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PubMed2001

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) inhibition of coronary development is preceded by a decrease in myocyte proliferation and an increase in cardiac apoptosis.

BACKGROUND: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) causes cardiovascular toxicity, culminating in edema, hemorrhage, and mortality in piscine, avian, and mammalian embryos. To elucidate the mechanism of the cardiovascular teratogenicity of TCDD, we used a chick embryo model to determine whether TCDD alters coronary artery development and whether this alteration was associated with apoptosis and/or changes in myocyte proliferation. METHODS: Fertile chicken eggs were injected with corn oil (control), 0.24, or 0.40 pmol TCDD/g in corn oil before incubation. To evaluate effects of TCDD on differentiation of coronary arteries, chick embryo hearts from incubation days 8 (D8), D10, and D12 were stained with anti-alpha-smooth muscle actin. Myocyte proliferation was measured by BrdU incorporation on D6, 8, 10, and 12 after TCDD treatment. In addition, temporal and spatial patterns of apoptosis were detected by TUNEL on D3, D5, D6, D8, and D10, and immunohistochemistry was used to identify the origin of apoptotic cells on D6. RESULTS: TCDD increased apoptosis in structures where cell death normally occurs, including the outflow tract, endocardial cushion of the atrioventricular canal, and dorsal mesocardium, peaking in intensity on D6. Immunohistochemistry revealed that cells undergoing TCDD-induced apoptosis in the dorsal mesocardium were not neural or epicardial in origin. On D8 and D10 TCDD reduced myocyte proliferation. On D10, TCDD reduced coronary artery size and on D10 and D12 TCDD induced a dose-dependent decrease in coronary artery number. CONCLUSIONS: The reduction of myocyte proliferation by TCDD preceded the reduction in coronary artery number and size, suggesting that changes in coronary development may be a consequence of reduced myocyte proliferation and a thinner ventricle wall. The peak of TCDD-induced increase in apoptosis occurred even earlier in embryo development and thus may contribute to changes in myocyte proliferation, coronary development, and cardiac structural malformations; however, a cause-and-effect relationship between apoptosis and these other events has yet to be established.

Actins↗

PubMed1990

The avian embryo as a model for early developmental endocrinology.

Studies utilizing the developing chicken embryo have significantly augmented our understanding of the ontogeny of endocrine regulation during major critical periods of embryonic development. These embryos currently provide the only available models for elucidating the onset of endocrine function during all stages of in situ amniote development, for examining chronic calcium deficiency during embryogenesis, and for experiments in basic renal function during periods when only the mesonephros is normally functioning, as well as mixed meso/metanephric function and solely metanephric kidney function.

Animals↗

PubMed2000

Acute hypoxic hypoxia transiently reduces GABA(A) binding site number in developing chick optic lobe.

The Central Nervous System is known to be critically affected in the prenatal-perinatal period by hypoxic-ischemic insults, which produce several disorders such as loss of neural projections, increased susceptibility to seizures, apoptosis and an imbalance in normal activity of glutamatergic and GABAergic neurones, resulting in acute cell excitotoxicity. The aim of the present work was to establish a chick embryo model of normobaric acute hypoxic hypoxia as well as to evaluate modifications in GABA(A) receptor complex from chick optic lobe, that may result from this injury. Fertile chicken (Gallus gallus domesticus) eggs from White Leghorn were incubated and at embryonic days (ED) 12 to 18, subjected to a stream of 8%O(2)/92%N(2) during1 h, and then were either returned to their shelves in the incubator for recovery, or immediately processed for biochemical studies. Hypoxic treatment produced a significant age dependent reduction in GABA binding sites showing the greatest decrease at the earliest stages studied (ED12-ED16). Saturation curves of GABA binding performed at ED12 showed a decrease in B(max), (control, 5.48+/-0.20, hypoxic, 3.90+/-0.39 pmol/mg protein), but no significant change in K(d). Following 48 h in normoxic atmosphere post-hypoxia reduction in [3H]GABA binding was reversed. Pharmacological properties of GABA(A) receptor at ED12 showed that positive allosteric modulation effects of the steroid 3alpha-hydroxy-5alpha-pregnan-20-one and the barbiturate pentobarbital sodium were enhanced by the treatment. This model of acute prenatal hypoxic hypoxia produced marked alterations in inhibitory CNS neurotransmission that proved reversible and age dependent.

Acute Disease↗

PubMed2001

Endocrine disrupting compounds: effect of octylphenol on reproduction over three generations.

