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PubMed1999

Lung macrophage differentiation antigens in developing fetal and newborn rat lungs: A quantitative flow cytometric analysis with immunohistochemistry.

Relative deficiencies in the number and function of alveolar macrophages (AMs) are present immediately after birth and contribute to increased susceptibility to infection. We used immunohistochemical localization with a panel of monoclonal antibodies to macrophage differentiation markers to characterize lung macrophage antigens relevant to development, and we present here the first study to quantitate these markers using flow cytometric analysis. Rat lung macrophages undergo immunophenotypic maturation seen by a changing number (OX-1, ED-1, ED-2, and ED-9) and distribution (ED-2) of certain lung macrophage differentiation antigens. Quantification of these antibodies revealed that labeling for ED-1 and ED-9 was less on lavageable AMs from early postnatal days than on mature adult AMs. In vitro treatment of adult rat AMs with murine granulocyte-macrophage colony-stimulating factor produces a proliferating population of AMs with a high proliferation index and an immature phenotype, similar to that of newborn AMs. This in vitro model was useful in validating our quantitation of neonatal lung macrophage differentiation antigens. Our quantitative studies of potential markers of AM differentiation in the developing lung may help to focus the study of macrophages in the developing lung on specific cellular and molecular pathways that may control immunologic events during this critical period.

Animals↗
PubMed2005

Effects of aflatoxin B1 on embryo fetal development in rabbits.

Aflatoxin B1 (AFB1), is a food borne mycotoxin produced by fungal species of the genera Aspergillus. To elucidate the teratogenic effects, AFB1 was dissolved in corn oil and given orally to New Zealand White rabbits during 6-18 days of gestation with the dose levels of 0.025, 0.05 and 0.1 mg/kg body weight. To assess pathomorphological features of the anomalies induced by AFB1, the fetal serial sections were histologically examined. There was no maternal mortality in any group. There was non-significant decrease in percent of live fetuses and increase in the percent resorptions and post-implantation losses at 0.1 mg/kg dose group as compared with those of controls. The mean crown to rump lengths of 0.05 and 0.1 mg/kg dose groups were significantly reduced than that of the control. The mean fetal weights were significantly reduced in 0.1 mg/kg dose group than that of other treated groups. The gross anomalies observed included wrist drop and enlarged eye socket whereas, skeletal anomalies were agenesis of caudal vertebrae, incomplete ossification of skull bones and bent metacarpals. The visceral anomalies of microphthalmia and cardiac defects were seen at 0.1 mg/kg dose group. The characteristic histological findings of fetal tissues were distortion of normal hepatic cord pattern and reduced megakaryocytes in liver, fusion of auriculo-ventricular valves, mild degenerative changes in myocardial fibers, microphthalmic eyes and lenticular degeneration. The results of this study indicated that AFB1 was found to be teratogenic in rabbits when given by oral route during gestation days 6-18 and the dose of 0.1 mg/kg could be considered as the minimum oral teratogenic dose. The histological examination of the fetal tissues indicated its importance in identifying the visceral anomalies which were otherwise not visible.

Administration, Oral↗
PubMed1976

[The influence of the N-mustard derivative "cytostasan" on pregnancy and fetal development in the rat].

This presentation describes the action of Cytostasan, a nitrogen mustard compound of benzimidazole, on reproduction and embryonic development of Wistar rats. Single doses from 20 through 100 mg/kg body weight were given intraperitoneally on the 4th, 7th, 9th, 11th or 13th day post coitum. All test animals were sacrificed on the 20th day of pregnancy. The following parameters served as a base for evaluation: the means of implantation rates, resorption rates, fetal body weights and the number of dead and living fetuses. Malformations were detected by outer inspection for gross anomalies, by means of the razor blade technique for malformations of organs and by alizarin preparations for detecting anomalies of the osseuos skeleton. All results were compared with those of an untreated control group and evaluated by statistical means. Cytostasan exerts embryotoxic and teratogenic effects in appropriate dosage. Notwithstanding the fact of giving high doses (1/2 LD 50) there is no loss of blastocysts before implantation: the number of implantation sites equals that of the control group. The resorption rate increases at all examined days of development after application of 40 mg/kg, but 20 mg/kg exert effects only on days 4, 7, and 11 p. c. There is no action on the number of living fetuses after injection of 20 mg Cytostasan/kg body weight. After application of 40 mg/kg the number of living fetuses decreases especially on the 7th, 9th, and 13th day p. c. There is a dose-dependent stunting: the fetal body weight is not reduced after a dosage of 20 mg/kg, but 40 mg/kg cause a considerable loss of weight during embryogenesis (days 9, 11, 13). It is impossible to induce stunting during blastogenesis (days 4 and 7). The observed patterns of malformation are relatively uniform: kinked tails, omphaloceles, hydronephroses, hydrocephali. Skeletal defects are absent. The results received are compared with other findings on aklylating antitumour drugs.

