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TEM through the cerebellar Purkinje cells at 16th day of incubated eggs of chick embryo of control group (A-A2) and nicotine treated group (B-B7). M: mitochondria, RER: rough endoplasmic reticulum, NG: Nissl granules, G: Golgi bodies. EH: euchromatin, HH: heterochromatin. The arrows refer to the separation of two nuclear membranes, lipofuscin, V: vacuoles, VM: vacuolated mitochondria, IG: irregular grooves, NP: nuclear pyknosis, ANG: aggregated Nissl granules. The cisternal fragmentation of Golgi bodies (star) 4000×.
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Long-acting nicotine is known to exert pathological effects on almost all tissues including the cerebellar cortex. The present work was designed to elucidate the effect of nicotine on the development of cerebellar cortex of chick embryo during incubation period.
The fertilized eggs of hen (Gallus gallus domesticus) were injected into the air space...
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Context 1
... shown in Fig. 5 and Table 1; the mean percentage of cerebellar apoptosis for all stages of nicotine treated group was significantly (P < 0.001) lower than that of control groups. Also, in control group the ratio of apoptosis in 16th day chick embryo was significantly (P < 0.001) higher than that of the other two stages (8th, 12th days) (Fig. ...
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Citations
... Nicotine affects the fertility rate, it alters the morphology of oocytes resulting in mitochondrial alterations, and disrupts fetal development [3,6]. This highly addictive, toxic alkaloid compound is dangerous not only to adults, but to a developing fetus, infants, children, and adolescents [3,7]. Nicotine affects the fertility rate, it alters the morphology of oocytes resulting in mitochondrial alterations, and disrupts fetal development [3,6]. ...
... Initially, nicotine stimulates the brain and then inhibits it, and when it is consumed during pregnancy it compromises the brain and its neural pathway's development [42]. In chicken embryos, nicotine was found to inhibit this ODC activity, and dose-dependently cause paralleled reductions in embryo size and brain weight [23,41,42], and a decrease in head size, and trunk diameter [7]. Nicotine-treated embryos had correlated reductions of glucose and Glut 1 55 kilodalton isoform concentrations in the developing brain but produced no changes to the level of Glut 3 transporter proteins [42]. ...
... Nicotine exposure also resulted in a reduction in mature Purkinje cells, the largest neuronal cells in the cerebellar cortex [7]. During the fourth day of incubation, the cerebellum in the chicken embryo begins to undergo a series of segmentation. ...
Background: Studies have shown that 22.3% of the world's population use tobacco and nicotine exposure during pregnancy remains a concern in embryonic development. Cigarette smoke contains several toxic and carcinogenic chemicals and has been known to cause pregnancy complications including premature births, low birthweights, and stillbirths. Purpose: This review aims to study nicotine exposure in chicken embryo development comprehensively. Methods: PubMed, Centers for Disease Control and Prevention (CDC), and Antpedia sites were used to search for studies using chicken embryos as a model. Studies that reported findings on nicotine's effects on various developmental processes were considered for this review. Conclusion: In total, 55 published articles were included in this review to discuss findings of nicotine-induced alterations during chicken embryo development. Findings have shown that nicotine affects angiogenesis, and embryonic and chorioallantoic membrane (CAM) growth by inhibiting cell proliferation. Nicotine affects brain and cerebellar cortex development by suppressing tumor protein p53 reactions. Nicotine also causes abnormal axial rotation and incomplete formation and closure of neural tubes. The compounds like green tree extract, vitamin C, and folic acid can reduce the effects of nicotine to suppress femur growth, decrease the contractility of cardiomyocytes, and reduce survival rates. These compounds are not protective measures to completely overcome the teratogenic effects of nicotine.
... While many teratogens have been identified that are known to cause birth defects, how they cause the birth defects has remained unclear. Given the advantages of the chicken embryo, many teratogenic agents mechanistic bases have begun to be identified and include thalidomide, valproic acid, alcohol, cocaine, nicotine, retinoic acid and cadmium just to mention a few (Wiens et al., 1992;Venturini and Sparber, 2001;Cullinane et al., 2009;Therapontos et al., 2009;Ito et al., 2010;Hsieh et al., 2012;Yamamoto et al., 2012;El-Beltagy et al., 2015). Understanding the mechanisms of teratogenicity of a factor can shed light on the biological action of the compound as well as how it causes congenital anomalies, which can lead to potential ways of making safer drugs. ...