With the growing concern that environmental chemicals might impair human and animal fertility, it is important to investigate the possible influence of these substances on sexual differentiation and genital development of mammals. Many of these substances are suspected to interfere with endocrine processes, and exposure during critical periods of prenatal development might affect reproductive performance over several generations. Alkylphenols and their metabolites are lipophilic substances exerting apparent estrogenic action in in vitro and in vivo testing systems. With the widespread industrial use of alkylphenols, these are disseminated in the environment with sewage sludge, and domestic animals and humans are likely to be exposed via the food chain. Using the pig as an in vivo model, we studied the effect of intrauterine exposure to tertiary octylphenol (OP) on essential reproductive parameters over 3 generations. Sows were treated daily from D 23 to 85 of pregnancy with either 0, 10 or 1000 micrograms OP/kg body weight. Treatment with OP extended pregnancy length and induced basal cell proliferation in the cervical epithelium of the parental generation. In F1 offspring of sows treated with the low dosage of OP, onset of puberty was accelerated. Furthermore, when F1 gilts and F1 boars originating from sows treated with high dosages of OP were bred, the litter size was reduced. The results of the present study are compared with previous reports on estrogenicity of OP, and the usefulness of in vivo animal or embryo models for the evaluation of possible consequences of human exposure to endocrine disrupting compounds is discussed. Furthermore, possible consequences of exposure to endocrine disrupting compounds for the embryo transfer industry are addressed.

Animals↗

PubMed1981

Effect of siderophores on virulence of Neisseria gonorrhoeae.

The virulence of Neisseria gonorrhoeae for chicken embryos can be modified in a predictable manner by the addition of microbial siderophores to the inoculum. "Meningobactin" and "gonobactin," siderophores isolated from iron-limited cultures of meningococci and gonococci, respectively, enhance the virulence of the relatively avirulent colony type 3 (T3) organisms, but have essentially no effect on the virulence of T1 organisms. Both of these compounds were found previously to stimulate in vitro growth of the pathogenic Neisseria spp. under conditions made iron limiting by the addition of conalbumin, the transferrin counterpart of chickens. Similarly, ferrated schizokinen and arthrobactin, both dihydroxamate siderophores which stimulated growth in iron-limited conditions in vitro, also enhanced virulence of T3 organisms, whereas desferrioxamine B mesylate (Desferal), a trihydroxamate previously shown to be inhibitory in vitro, decreased the virulence of the T1 colony form. This was due to the iron-binding function of the molecule, as the iron-saturated form, ferrioxamine B mesylate, did not affect virulence. An additional trihydroxamate siderophore, ferrichrome A, which was inactive on Neisseria spp. in either the deferri- or ferrated forms in vitro, likewise did not affect virulence in the chicken embryo model. The neisserial siderophores were more effective than the other microbial siderophores in enhancing virulence of T3 gonococci. The results add to the evidence that the ability to acquire iron is an important determinant of virulence.

Animals↗

PubMed2006

Combination therapy using aspirin-enhanced photodynamic selective drug delivery.

In photodynamic therapy (PDT), excitation of a drug by light leads to a cascade of biochemical processes that can cause closure of blood vessels. It has been observed clinically that significant short-term leakage from the irradiated vasculature can occur prior to vessel closure and blood flow stasis. In this paper we demonstrate in a chicken embryo model that this leakage can be significantly enhanced by the presence of the cyclo-oxygenase inhibitor, aspirin. We also observe that following this aspirin-enhanced leakage, blood vessels close as effectively as after PDT in the absence of aspirin. Consequently we propose that this PDT-induced aspirin-enhanced leakage can be used to locally deliver a drug for combination therapy. This is then demonstrated in the chicken embryo using Visudyne as a PDT agent in combination with aspirin and fluorescein isothiocyanate dextran 10 kDa as leakage indicator. The latter represents a hypothetical drug to be delivered in various kinds of combination therapy. Two examples of this procedure would be the photodynamic treatment of choroidal neovasculature associated with exudative age-related macular degeneracy (AMD) where local delivery of an anti-angiogenic or an anti-inflammatory drug has been shown to be effective, or PDT of cancer where local dosing of a chemotherapeutic drug may well increase the treatment efficacy.

Animals↗

PubMed2006

Virulence phenotyping and molecular characterization of a low-pathogenicity isolate of Listeria monocytogenes from cow's milk.