Abnormalities, Drug-Induced↗
PubMed1979

Effect of maternal thyroparathyroidectomy before gestation on fetal development in rats.

Female rats were thyroparathyroidectomized (TPTX) at 24 (immature), 40 (pubertal) and 75 (matured) days of age, at least 21 days before mating. Thyroxine (2.5 microgram/kg) or parathyroid hormone (150 USP units/kg x 2) was replaced in two TPTX groups. Thyroxine deficient groups of all ages had reduced body weight, litter size and serum thyroxine and calcium level. Fetal weights at 20 days of gestation in all thyroxine deficient groups were significantly reduced but placental weight was generally increased. Maternal serum thyroxine and fetal weight was positively related when all groups were taken together, but maternal serum calcium and fetal weight was not related. There were no significant differences in gross, visceral or skeletal anomalies in the fetuses in any group.

Animals↗
PubMed1979

Water relations of fetal development.

Normal pregnancy is accompanied by a remarkable increase in total body water, due partly to the growth and development of the conceptus and partly to water retention by the mother. An evaluation of the changes in body water during pregnancy suggests that they could very largely be brought about by the hydrostatic element of osmotic water regulation and are mainly under fetal, rather than maternal control. The results also suggest that pathological disorders of water in pregnancy are essentially secondary, and not primary manifestations of disease.

Amniotic Fluid↗
PubMed2002

The human prostate expresses sonic hedgehog during fetal development.

PURPOSE: The keynote event of prostate ductal development is the formation of epithelial buds that invade the urogenital sinus mesenchyma. Studies in mice have shown that budding requires the signaling peptide, which is expressed in the epithelium of the prostatic anlagen. We report our characterization of (SHH) expression in the human fetal prostate. MATERIALS AND METHODS: Reverse transcriptase-polymerase chain reaction was performed in fetal prostate RNA isolated at 15.5 and 18 weeks of gestation, respectively. Immunostaining was performed on sections from 7 male fetuses at 9.5 to 34 and in 4 female fetuses at 9 to 18 weeks of gestation. RESULTS: Weak staining for was seen in the prostatic urethra at 9.5 weeks. Intense staining was seen at 11.5 and 13 weeks in the prostatic urothelium and nascent prostatic buds. Staining was slightly diminished at 16.5, further diminished at 18 to 20 and absent at 34 weeks. expression at 15.5 and 18 weeks was confirmed by reverse transcriptase-polymerase chain reaction assay of freshly isolated prostate tissue. Comparative immunostaining in the female showed urothelial staining at 9 and 12 weeks with staining greatest above the entrance of the müllerian ducts. Staining diminished earlier in the female (14 weeks) than in the male and was almost absent at 18 weeks. CONCLUSIONS: expression in the human fetal prostate is contemporaneous with the fetal testosterone surge and with ductal budding of the prostatic urothelium. expression is also present in the female urogenital sinus but in the absence of testosterone it is not associated with ductal budding.

Female↗
PubMed1992

Descriptive morphology of developing fetal neostriatal allografts in the rhesus monkey: a correlated light and electron microscopic Golgi study.

Primate fetal striatal neurons were transplanted into the ibotenic acid lesioned rhesus monkey striatum. Ten weeks after transplantation the monkeys were transcardially perfused and graft tissue was histologically stained. Golgi impregnated, and processed for electron microscopy. The monkeys received magnetic resonance imaging (MRI) scans before lesioning, after lesioning, and ten weeks after transplantation to noninvasively study the striatal grafts. The study demonstrated that fetal striatal grafts, measuring up to 0.4 x 0.8 cm, can survive for extended periods of time in the non-human primate. Hematoxylin-eosin stained sections of the transplant demonstrated that neuronal, glial, vascular, and lymphocytic cells were present in the graft. The majority of the neurons had somatic diameters between 8 and 20 microns and were characterized by nuclei containing multiple nucleoli. A few neurons within the graft had somatic diameters up to 40 microns. These larger neurons exhibited more mature cytoplasm containing a moderate amount of Nissl substance. Some of the blood vessels within the graft were surrounded by a large number of plasma cells, but there was no evidence of hemorrhage or necrosis. Bielschowsky staining and Golgi impregnation of the transplanted tissue demonstrated that there were neurons at various degrees of differentiation. Some of the neurons had varicose dendrites, growth cones, and filopodia, which are all characteristics of immature neurons, while others had a much more mature appearance, including a moderate number of dendritic spines. Some of these neurons had an appearance typical of differentiating "medium spiny" neurons of the normal striatum. Electron microscopic analysis of the transplanted tissue and individual Golgi-impregnated neurons within the transplant confirmed that there were developing neurons within the graft. These neurons had an increased nuclear-to-cytoplasmic ratio and had nuclei containing multiple nucleoli. The neuropil surrounding these neurons was loosely organized and contained large areas of extracellular space. The neuropil exhibited developing dendrites, numerous growth cones, and mature synapses. In summary, the study demonstrated that fetal striatal allografts can survive for up to three months in the rhesus monkey and undergo normal differentiation as assessed by Golgi impregnation and electron microscopy.

