[Drugs and embryonic-fetal development].
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Drug-Related Side Effects and Adverse Reactions↗
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Central vagal sensory and motor connections: human embryonic and fetal development.
The embryonic and fetal development of the nuclear components and pathways of vagal sensorimotor circuits in the human has been studied using Nissl staining and carbocyanine dye tracing techniques. Eight fetal brains ranging from 8 to 28 weeks of development had DiI (1,1'-dioctadecyl-3,3,3',3' tetramethylindocarbocyanine perchlorate) inserted into either the thoracic vagus nerve at the level of the sternal angle (two specimens of 8 and 9 weeks of gestation) or into vagal rootlets at the surface of the medulla (at all other ages), while a further five were used for study of cytoarchitectural development. The first central labeling resulting from peripheral application of DiI to the thoracic vagus nerve was seen at 8 weeks. By 9 weeks, labeled bipolar cells at the ventricular surface around the sulcus limitans (sl) were seen after DiI application to the thoracic vagus nerve. Subnuclear organization as revealed by both Nissl staining and carbocyanine dye tracing was found to be advanced at a relatively early fetal age, with afferent segregation in the medial Sol apparent at 13 weeks and subnuclear organization of efferent magnocellular divisions of dorsal motor nucleus of vagus nerve noticeable at the same stage. The results of the present study also confirm that vagal afferents are distributed to the dorsomedial subnuclei of the human nucleus of the solitary tract, with particular concentrations of afferent axons in the gelatinosus subnucleus. These vagal afferents appeared to have a restricted zone of termination from quite early in development (13 weeks) suggesting that there is no initial exuberance in the termination field of vagal afferents in the developing human nucleus of the solitary tract. On the other hand, the first suggestion of afferents invading 10N from the medial Sol was not seen until 20 weeks and was not well developed until 24 weeks, suggesting that direct monosynaptic connections between the sensory and effector components of the vagal sensorimotor complex do not develop until this age.
Carbocyanines↗
Blood coagulation factors in human embryonic-fetal development: preferential expression of the FVII/tissue factor pathway.
The expression of a number of blood coagulation factors (F) (FX, FIX, FVIII, FVII, alpha-, beta-, gamma-fibrinogen chains, protein C, and antithrombin III [AT III]) was analyzed at RNA and protein level in 5- to 10-week-old human embryos and fetuses. FX, FIX, and FVII were also analyzed at protein level. Total and poly(A)+ RNA, extracted from embryonic-fetal (FL) and adult liver (AL), were analyzed by dot and Northern blot hybridization with specific cDNA probes. The results indicate that: (1) the size of the messenger RNAs of these factors is equivalent in FL and AL; (2) in the 5- to 10-week period, their abundance in FL increases from 30% to 50% of the adult level except for FIX (from 2% to 10%) and FX (always 100% of the adult value). Western blot analysis of FIX, FX, and FVII in 5- to 10-week soluble liver proteins and 6- to 8-week plasma showed a low level of FIX versus a higher concentration of both FVII and FX, when compared with corresponding adult values, ie, a liver protein level of 10% versus 100% and a plasma concentration level of 10% versus 40%. Although little is known so far on the activity and the functional role of the clotting factors in early human ontogenic development, these studies suggest an activation of FX via the FVII/tissue factor activity rather than the FIXa/FVIIIa phospholipid complex in human embryonic and early fetal life.
Blood Coagulation Factors↗
Erythroid progenitor cells and stimulating factors during murine embryonic and fetal development.