A low-pathogenicity isolate of Listeria monocytogenes from cow's milk, as screened in mouse and chicken embryonated egg models, was examined for virulence-related phenotypic traits. Corresponding virulence genes (iap, prfA, plcA, hly, mpl, actA, plcB, InlA and InlB) were compared with L. monocytogenes reference strains 10403S and EGD to elucidate the possible molecular mechanisms of low virulence. Although L. monocytogenes H4 exhibited similar patterns to strain 10403S in terms of hemolytic activity, in vitro growth and invasiveness and even had higher adhesiveness, faster intracellular growth and higher phospholipase activity in vitro, it was substantially less virulent than the strain 10403S in mouse and chicken embryo models (50% lethal dose: 10(8.14) vs. 10(5.49) and 10(6.73) vs. 10(1.9), respectively). The genes prfA, plcA and mpl were homologous among L. monocytogenes strains H4, 10403S and EGD (>98%). Genes iap, hly, plcB, InlA and InlB of L. monocytogenes 10403S had higher homology to those of strain EGD (>98%) than isolate H4. The homology of the gene hly between strain 10403S and isolate H4 was 96.9% at the nucleotide level, but 98.7% at the amino acid level. The actA gene of isolate H4 had deletions of 105 nucleotides corresponding to 35 amino acid deletions falling within the proline-rich region. Taken together, this study presents some clues as to reduced virulence to mice and chicken embryos of the isolate H4 probably as a result of deletion mutations of actA.

Amino Acid Sequence↗

PubMed1989

Development of receptors for insulin and insulin-like growth factor-I in head and brain of chick embryos: autoradiographic localization.

In whole brain of chick embryos insulin receptors are highest at the end of embryonic development, while insulin-like growth factor-I (IGF-I) receptors dominate in the early stages. These studies provided evidence for developmental regulation of both types of receptors, but they did not provide information on possible differences between brain regions at each developmental stage or within one region at different embryonic ages. We have now localized the specific binding of [125I]insulin and [125I]IGF-I in sections of head and brain using autoradiography and computer-assisted densitometric analysis. Embryos have been studied from the latter part of organogenesis (days 6 and 12) through late development (day 18, i.e. 3 days before hatching), and the binding patterns have been compared with those in the adult brain. At all ages the binding of both ligands was to discrete anatomical regions. Interestingly, while in late embryos and adult brain the patterns of [125I]insulin and [125I] IGF-I binding were quite distinct, in young embryos both ligands showed very similar localization of binding. In young embryos the retina and lateral wall of the growing encephalic vesicles had the highest binding of both [125I]insulin and [125I]IGF-I. In older embryos, as in the adult brain, insulin binding was high in the paleostriatum augmentatum and molecular layer of the cerebellum, while IGF-I binding was prominent in the hippocampus and neostriatum. The mapping of receptors in a vertebrate embryo model from early prenatal development until adulthood predicts great overlap in any possible function of insulin and IGF-I in brain development, while it anticipates differential localized actions of the peptides in the mature brain.

Animals↗

PubMed1992

Possibility of separating toxins from bacteria associated with sudden infant death syndrome using anion exchange chromatography.

AIMS: To develop techniques for the characterisation of toxins elaborated by a strain of Escherichia coli associated with sudden infant death syndrome (SIDS). METHODS: E coli SIDS 04, isolated from the nasopharynx of a case of SIDS, was studied. Cell-free toxin preparations were standardised, their protein measured, and analytical separation of proteins achieved using sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE). Acetone precipitation of proteins was required prior to Coomassie blue staining of bands. Preparative separation was achieved on an anion exchange column using a programmed concentration gradient of NaCl in TRIS buffer. Fractions were tested individually or pooled for presence of lethal toxin including endotoxin. Lethal toxin was detected with the chick embryo test system. Endotoxin was measured using a chromogenic modification of the Limulus amoebocyte assay. RESULTS: Twenty one peaks were detected by chromatography. Ten individual, or pooled, fractions were assayed for endotoxin which ranged from 27-33 pg/ml. Much greater variation was found when the same fractions were assayed in chick embryos. E coli fractions varied considerably in lethal toxicity, from 0/10 to 10/10 chick embryos killed/tested. Certain E coli fractions tested individually (lethality four out of 10 to eight out of 10) proved more lethal (10 out of 10) if pooled prior to testing. CONCLUSIONS: In E coli infection associated with SIDS relatively low concentrations of extracellular protein are lethally toxigenic for the chick embryo model of SIDS. These proteins can be separated analytically by SDS-PAGE and preparatively by anion exchange chromatography. Toxicity of individual fractions is not correlated with endotoxin concentrations in samples tested.

Animals↗

PubMed1990

Arachidonic acid metabolism by dioxin-induced cytochrome P-450: a new hypothesis on the role of P-450 in dioxin toxicity.

Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD) is a highly potent inducer of cytochrome P-450. The role of the induced P-450 in TCDD toxicity has been obscure as P-450 neither detoxifies TCDD nor activates it to genotoxic or cytotoxic metabolites. We show, using a chick embryo model, that TCDD causes major increases in the NADPH dependent metabolism of arachidonic acid (AA), a predominant cell membrane fatty acid, that it does so with extremely high potency (ED50, 6.3 pmol per egg) and that this metabolism is catalyzed by TCDD-induced cytochrome P-450 species. Thus, TCDD treatment increased by six to ten fold the P-450 mediated hepatic microsomal metabolism of AA to epoxides and monohydroxyeicosatetraenoic acids, products whose diverse biological activities suggest links to TCDD's toxic effects. In contrast only x and x-1 hydroxy AA, inactive products, were significantly formed by the controls. These findings open a new perspective on how P-450 induction could be related to the diverse toxic effects of TCDD. They lead to the novel hypothesis that TCDD-induced cytochrome P-450 metabolizes an endogenous fatty acid to reactive products that in turn mediate or modulate varied manifestations of TCDD toxicity.

Animals↗

PubMed2004

Myogenic regulatory factors: redundant or specific functions? Lessons from Xenopus.

The discovery, in the late 1980s, of the MyoD gene family of muscle transcription factors has proved to be a milestone in understanding the molecular events controlling the specification and differentiation of the muscle lineage. From gene knock-out mice experiments progressively emerged the idea that each myogenic regulatory factor (MRF) has evolved a specialized as well as a redundant role in muscle differentiation. To date, MyoD serves as a paradigm for the MRF mode of function. The features of gene regulation by MyoD support a model in which subprograms of gene expression are achieved by the combination of promoter-specific regulation of MyoD binding and MyoD-mediated binding of various ancillary proteins. This binding likely includes site-specific chromatin reorganization by means of direct or indirect interaction with remodeling enzymes. In this cascade of molecular events leading to the proper and reproducible activation of muscle gene expression, the role and mode of function of other MRFs still remains largely unclear. Recent in vivo findings using the Xenopus embryo model strongly support the concept that a single MRF can specifically control a subset of muscle genes and, thus, can be substituted by other MRFs albeit with dramatically lower efficiency. The topic of this review is to summarize the molecular data accounting for a redundant and/or specific involvement of each member of the MyoD family in myogenesis in the light of recent studies on the Xenopus model.

Animals↗

PubMed2006

The expression of the NR1-subunit of the NMDA receptor during mouse and early chicken development.

It has been suggested that homocysteine-induced defects are mediated by the inhibition of the N-methyl-d-aspartate (NMDA) receptor on neural crest cells. However, the majority of this work has been performed using the chicken embryo model. In an effort to better understand the molecular events involved a murine model of homocysteine-induced defects was sought. However, it has been previously shown that homocysteine failed to induce congenital defects in several strains of mouse. Therefore, in an effort to better understand the difference in the susceptibility between these two species we investigated the ontogeny of the NMDA receptor in the mouse and chicken. To determine the expression of the NMDA receptor we performed Western blot analysis using an antibody to the NR1-subunit of the NMDA receptor in both the chicken and mouse embryos. Further, we used RT-PCR to determine the temporal expression of this subunit in the murine embryos from gestational day 8.5 to 18.5 to confirm our Western blot analysis. Results from these studies demonstrated that the expression of the NMDA receptor was expressed during the early stages of development in the chick embryo but neither the transcript nor the protein was detected in mouse embryos until later in development. These results demonstrate that during the stages of neurulation and/or early heart development the expression of the NR1-subunit of the NMDA receptor was not detected. The expression of this gene increased and was detectable by gestational days 14.5-15.5 and continued to increase in its expression until term. Therefore, these experiments suggest that homocysteine-induced defects may be mediated via the NMDA receptor.

Animals↗

PubMed1997

[Significance of glycosaminoglycans content in developing mechanism of cleft palate].

To explore significance of Glycosaminoglycans content in the development of embryo and forming mechanism of cleft palate, Dexamethason acetate was injected into the abdomen of NIH mouse on the 12th day of gestation to induce cleft palate mouse embryo model. Then by taking cranio-maxillary coronary sections, stained with Alcian blue/PAS and quantitatively analysing the area of the palatal process covered by glycosaminoglycans using a TDS-90 photodigital system with computer. Results indicate that on 13(12) day(hour) of gestation the colour of Alcian blue starts to show in the palatal process. By then, the area covered by glycosaminoglycans in the normal group is 4.69 mm whereas for the experimental group is 2.40 mm, showing a significant statistical difference (P < 0.05). The area of the palatal process covered by glycosaminoglycans gradually increases as the embryo developes, but is distinctly smaller in experimental than in the normal group (P > 0.05). This proves that there's a relationship between the level of glycosaminoglycans in the palatal process and development of cleft palates.