Animals↗
PubMed1985

Fetal development in mice exposed to isoflurane.

The developmental toxicity of trace (0.006%), subanesthetic (0.06%), and light anesthetic (0.6%) exposure to isoflurane was examined in Swiss/Webster mice. No adverse effects were demonstrated following exposure of dams to 0.006% (n = 26) and 0.06% (n = 27) isoflurane for 4 hr daily on days 6-15 of pregnancy. Exposure to 0.6% isoflurane (n = 23) for the same period resulted in significantly decreased fetal weight, decreased skeletal ossification, minor hydronephrosis, and increased renal pelvic cavitation. The incidence of cleft palate also was significantly increased, abnormalities occurring in 12.1% of fetuses and affecting 11 of 23 litters. This incidence was considerably higher than that of the combined treatment and colony control groups (0.75%) and those that we have found in previous experiments with this mouse strain following exposure to halothane (1.2%) or enflurane (1.9%).

Abnormalities, Drug-Induced↗
PubMed1979

Morphological alterations in the developing fetal rat limb due to maternal injection of chlorambucil.

On day 14 of pregnancy, rats were injected i.p. with 9.5 mg/kg of chlorambucil. At term, all the fetuses were stunted and had obvious skeletal malformations. From days 15-20 of gestation there was a steady progression of cell death and histologic derangement in long bone formation. This began on day 15, the day following exposure to chlorambucil, with extensive cell death of chondroblasts in the long bone primordia. By day 16, dead or dying cells were located in the cartilage model and became associated with a higher than normal matrix to cell ratio. In day 17 limbs, many cells of the cartilage model were irregular in size and shape so that the normally precise cellular arrangement was lacking. On day 18, periosteal and enchondrial calcification was delayed and scanty. The fibular hemimelia observed in all drug-treated term fetuses stained with alizarin appeared to result from lack of development of the proximal half of the cartilage model. The observed alterations, particularly bowing of the ulna, in the teratogen-treated fetuses appeared to result primarily from specific cell death and formation of aberrant cell types but abnormal cell products may also play a role.

Animals↗
PubMed1988

In situ localization of T cell receptor beta chain in the murine thymus: changes in the intrathymic distribution of thymocytes expressing beta chain during fetal development.

The expression of T cell receptor beta chain in the developing thymus was examined at the light and electron microscopic levels using the monoclonal antibody F23.1. Cells expressing cytoplasmic forms of beta chain were first observed at Day 16 of gestation, while thymocytes expressing cell surface beta chain were detected about a day later. Clustering of cortical F23.1+ cells was more pronounced in fetal thymus when compared to adult. The density of F23.1+ cells in the subcapsular areas of the thymus was initially lower than that in the rest of the cortex or the medulla. Within the subcapsular and cortical areas of the thymus there was an inverse relationship between the density of F23.1+ cells and cells labeled with the lectin from Dolichos bifloris, which binds to terminal alpha-linked N-acetylgalactosamine residues preferentially expressed by L3T4-/Lyt2- thymocytes. Although this pattern was less pronounced with increasing gestational age, it was still apparent at birth.

Animals↗
PubMed1981

Maternal ethanol consumption and fetal development in the rat: a comparison of ethanol exposure techniques.

Comparison of the polydipsia and liquid diet procedures for ethanol exposure were used in female rats, either before and/or during gestation. Autopsy of the fetuses on day 20 of gestation found a significant weight reduction in the polydipsia-exposed animals that could be attributed to ethanol. No such effect was found in the liquid diet-exposed animals. The data are discussed in relation to the human fetal alcohol syndrome.

Animals↗
PubMed1978

Subcellular localization of gonadotropins and testosterone in the developing fetal rat testis.