Murine embryonic and fetal yolk-sacs, peripheral blood, and livers were assayed for hemopoietic multipotential and progenitor cell content between days 6 and 13 of gestation. Multipotential cells (Mix-CFC), erythroid-committed progenitor cells (BFU-E), and nonerythroid progenitor cells (predominantly GM-CFC) were assayed by their ability to form hemopoietic colonies in vitro when stimulated by pokeweed-mitogen-stimulated spleen-cell-conditioned media (as a source of Multi-CSF) and either human or murine erythropoietin. Late erythroid progenitor cells (CFU-E) were stimulated to form colonies by erythropoietin. Mix-CFC, BFU-E, and nonerythroid cells were first detected on day 8 in yolk-sacs, day 9 in peripheral blood, and day 11 in liver. Maximum absolute numbers of yolk-sac Mix-CFC (182), BFU-E (331), and non-erythroid CFC (1358) occurred at 11 days of gestation. The maximum frequency of peripheral blood mix-CFC (24/10(5) cells) and BFU-E (55/10(5) cells) occurred at ten days of gestation. The absolute numbers of hepatic Mix-CFC, BFU-E, nonerythroid CFC, and CFU-E increased exponentially from 11 to 13 days' gestation. CFU-E were first detected at nine days in peripheral blood, at ten days in yolk-sac, and 11 days in liver and at all ages were equally responsive to erythropoietin. The maximum frequency (151/10(5) cells) of CFU-E in the peripheral blood and the maximum number per yolk-sac (1699) both occurred on day 11 of gestation. In confirmation of previous studies, yolk-sac fluid was found to contain a macrophage colony-stimulating activity. In addition, an activity capable of stimulating fetal liver CFU-E was also detected in yolk-sac fluid. However, no activity (Multi-CSF) capable of stimulating Mix-CFC or BFU-E was detected in either yolk-sac fluid or fetal plasma.
Animals↗
Superovulation of female mice delays embryonic and fetal development.
Mouse and human embryos, cultured in vitro, undergo a delay in development compared with those grown in vivo. This delay can be caused by suboptimal culture conditions, but possible influences of ovarian stimulation cannot be excluded. The objective of this study was to test the hypothesis that both in vitro and in vivo, preimplantation embryonic development and postimplantation fetal development are impaired in superovulated female mice when compared with naturally cycling controls. A delay in in-vitro blastocyst hatching and in-vivo blastocyst formation (P < 0.03 and P < 0.0001 respectively) and a 40% fetal growth retardation (P < 0.0001) were observed after superovulation in comparison with naturally cycling controls. After transfer to non-stimulated foster mothers, blastocysts from stimulated females had a lower implantation rate (P < 0.005), and developed into fewer living fetuses (P < 0.02), more resorption sites (P < 0.02) and had more pronounced growth retardation (P < 0.0001) when compared with blastocysts from naturally cycling controls. In conclusion, superovulation in the mouse causes a delayed embryonic development in vitro and in vivo, an increased abnormal blastocyst formation, a pronounced fetal growth retardation, and an increased number of resorption sites. If this observation in mice can be extrapolated to humans, it may offer an explanation for the delay in embryonic development and the low birth weight observed after IVF.
Animals↗
Magnetic resonance imaging of embryonic and fetal development in model systems.
We give an overview of the applications and methods of high-resolution anatomical magnetic resonance imaging (MRI) in the study of embryonic and fetal development in animal models. Challenges associated with performing in utero studies are described. Recent in utero images in mouse and in nonhuman primates are presented. Results using magnetic resonance microscopy in fixed mouse embryos and in amphibian embryos in vivo are reviewed. We discuss how studies of pregnancy in animal models aid in the translation of innovative new MRI techniques to clinical applications.
Animals↗
Secretory immune system in human embryonic and fetal development: joining chain and immunoglobulin transport (Review).