Animals↗

PubMed2006

EMAGE: a spatial database of gene expression patterns during mouse embryo development.

EMAGE (http://genex.hgu.mrc.ac.uk/Emage/database) is a freely available, curated database of gene expression patterns generated by in situ techniques in the developing mouse embryo. It is unique in that it contains standardized spatial representations of the sites of gene expression for each gene, denoted against a set of virtual reference embryo models. As such, the data can be interrogated in a novel and abstract manner by using space to define a query. Accompanying the spatial representations of gene expression patterns are text descriptions of the sites of expression, which also allows searching of the data by more conventional text-based methods.

Animals↗

PubMed1993

Comparative kinetics of embryo development.

A model of embryo energetics was fitted to data from the literature for species as different as snails and mammals. The model is based on assumptions about energy uptake, storage and utilization. It describes the animal by two state variables: volume and energy storage. Embryo weight is taken to be proportional to volume, yolk weight to energy storage, and respiration rate to storage utilization rate. The fits were good, with minor deviations occurring only in the early phases of development. For altricial birds, good model fits were obtained, but the parameter values markedly differed from those of other species. We hypothesized that, due to an increase in energy utilization towards hatching, the temperature of the embryo increases. As a result, metabolic processes are accelerated. When this was taken into account, parameter values were obtained that correspond better with those of other animals.

Animals↗

PubMed1999

Polychlorinated biphenyls (PCBs) selectively disrupt serotonergic cell growth in the developing Spisula embryo.

Polychlorinated biphenyls (PCBs) are ubiquitous environmental contaminants that exert neurotoxic effects during embryonic development. The present study demonstrates that early embryonic exposure to a mixture of PCBs (Aroclor 1254) results in a decrease in serotonergic cell growth. Using a novel, marine invertebrate embryo model, Spisula solidissima, immunocytochemistry, and confocal microscopy techniques, a dose-dependent decrease in serotonergic cell number was quantified within 24 h of exposure. This effect was seen with doses as low as 1 ppm Aroclor 1254. These findings demonstrate that environmentally relevant doses of Aroclor 1254 impair development of the serotonergic nervous system.

Animals↗

PubMed1994

JM9 strains, a new type of group B streptococci from Japan.

JM9 strains isolated from human carriers and patients in several districts of Japan, represent a new serotype of group B streptococci (GBS, Streptococcus agalactiae). They were first detected in 1983 but are meanwhile prevailing among all other GBS serotypes in Japan. Outside of Japan, strains of this type have not been reported until now. In the present work, N-acetylneuraminic acid was detected in all strains investigated, by chemical analysis as well as by interaction with a sialic acid-binding lectin. This component is characteristic of all analyzed GBS type polysaccharides. In a chicken embryo model, all strains exhibited a very strong virulence. Examination of the antibiotic sensitivity revealed that all strains were susceptible to penicillin, cephalothin, clindamycin, mezlocillin, azlocillin, erythromycin, methicillin, chloramphenicol, tetracyclin, oxacillin and sulfamethoxazole/trimethoprim, whereas all strains were resistant against gentamicin, kanamycin and neomycin. Electron microscopic studies revealed for these strains relatively small capsules but unusually thick cell walls. By immunogold labelling, the type polysaccharide, the group polysaccharide, the lipoteichoic acid and in some strains, the protein R were localized.

Animals↗

PubMed2005

Toxicological effects of mainstream whole smoke solutions on embryonic movements of the developing embryo.

Cigarette smoking is unrivaled among developmental toxicants in terms of total adverse impact on the human population. Maternal tobacco use during pregnancy adversely affects prenatal and postnatal growth and increases the risk of behavioral and developmental defects in children and adolescents. In the current study, the effects of different preparations of nicotine and mainstream whole smoke solutions (MSWSS) on embryonic movements during neonatal development were examined in vivo, using the chicken embryo model, recorded in real-time by a video camera. It was observed that low doses of nicotine induced hyperactivity and higher doses induced hypoactivity. Accordingly, a significant (p < 0.01) decrease in movements was observed by application of 10 microg of nicotine and different preparations of MSWSS. A dose-dependent decrease in embryonic movements was observed, which did not recover by the end of experiment. It was concluded that nicotine could alter embryonic movements, which are important during embryogenesis for differentiation and maturation of the body systems.

Animals↗