Gonadotropins and testosterone were immunocytochemically localized in the fetal rat testes 16-18 days of gestation with the unlabeled antibody-peroxidase anti-peroxidase complex technique. Maximum staining for gonadotropins with antiserum to the beta chain of human chorionic gonadotropin (anti-hCGbeta) occurred at 16 days gestation in the seminferous tubule and 17 days gestation in interstitial (Leydig) cells. Anti hCGbeta sites were on the plasma membranes at the luminal aspects of Sertoli cells at 16 days gestation. In addition, intracellular hCGbeta sites were evident including the nucleus, nucleolus, ribosomes, some vesicles, lysosomes and centrioles. The stain for hCGbeta disappeared rapidly and by 17 days was limited to patches in the cytoplasm and nuclei. In the fetal testes, staining for anti-testosterone binding sites was most intense at 18 days of gestation either in lipid droplets or on nuclei of Leydig and Sertoli cells. Very little testosterone stain was observed before 18 days of gestation. These findings agree with physiologic data that suggest that gonadotropins bind to receptors and stimulate testicular development and the capacity for testosterone production.

Animals↗
PubMed1993

Androgen regulation of epidermal growth factor receptor binding activity during fetal rabbit lung development.

Fetal lung development progresses in a sex-specific manner with male fetuses exhibiting delayed maturation. Androgens, both exogenous and endogenous, inhibit while epidermal growth factor (EGF) enhances fetal lung development. We hypothesized that one mechanism responsible for the delay in male fetal lung development is an androgen-induced delay in EGF receptor binding activity. We measured EGF binding in sex-specific fetal rabbit lung plasma membranes isolated from control fetuses (days 21, 23, 25, 27, 29, and 30 of gestation) and from androgen-treated fetuses (days 21, 23, and 27 of gestation) that had been continuously exposed in vivo to exogenous 5 alpha-dihydrotestosterone from day 12 through 27 of gestation. Specific binding of EGF was significantly lower in male than in female fetal lung tissue isolated from controls at day 21 of gestation. Scatchard analysis revealed that this decrease in EGF binding was associated with decreased EGF receptor density without any significant change in affinity. Prenatal exogenous androgen treatment led to decreased EGF binding in fetal rabbit lung tissue from both sexes secondary to a decrease in EGF receptor density. These findings suggest that one mechanism responsible for the delay in male fetal lung maturation is an androgen-induced delay in EGF receptor binding activity during fetal lung development.

Androgens↗
PubMed1982

Rat fetal development and maternal exposure to trichloroethylene 100 p.p.m.

Thirty-two inbred Wistar rats (study group) were exposed to trichloroethylene 100 p.p.m. in air for 4 h daily from day 8 to day 21 of pregnancy. A control group (31 rats) was exposed to the same experimental conditions but without the addition of trichloroethylene. All the rats were sacrificed on the 21st day of pregnancy and the ovaries, uterus, liver, lungs, heart and the fetuses were examined. There was no evidence of teratogenesis, but a delay in fetal maturation was suggested by reduced fetal weight (P less than 0.05) and by an increase in bipartite or absent skeletal ossification centres (P less than 0.005).

Abnormalities, Drug-Induced↗
PubMed1982

The effects of hyperphenylalaninemia on fetal development: a new animal model of maternal phenylketonuria.

A new model has been developed for the study of maternal phenylketonuria. Beginning on the 12th day of gestation the diet of pregnant rats was supplemented with 0.5% alpha-methylphenylalanine and 3% phenylalanine. This resulted in an 83% reduction of hepatic phenylalanine hydroxylase activity. The maternal plasma phenylalanine was elevated 10-20-fold for two-thirds of the day, but the degree and persistence of the fetal hyperphenylalaninemia may have been even greater. The brain phenylalanine concentrations in the fetus were raised up to 2900 nmole/g brain, whereas the highest level observed in the dam was 382 nmole/g. Experimentally-treated fetuses showed small reductions in both body and brain weight when compared to age-matched controls; however, no differences were seen in crown to rump length, litter size, DNA and protein concentrations per g, or in postnatal survival. Initiation of the diet at conception rather than on the 12th day caused a significantly greater inhibition of fetal growth, and 21% mortality. The fetal cerebral concentrations of methionine and the branched chain amino acids (valine, leucine and isoleucine) were decreased by hyperphenylalaninemia. From the 16th day on, the concentration of the inhibitor neurotransmitter glycine was elevated. Cerebral serotonin showed a 20-30% deficit and its primary metabolite 5-hydroxyindoleacetic acid a 71-77% deficit. Of twelve enzymes quantified in the brains of hyperphenylalaninemic fetuses only phosphoserine phosphatase showed any change. From the 20th to the 22nd day of gestation its activity was 46-67% higher in experimental than in normal fetuses. Measurement on the 22nd day of gestation showed that the increases in phosphoserine phosphatase activity and glycine content were present in brain stem, cerebellum, and forebrain.

Animals↗