The role of joining (J) chain, one of the protein components of the secretory immune system (SIS), in the immune reactions of the human embryo and fetus was analyzed on the basis of data from the literature and our previous studies. All organs and structures, including extra-corporeal ones, of 18 embryos (4-8 weeks of development) and 45 fetuses (9-38 weeks) were studied using methods of pathomorphology, immunohistochemistry and morphometry. This approach enabled us to analyze the problem in the whole organism throughout its embryonic and fetal development. J chain, as well as polymeric immunoglobulin (Ig) receptor-secretory component (pIgR/SC) and Igs, are already widely distributed in 4-week-old embryos before the appearance of the common immune system. The whole complex of protein components of the SIS was seen in mucous layers, and in blood-tissue and tissue-tissue barrier structures. Therefore, we can consider two parts of the SIS: mucosal and barrier. Already in embryos, an increase in the functional activity of the SIS following massive antigenic attack in cases of acute chorioamnionitis reflects the increased exocrine secretion of Igs. The J chain appears to participate in the endocytosis but not exocytosis of Igs. J chain and Igs, but not pIgR/SC, were present in cells of the heart, endocrine glands, gonads and some other organs. The exocrine secretion of Igs, the main function of the SIS, is absent in these organs, and, they are therefore, not considered part of the SIS.
Embryonic Development↗
Feed and forage toxicants affecting embryo survival and fetal development.
Early embryonic and fetal development in mammals is sensitive to deficiencies and excesses of specific nutrients and toxicants. Operating directly and/or indirectly, these deficiencies and excesses can result in embryonic death or, in less severe circumstances, disruption of normal embryo and fetal growth. This paper explores the threats posed by feed and forage toxicants to the developing embryo and their impact on early programming of fetal development. Using significant examples, we consider the relevance of temporal sensitivities during early development in utero, and their implications for the morphology and functional competence of specific organs and tissues.
Animal Feed↗
Effects of exposure of a surfactant, polyoxyethylene(10)nonylphenyl ether (NP-10), to sperm on embryonic and fetal development in rabbits.
The effects of exposure of a surfactant, nonoxynol(NP-10), to sperm on embryonic and fetal development were studied using rabbits. In the preliminary test, the concentration of NP-10 at which total sperm immobility was 0.01% and nonfertilizing was 0.008% in vitro. No implantation was observed at the concentration of 0.032% NP-10 in vivo. Based on these results, the rabbit semen was treated either with 0.04, 0.01 or 0.0025% NP-10 solution, and used for artificial insemination to examine if the sperm was fertile as well as to determine the effect of NP-10-treated sperm on embryonic and fetal development. Gestation was not observed after insemination with semen treated with 0.04% NP-10; after insemination with semen treated with 0.01 and 0.0025% NP-10, it occurred without impairing the viability, organogenesis or growth of embryos or fetuses. These results may indicate that gestation may not be possible with sperm severely impaired by exposure to NP-10, but no untoward effect on embryonic or fetal development may be observed when gestation is initiated with exposed semen.
Animals↗
Localization of type I human skin collagenase in developing embryonic and fetal skin.
Type I human skin collagenase (HSC-1) was localized in developing embryonic and fetal skin ranging from 6 to 20 weeks estimated gestational age using an antigen-specific, affinity-purified, polyclonal antiserum to HSC-1 and an avidin-biotin alkaline phosphatase procedure. Double immunolabeling with monoclonal antibodies for Factor VIII-related antigen, type IV collagen, and the 68-kilodalton neurofilament subunit was performed using a direct peroxidase procedure. By 8 weeks estimated gestational age, HSC-1 localized to the periderm, the basal cell epidermal keratinocytes, dermal fibroblasts, and surrounding extracellular matrix. At 12 weeks estimated gestational age, HSC-1 immunolabeling showed a continued association with the epidermis and dermis. Dermal and subcutaneous blood vessels and the surrounding extracellular matrix were positive for HSC-1 labeling. HSC-1 staining was also found around developing nerves and in association with dermal fibroblasts. In the developing hair follicle, HSC-1 was present in keratinocytes of the pre-germ, germ, hair peg, and bulbous hair peg. HSC-1 immunoreactivity was also found in association with the hair canal, the bulge, and the dermal papillae, but was absent from the fetal sebaceous gland. These data demonstrate the association of HSC-1 with the development of interfollicular epidermis, the dermal collagenous matrix, the process of angiogenesis, the development of nerves, and hair follicle morphogenesis.
Antibodies, Monoclonal↗
Distribution of osteonectin mRNA and protein during human embryonic and fetal development.
