Teratogenicity of Ethanol in Different Chicken Strains

Becker, Stephanie R. Bupp; Shibley, Ivan A.

doi:10.1093/alcalc/33.5.457

Cited by 42 publications

(26 citation statements)

References 28 publications

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“…Although few of the environmental causes and none of the genetic factors have been fully identified in humans so far, numerous teratogens and nutritional factors have been suggested as possible causes. Exposure to chemicals is one of the known reasons for disorders related to nonclosure of the neural tube (3,5,(10)(11)(12). This critical period is the first month of pregnancy and it is known as gastrulation.…”

Section: Discussionmentioning

confidence: 99%

“…Stage eight embryos were generally chosen for these investigations since developing neural tissues exhibit a gradual variation on the degree of opening along its length that provides an excellent opportunity to study the effect of chemical agents on neural tube closure. Numerous chemical agents such as caffeine, phenytoin, alcohol, diazepam, methotrexate, meloxicam, and local anesthetics are known to cause NTDs in chick embryos (3,5,(10)(11)(12)(13). It is recently known that reactive oxygen species (ROS) are systemically increased upon certain stress factors such as excess glucose and aforementioned chemical agents which consequently interfere with cellular signaling pathways and expression of genes required for neural tube closure (6).…”

Section: Discussionmentioning

confidence: 99%

“…Oxidative stress triggers an acute inflammatory reaction locally in the airways with the potential to up-regulate systemic inflammatory processes. Moreover, particles can cross barriers into the circulation and may directly interact with tissues to cause effects at various sites (1)(2)(3)(4)(5)(6)(7)(10)(11)(12)(13)15,16,20,24).…”

Section: A B C Dmentioning

confidence: 99%

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The effects of diesel exhaust particles on neural tube development in the early stage chicken embryo

Şimşek

Çolak²,

Kaya³

et al. 2011

Turkish Neurosurgery

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AIm: Particulate matter is an important air-pollutant and its toxicity has been reported. Diesel exhaust particles (DEP) constitute a large portion of particulate matter. Therefore, we established our study to investigate the effects of DEP on neural tissue in early stage chicken embryos. mAterIAl and methOds: Four study groups and one control group, each of which included 24 objects were designed. Eggs were incubated for 30 hours. Solutions of DEP containing 10, 50, 100, and 200 µg/0.1 ml were prepared with serum saline. At the end of thirty hours diesel exhaust particle solutions were administered under the embryonic discs. After 72nd hour of the incubation, embryos were excised and evaluated macroscopically and histopathologically. results:The difference between the embryos that were defined as poorly and well developed, was found statistically significant (p<0.05). Neural tube defects were detected in 16 of 104 embryos. Statistically significant association between the administration of DEP and development of neural tube defect was identified (p=0.037).COnClusIOn: Thus, the direct neurotoxic effects of DEP, which the whole population encounters inevitably, have been shown in the early stages of embryonic development. Further studies are needed to identify the effects of these particles in the later stages of embryonic development. BulGulAr: Embriyolar arasındaki fark istatistiksel olarak anlamlı bulundu (p<0.05). 104 embriyonun 16 adedinde nöral tüp defekti saptandı. Tüm gruplarda dizel parçacığı verilmesiyle nöral tüp defekti gelişmesi arasında istatistiksel anlamlı ilişki bulundu (p=0.037). KeywOrdssOnuÇ: Böylece, kaçınılmaz şekilde tüm toplumun maruz kaldığı dizel egzoz parçacıklarının embriyonel gelişimin erken dönemlerinde doğrudan nörotoksik etkileri gösterildi. Bu parçacıkların embriyolojik gelişimin sonraki dönemlerindeki etkilerinin ortaya konabilmesi için ileri çalışmalara ihtiyaç vardır.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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The effects of diesel exhaust particles on neural tube development in the early stage chicken embryo

Şimşek

Çolak²,

Kaya³

et al. 2011

Turkish Neurosurgery

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“…Mouse [9], rat [10] and chick [11][12][13][14][15] embryos have been extensively used as models to address the mechanisms underlying the teratogenic effects of ethanol in various systems.…”

Section: Introductionmentioning

confidence: 99%

Ethanol exposure leads to disorder of blood island formation in early chick embryo

Wang

Chen

Wang

et al. 2017

Reproductive Toxicology

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exposure leads to disorder of blood island formation in early chick embryo.Reproductive Toxicology http://dx.doi.org/10. 1016/j.reprotox.2017.08.003 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. 2,2′-azobis-amidinopropane dihydrochloride, a ROS inducer, which gave a similar anti-vasculogenesis effect as ethanol and this anti-vasculogenesis effect could be reversed by vitamin C. Overall, exposing early chick embryos to ethanol represses blood island progenitor cell migration but disturbed differentiation at a different stage, so that the disorder of blood island formation occurs through excess ROS production and altered vascular-associated gene expression.

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“…This model has been well validated for studies on both blood vessel development [Stewart et al, 1990;Allen and Wilson, 1993;Hoper and Jahn, 1995;Ribatti et al, 1996;Giles and Bannigan, 1999;Hoper et al, 1999;Last and Bannigan, 2001] and FAS [Bupp and Shibley, 1998;Illanes et al, 1999;Cavieres and Smith, 2000;Debelak and Smith, 2000;Roda-Moreno et al, 2000;Miller et al, 2001;Su et al, 2001]. It has the advantage of allowing direct and continuous observation of all stages of vascular development and proper functioning of the cardiovascular system in the same embryo [Flamme et al, 1993].…”

Section: Introductionmentioning

confidence: 99%

The Effect of Ethanol Exposure on Extraembryonic Vascular Development in the Chick Area Vasculosa

Tufan

Şatıroğlu-Tufan

2003

Cells Tissues Organs

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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.

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Teratogenicity of Ethanol in Different Chicken Strains

Cited by 42 publications

References 28 publications

The effects of diesel exhaust particles on neural tube development in the early stage chicken embryo

The effects of diesel exhaust particles on neural tube development in the early stage chicken embryo

Ethanol exposure leads to disorder of blood island formation in early chick embryo

The Effect of Ethanol Exposure on Extraembryonic Vascular Development in the Chick Area Vasculosa

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