Congenital anomalies and its causes, particularly, by external factors are the aim of the field called teratology. The external factors studied by teratology are known as teratogens and can be biological or environmental factors for example, chemicals, medications, recreational drugs, environmental pollutants, physical agents (e.g., X-rays and maternal hyperthermia) and maternal metabolic conditions. Proving the teratogenicity of a factor is a difficult task requiring epidemiology studies as well as experimental teratology evidence from the use of animal models, one of which is the chicken embryo. This model in particular has the advantage of being able to follow development live and in vivo, with rapid development hatching around 21 days, is cheap and easy to manipulate and to observe development. All this allows the chicken embryo to be used in drug screening studies, teratogenic evaluation and studies of mechanisms of teratogenicity. The chicken embryo shares morphological, biochemical and genetic similarities with humans as well as mammalian species, making them ideal to ascertain the actions of teratogens, as well as screen drugs to test for their safety. Pre-clinical trials for new drugs are carried out in rodents and rabbits, however, chicken embryos have been used to screen new compounds or analogs of thalidomide as well as to investigate how some drugs can lead to congenital malformations. Indeed, the chicken embryo has proved valuable in understanding how many congenital anomalies, seen in humans, arise following teratogen exposure. The aim of this review is to highlight the role of the chicken embryo as an experimental model for studies in teratology, exploring its use in drug screening studies, phenotypic evaluation and studies of teratogenic mechanisms of action. Here, we discuss many known teratogens, that have been evaluated using the chicken embryo model including some medicines, such as, thalidomide, valproic acid; recreational drugs including alcohol; environmental influences, such as viruses, specifically ZIKV, which is a newly discovered human teratogen. In addition, we discuss how the chicken embryo has provided insight on the mechanisms of teratogenesis of many compounds and also how this impact on drug safety.
... A.E.-F.B.M. El-Beltagy et al. recorded the changes of cerebellum at different time points by hematoxylin and eosin staining assay. They testified that nicotine, a neurostimulant ingredient from tobacco caused irregular cerebellar foliations with interrupted cerebellar cortex and abnormal arrangement of Purkinje cells [109]. Besides, the potential CCD rescuers are also verified in chick embryo. ...
... Nicotine plasma levels of ~25-30 ng/ml of plasma nicotine in humans are equivalent to moderate to heavy smoking (~2 packs/day) (Benowitz, 1996;de Leon et al., 2002). In chicks, desirable nicotine levels can be 50 times higher (El-Beltagy-Ael at al., 2015). The dose we use in the current study is 300 ng/ml. ...
A large proportion of the United States population has been exposed to maternal smoking in utero. Mounting data suggests that nicotine can have a negative impact on neural system development. The goal of this study was to evaluate effects of nicotine exposure on chicken neural system. The early chick embryo is an established model of the first month of embryonic development in mammals. Nicotine (nicotine hydrogen bitartrate) or vehicle (sodium bitartrate monohydrate) solutions were injected in eggs prior to incubation (300ng/ml). Three cohorts of 24 eggs distributed between treatment groups were generated. After injections, eggs were sealed and placed in the incubator. Embryos were harvested on day 5 after injections, evaluated and measured, embedded in paraplast, sectioned, and stained with hematoxylin and eosin for histological analysis. Our data indicates that the nicotine treatment does not affect viability, weight, or length of the embryos. Nonetheless, nicotine notably affects the axial rotation of the embryos (defined as a change in the dorsoventral orientation of the head during development). In this study, altered axial rotation was observed in nicotine treated groups 4 times more often than in controls (p<0.05). Microscopic analysis demonstrated that atypical axial rotation was associated with incomplete closing of the embryonic neural tube in the cervical region, but not in other areas of the tube. Further research is needed to evaluate the exact mechanisms of the developmental insult onto neural system development observed in the present study.
Monosodium glutamate (MSG) is a popular flavor enhancer largely used in the food industry. Although numerous studies have reported the neurotoxic effects of MSG on humans and animals, there is limited information about how it affects embryonic brain development. Thus, this study aimed to determine the effects of in ovo administered MSG on embryonic brain development in chickens. For this purpose, 410 fertilized chicken eggs were divided into 5 groups as control, distilled water, 0.12, 0.6 and 1.2 mg/g egg MSG, and injections were performed via the egg yolk. On days 15, 18, and 21 of the incubation period, brain tissue samples were taken from all embryos and chicks. The mortality rates of MSG-treated groups were significantly higher than those of the control and distilled water groups. The MSG-treated groups showed embryonic growth retardation and various structural abnormalities such as abdominal hernia, unilateral anophthalmia, hemorrhage, brain malformation, and the curling of legs and fingers. The relative embryo and body weights of the MSG-treated groups were significantly lower than those of the control group on incubation days 18 and 21. Histopathological evaluations revealed that MSG caused histopathological changes such as necrosis, neuronophagia, and gliosis in brain on incubation days 15, 18, and 21. There was a significant increase in the number of necrotic neurons in the MSG-treated groups compared to the control and distilled water groups in the hyperpallium, optic tectum and hippocampus regions. Proliferating cell nuclear antigen (PCNA) positive cells in brain were found in the hyperpallium, optic tectum, and hippocampus regions; there were more PCNA(+) immunoreactive cells in MSG-treated groups than in control and distilled water groups. In conclusion, it was determined that in ovo MSG administered could adversely affect embryonic growth and development in addition to causing necrosis in the neurons in the developing brain.