We investigated the temporal and spatial distribution of osteonectin during human embryonic and fetal development, using in situ hybridization and immunohistochemistry. Osteonectin gene expression was generally found in cells exhibiting high rates of matrix production/proliferation. In mineralized tissue, a strong signal was obtained in osteoblasts, odontoblasts, and chondrocytes of the upper hypertrophic and proliferative zones. Chondrocytes of the mineralized zone showed no expression throughout the different stages of development. Strong osteonectin expression was found in odontoblasts of developing teeth. In addition, osteonectin mRNA and protein were detected in several non-mineralized tissues: steroid-producing cells of the adrenal gland and the gonads, kidney (glomeruli), lung (bronchi), skin, megacaryocytes, and large vessels. Histochemistry confirmed the results and detected extracellular osteonectin in bone and in the zone of mineralized cartilage only. The localization of osteonectin in bone, cartilage, and teeth is consistent with a role in the initiation of mineralization. However, the organ-specific distribution in non-mineralized tissues suggests an important multifunction role of this protein during human development.
Abortion, Spontaneous↗
Disruption of embryonic and fetal development due to preimplantation chemical insults: a critical review.
Descriptive teratology has developed several fundamental precepts, two of which can now be challenged on the basis of experimental evidence. The first is that prior to implantation the developing embryo is not susceptible to survivable defects from chemical injury. The second is that developmental defects cannot be due to mutational events since rare events seem unlikely to explain alterations in large populations of cells. This review presents current experimental evidence demonstrating that the effects of chemical exposure on blastocyst stage embryos may be manifest long after the time of insult and that subtle nonlethal mutations may have a role in poor fetal performance after early chemical exposures.
Animals↗
How does maternal diabetes disrupt embryonic and fetal development?
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Embryo, Mammalian↗
Assessing the effects of low boron diets on embryonic and fetal development in rodents using in vitro and in vivo model systems.
To date, boron (B) essentiality has not been conclusively shown in mammals. This article summarizes the results of a series of in vitro and in vivo experiments designed to investigate the role of B in mammalian reproduction. In the first study, rat dams were fed either a low (0.04 microg B/g) or an adequate (2.00 microg B/g) B diet for 6 wk before breeding and through pregnancy; reproductive outcome was monitored on gestation day 20. Although low dietary B significantly lowered maternal blood, liver, and bone B concentrations, it had no marked effects on fetal growth or development. The goal of the second study was to assess the effects of B on the in vitro development of rat postimplantation embryos. Day 10 embryos collected from dams fed either the low or adequate B diets for at least 12 wk were cultured in serum collected from male rats exposed to one of the two dietary B treatments. Dams fed the low B diet had a significantly reduced number of implantation sites compared to dams fed the B-adequate diet. However, embryonic growth in vitro was not affected by B treatment. The aim of study 3 was to define the limits of boric acid (BA) toxicity on mouse preimplantation development in vitro. Two-cell mouse embryos were cultured in media containing graded levels of BA (from 6 to 10,000 microM). Impaired embryonic differentiation and proliferation were observed only when embryos were exposed to high levels of BA (>2000 microM), reflecting a very low level of toxicity of BA on early mouse embryonic development. Study 4 tested the effects of low (0.04 microg B/g) and adequate (2.00 microg B/g) dietary B on the in vitro development of mouse preimplantation embryos. Two-cell embryos obtained from the dams were cultured in vitro for 72 h. Maternal exposure to the low B diet for 10, 12, and 16 wk was associated with a reduction in blastocyst formation, a reduction in blastocyst cell number, and an increased number of degenerates. Collectively, these studies support the concept that B deficiency impairs early embryonic development in rodents.
Animals↗
[Effect of cefuroxime on embryonic and fetal development in an experiment].
