposure to dexamethasone, which preceded the natural appearance of fetal corticosteroids, markedly accelerated the normal perinatal course of fluidization of this membrane. The lipid apparent microviscosity, which was determined by measurement of fluorescence polarization, decreased in 21-days-old treated fetuses to values that were indistinguishable from those of untreated newborn rats. This dexamethasone-mediated acceleration of membrane fluidization was associated with an increase in the index of unsaturation of the fatty acyl moiety of microsomal lipids. Dexamethasone caused a significant increase in the microsomal content of polyunsaturated fatty acids (arachidonic and linoleic acid), which was accompanied by a decrease in content of monoenoic fatty acids (oleic and palmitoleic acid). This early exposure in utero to dexamethasone precociously induced the changes in fatty acid composition of fetal-rat liver microsomal lipids that normally occur between the last day of pregnancy and the first day of extra-uterine life. These results suggest that endogenous glucocorticoids play a major role in the perinatal fluidization of the rat liver microsomal membrane.

scholarly journals Efficacy of Low Molecular Heparin on Preeclampsia by Inhibiting Apoptosis of Trophoblasts via the p38MAPK Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Dandan Quan ◽  
Li Li ◽  
Manzhen Zuo
Keyword(s):  
Blood Pressure ◽  
Signaling Pathway ◽  
Heparin Group ◽  
Pregnant Rats ◽  
Apoptosis Rate ◽  
Protein Levels ◽  
Fetal Rats ◽  
P38mapk Signaling ◽  
Tissue Cells ◽  
And Migration

Objective. To explore the efficacy of low molecular heparin on preeclampsia by inhibiting apoptosis of trophoblasts via the p38MAPK signaling pathway. Methods. A preeclampsia rat model was established, and the effects of low molecular heparin on preeclampsia via the p38MAPK signaling pathway were analyzed based on intervention of the rats with different combinations of low molecular heparin and p38MAPK signaling pathway activator. Furthermore, a hypoxia/reoxygenation model of trophoblasts in vitro was established to explore the effects of low molecular heparin on trophoblasts via the p38MAPK signaling pathway. Results. After treatment with low molecular heparin, pregnant rats in the heparin group showed significantly decreased blood pressure, 24 h proteinuria, and p38MAPK protein levels in placenta tissues and decreased apoptosis rate of placenta tissue cells (all P < 0.05 ) and showed more fetal rats and lowered weight of them (both P < 0.05 ) but showed no significant change in the weight of placenta (all P > 0.05 ). Pregnant rats treated with low molecular heparin and p38MAPK activator showed significantly higher blood pressure, 24 h proteinuria, and p38MAPK protein levels in placenta tissues and apoptosis rate of placenta tissue cells than those of pregnant rats in the heparin group (all P < 0.05 ) and also showed less fetal rats and lighter fetal rats than those in the heparin group (both P < 0.05 ) but showed no difference with them in the weight of placenta ( P > 0.05 ). Further analysis revealed that low molecular heparin could protect the survival and migration of trophoblasts under hypoxia/reoxygenation conditions and reduce apoptosis of them (all P < 0.05 ). Conclusion. Low molecular heparin can alleviate preeclampsia by inhibiting the p38MAPK signaling pathway and can inhibit apoptosis of trophoblasts and promote proliferation and migration of them.

Erythroid colony formation by fetal rat liver and spleen cells in vitro: inhibition by a low relative molecular mass component of fetal spleen

Development ◽  
1992 ◽  
Vol 114 (1) ◽  
pp. 213-219
Author(s):  
M.D. Nagel ◽  
J. Nagel
Keyword(s):  
Molecular Mass ◽  
Lethal Effect ◽  
Relative Molecular Mass ◽  
Spleen Cells ◽  
Fetal Rat ◽  
Fetal Rats ◽  
Percoll Gradients ◽  
Fetal Rat Liver ◽  
Liver Fraction

Liver and spleen hematopoietic cell suspensions from 20-day-old-fetal rats were fractionated on Percoll gradients. A granulocyte-rich splenic fraction inhibited CFUe production by cultures of a CFUe-enriched liver fraction, and by cultures of unfractionated liver and spleen hematopoietic cells. Conditioned medium from the spleen cell fraction contained an inhibitor of relative molecular mass, Mr, 25–35 × 10(3). The sensitivity of spleen cells to the inhibitor varied with the age of the fetus from which they were derived (20-day-old less than 18-and 19-day-old). No such age-dependence was found for liver cells. The inhibitor affects cycling CFUe, blocks the lethal effect of AraC, does not appear to be lineage-specific and its influence can be reversed by washing.

scholarly journals The development of the sinusoids of fetal rat liver: localization of endogenous peroxidase in fetal Kupffer cells.

1979 ◽  
Vol 27 (2) ◽  
pp. 643-652 ◽  
Author(s):  
R M Pino ◽  
P W Bankston
Keyword(s):  
Rat Liver ◽  
Kupffer Cells ◽  
Serial Sections ◽  
Adult Liver ◽  
Monocytic Cells ◽  
Dense Bodies ◽  
Fetal Rat ◽  
Endogenous Peroxidase ◽  
Fetal Rat Liver ◽  
Cytochemical Marker

Endogenous peroxidase is the cytochemical marker used to identify Kupffer cells in the adult liver. In this study, we show by ultrastructural cytochemistry that Kupffer cells of the fetal rat liver are endogenous peroxidase positive. The reaction product is localized in the endoplasmic reticulum including the perinuclear cisternae and in a few lysosome-like dense bodies. Serial sections of Golgi regions suggest that GERL and not the Golgi stacks, is peroxidase positive. As in the adult liver, peroxidase is not localized in endothelial cells. Kupffer cells do not appear to transform from endothelial or extravascular developing monocytic cells and are present prior to bone marrow formation. The relevance of these observations with respect to the possible origin of the Kupffer cell is discussed.

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