The effect of ethanol exposure on extraembryonic vascular development in the chick area vasculosa
| Autor: | A. Cevik Tufan, N. Lale Satiroglu-Tufan |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Reactive oxygen species metabolism
cell infiltration alpha-Tocopherol Chick Embryo reactive oxygen metabolite alpha tocopherol Mesoderm chemistry.chemical_compound angiogenesis ?-Tocopherol Fetal alcohol syndrome Pregnancy dose response Vasculogenesis retinoic acid oxidative stress mesenchyme cell Growth Substances statistical significance alcohol messenger RNA drug effect article Embryo Cell Differentiation Up-Regulation Vascular endothelial growth factor Survival Rate Dose–response relationship priority journal embryonic structures sodium chloride immunohistochemistry Female Anatomy Organ Culture Technique Animals Blood Vessels/*abnormalities/*drug effects/pathology Cell Differentiation/*drug effects/genetics Chick Embryo/*drug effects/growth & development/pathology Dose-Response Relationship Drug Drug Administration Schedule Ethanol/*toxicity Growth Substances/genetics Humans Mesoderm/cytology/drug effects/metabolism Neovascularization Physiologic/*drug effects/physiology Organ Culture Techniques Oxidative Stress/drug effects/genetics RNA Messenger/drug effects medicine.medical_specialty Validation study animal structures Histology chicken embryo growth retardation Neovascularization Physiologic Tretinoin Biology All-trans-retinoic acid animal tissue α-Tocopherol Internal medicine medicine Reaction Time controlled study RNA Messenger tissue culture nonhuman Ethanol vasculotropin Ethanol exposure embryo development mortality Oxidative Stress Endocrinology chemistry exposure gene expression Northern blotting Blood Vessels Reactive Oxygen Species |
| Zdroj: | Cells, tissues, organs. 175(2) |
| ISSN: | 1422-6405 |
| Popis: | The effect of ethanol (EtOH) exposure on extraembryonic vascular development was examined using the chick embryo area vasculosa (AV) in shell-less culture. Embryos were placed in cultures at Hamburger Hamilton (HH) stage 11/12 and a single dose of EtOH (10, 30 or 50%) was applied to the center of the blastodisc. Untreated/sodium-chloride-treated controls showed normal embryonic growth and well-developed extraembryonic vessels at 24/48 h of treatment. At doses of 30 and 50%, the mortality rate was significantly increased, and survivors demonstrated significant growth retardation and inhibition of normal vascular development in a dose-dependent manner. Immunostaining for vascular endothelial growth factor (VEGF) showed that mesenchymal cells continued to differentiate into angioblasts to form blood islands, but their assembly into primitive vessels was perturbed in a dose-dependent manner. Northern blot analyses of basic fibroblast growth factor, VEGF, Flt-1 and Flk-1 mRNA expression supported these findings and showed a dose-dependent decrease in EtOH-treated cultures compared to controls. Co-treatment with α-tocopherol (0.05 M) or all-trans-retinoic acid (10–8M) significantly decreased the mortality rate and improved both embryonic growth and extraembryonic vascular development in the cultures. On the other hand, almost all embryos treated with 10% EtOH survived the first 48 h after treatment. However, the complexity of the vascular tree measured as the relative vasculogenesis index, the surface area of the AV and the mRNA expression of vasculogenic molecules were increased during the first 24 h. This acute effect disappeared 48 h after treatment and the vascular tree continued to develop parallel to the controls. No significant growth retardation was observed in this group. These results suggest that, in terms of extraembryonic vascular development, an early, single, low-dose EtOH exposure may have an acute, short-term positive effect, whereas moderate- or high-dose EtOH exposure may severely perturb this process disabling the necessary absorption of the nutrients for the embryo to develop properly. The mechanisms of action of EtOH on extraembryonic vascular development may involve the establishment of reactive oxygen species, resulting in the initiation of oxidative stress and perturbation of retinoic acid signaling and alterations in the expression of growth-regulatory vasculogenic factors and their receptors. |
| Databáze: | OpenAIRE |
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