The direct and indirect effects of cefuroxime on the embryo and fetus were studied in vitro and in vivo at different gestation times. The placenta, liver and kidneys of the mother and fetus were investigated morphologically. It was shown that in a dose of 250 mg/kg the antibiotic did not induce disorders in the fetus development. The histological examination of the fetus placenta and liver revealed no changes as compared to the controls. However, in the renal tubules of the mother and fetus, pathological lesions in the form of the cytoplasm granular degeneration and nucleus swelling, lysis and necrosis were observed. These lesions were of a dose-dependent character. The possible nephrotoxic effect of cefuroxime prevents its use as a drug of choice in treatment of gestation pyelonephritis.
Abnormalities, Drug-Induced↗
Nutrition in embryonic and fetal development.
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Embryonic and Fetal Development↗
Embryonic and fetal development in a commercial dam-line genotype.
During depopulation of a breeding unit within Swine Graphics Enterprises, extensive data were collected and used to examine relationships among ovulation rate, the pattern of prenatal loss, and placental and fetal development. Groups of Large White x Landrace females (n=447) were slaughtered between day 20-30, 50-55 or 85-90 of gestation, with approximately equal numbers of animals representing gilts and parity 1 (G/P1), parity 2-3 (P2/3), and parity >4 (P4+). Ovulation rate and embryo number were recorded for all animals. With the exception of the G/P1 animals, embryonic and placental weight were recorded for four conceptuses per sow on day 20-30; on day 85-90 two conceptuses per sow were dissected to determine placental and fetal development. Ovulation rate (22.7 +/- 0.2 overall) was higher (P <0.05) in P2/3 (23.6 +/- 0.4) and P4+ (24.7 +/- 0.4) than in G/P1 (20.2 +/- 0.5). Embryonic/fetal survival was 61.8 +/- 2.1% at day 20-30, 50.2 +/- 2.2% at day 50-55 and 48.7 +/- 1.9% at day 85-90 and the number of surviving conceptuses was higher (P <0.05) in the P2/3 sows than in other parity groups. There was no relationship between ovulation rate and number of live embryos at day 20-30 or 85-90. At day 20-30 and 85-90, embryo weight was positively correlated with placental weight, but neither placental weight nor embryonic/fetal weight was correlated with number of viable embryos. A parity by gestation day interaction existed; placental weight for P4+ (3.42 +/- 0.43 g) was less than for P2/3 (7.55 +/- 0.40 g) at day 20-30 (P <0.0001), whereas at day 85-90, placental weight of P2/3 (209.5 +/- 8.5 g) was less (P=0.05) than both G/P1 (235.7 +/- 7.3g) and P4+ (235.4 +/- 7.1 g). At day 85-90, fetal brain weight, relative to body weight (R2=0.61, P <0.0001), and fetal brain:liver weight ratio (R2=0.35; P <0.0001) were negatively related to mean fetal weight, and brain:liver weight ratio showed a trend towards a relationship with number of viable fetuses (P=0.08). Parity also affected brain:liver weight ratio (P=0.01). Clearly, high ovulation rates in the higher parity sows have the potential to cause excessive in utero crowding of conceptuses in the post-implantation period. Even with moderate crowding, increased brain:liver weight ratios in smaller fetuses in late gestation indicate that uterine capacity impacts fetal development as well as the number of surviving fetuses.
Animals↗
Embryonic and fetal development: fundamental research.
Much progress has been made over the past decades in the development of in vitro techniques for the assessment of chemically induced effects in embryonic and fetal development. In vitro assays have originally been developed to provide information on the mechanism of action of normal development, and have hence more adequately been used in fundamental research. These assays had to undergo extensive modification to be used in developmental toxicity testing. The present paper focuses on the rat whole embryo culture system, but also reviews modifications that were undertaken for the in vitro chick embryo system and the aggregate cultures of fetal rat brain cells. Today these tests cannot replace the existing in vivo developmental toxicity tests. They can, however, be used to screen chemicals for further development or further testing. In addition, these in vitro tests provide valuable information on the mechanisms of developmental toxicity and help to understand the relevancy of findings for humans. In vitro systems, combined with selected in vivo testing and pharmacokinetic investigations in animals and humans, can thus provide essential information for human risk assessment.
Animals↗