The effect of diclofenac sodium on neural tube development in the early stage of chick embryos

Ertekın, Tolga; Bilir, Abdülkadir; Aslan, Esra; Koca, Buğra; Turamanlar, Ozan; Ertekin, Ayşe; Albay, Soner

doi:10.5603/fm.a2018.0080

Cited by 23 publications

(19 citation statements)

References 41 publications

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“…The early chick embryo model corresponds to the first month of mammalian embryonic development [59]. The development of neuron and spinal cords in chick embryo is very similar to the development of human embryos [60]. Therefore, it is feasible to use chicken embryos to study the development of human embryos in the early stage of embryo development, which can reveal the development of human embryos to a great extent.…”

Section: Discussionmentioning

confidence: 99%

Okadaic Acid Exposure Induced Neural Tube Defects in Chicken (Gallus gallus) Embryos

Jiao

Wang

et al. 2021

Marine Drugs

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Okadaic acid (OA) is an important liposoluble shellfish toxin distributed worldwide, and is mainly responsible for diarrheic shellfish poisoning in human beings. It has a variety of toxicities, including cytotoxicity, embryonic toxicity, neurotoxicity, and even genotoxicity. However, there is no direct evidence of its developmental toxicity in human offspring. In this study, using the chicken (Gallus gallus) embryo as the animal model, we investigated the effects of OA exposure on neurogenesis and the incidence of neural tube defects (NTDs). We found that OA exposure could cause NTDs and inhibit the neuronal differentiation. Immunofluorescent staining of pHI3 and c-Caspase3 demonstrated that OA exposure could promote cell proliferation and inhibit cell apoptosis on the developing neural tube. Besides, the down-regulation of Nrf2 and increase in reactive oxygen species (ROS) content and superoxide dismutase (SOD) activity in the OA-exposed chicken embryos indicated that OA could result in oxidative stress in early chick embryos, which might enhance the risk of the subsequent NTDs. The inhibition of bone morphogenetic protein 4 (BMP4) and Sonic hedgehog (Shh) expression in the dorsal neural tube suggested that OA could also affect the formation of dorsolateral hinge points, which might ultimately hinder the closure of the neural tube. Transcriptome and qPCR analysis showed the expression of lipopolysaccharide-binding protein (LBP), transcription factor AP-1 (JUN), proto-oncogene protein c-fos (FOS), and C-C motif chemokine 4 (CCL4) in the Toll-like receptor signaling pathway was significantly increased in the OA-exposed embryos, suggesting that the NTDs induced by OA might be associated with the Toll-like receptor signaling pathway. Taken together, our findings could advance the understanding of the embryo–fetal developmental toxicity of OA on human gestation.

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Section: Discussionmentioning

confidence: 99%

Okadaic Acid Exposure Induced Neural Tube Defects in Chicken (Gallus gallus) Embryos

Jiao

Wang

et al. 2021

Marine Drugs

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“…Neural and spinal development stages of chick embryo closely resemble the development stages of human embryos (Ertekin et al, 2019;Umur et al, 2013). Human embryo development is evaluated according to Carnegie stage (O'Rahilly & Müller, 2010).…”

Section: Discussionmentioning

confidence: 99%

“…Birth defects are seen in 3–5% of neonates and NTD account for 7% of newborn deaths due to birth defects (Cragan et al, 1995). There are many studies in the literature on NT development using the chicken embryo model (Crump, Chiu, & Williams, 2018; Ertekin et al, 2019; Guvenc et al, 2013, 2016; Kantarcioglu et al, 2018; Sravani, Padmaja, & Srilatha, 2017; Taskapilioglu et al, 2016). There are also some studies on the effect of BPA on various organs and systems of the chicken embryo (Kandil & Sur, 2018; Mathisen et al, 2013; Saito et al, 2012; Sashihara, Yamashita, Takagi, Nakanishi, & Furuse, 2003; Sravani et al, 2017; Tian et al, 2014; Yu et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

“…Previously, substances that were thought to be toxic for the neural tube (NT) during pregnancy were investigated using the chicken embryo model (Emon, Orakdogen, Uslu, & Somay, 2015;Mete et al, 2016). In these studies, the effect of teratogenic substances was investigated on NT closure (Ertekin et al, 2019;Guvenc et al, 2013Guvenc et al, , 2016. In addition, the effects of factors other than teratogenic agents have been investigated in recent chicken embryo studies (Kantarcioglu et al, 2018).…”

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confidence: 99%

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Impact of Bisphenol A on neural tube development in 48‐hr chicken embryos

Atay

Ertekin

Bozkurt

et al. 2020

Birth Defects Research

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Objectives: Bisphenol A (BPA) is one of the most heavily produced chemicals in the world. BPA is involved in the production of many substances such as cosmetics, various foodstuffs, toys, personal care products, detergents and plastic bottles all that are frequently used in daily life. Depending on BPA exposure, sexual maturation and reproductive function, and bone and brain development are adversely affected. The aim of this study is to investigate the possible effects of BPA on the development of the nervous system and neural tube in 48-hr chicken embryos. Methods: Thirty specific pathogen-free (SPF) fertilized eggs were used in the study. SPF eggs were placed in the incubator and divided into three groups at 28 hr of incubation; control, BPA 1 and BPA 2 (10 eggs in each group). At this stage of incubation, two different doses of BPA were injected subblastodermically with the Hamilton microinjector. At the end of 48 hr of incubation, all eggs were opened and embryos were dissected and separated from the embryonic membrane. All embryos were evaluated morphologically and histopathologically. Results: As the BPA dose increased, delays in the development of the nervous system and midline closure increased in the early period of chicken embryos. Depending on the dose, it was found that the embryo's crown-rump length and somite number decreased (p < .05). Conclusion: It was determined that BPA application on early chicken embryos adversely affected neural tube development. It was also found to delay midline closure.

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“…Environmental factors, genetic causes, and drug use during pregnancy are most common. Although the pregnancy categories of the new generation drugs used during pregnancy are certain, it is not known exactly whether they cause malformation due to their low use [6,7]. It is the chick embryo that is most similar in development to the human embryo [7].…”

Section: Introductionmentioning

confidence: 99%

Effect of ondansetron application on neural tube development in 48-hour chick embryos

2021

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The study aims to show that ondansetron, which is used safely in pregnant women, can cause serious side effects. Neural tube defects are among the most common congenital malformations of the central nervous system. It is known that genetic predisposition, environmental factors, and some drugs play an important role in the development of neural tube defects. Ondansetron is a selective 5-hydroxytryptamine-3 receptor antagonist used in the treatment of cancer, nausea, and vomiting during pregnancy and after anesthesia. In the literature studies, it was not found that developmental anomalies were observed. Seventy-five free specific pathogen eggs were incubated for 32 hours and divided into five groups of 15 eggs each, including a control group. Ondansetron was administered to these five groups by sub-blastoderm route in 4 different doses with a Hamilton microinjector. At 48 hours of incubation, the embryos were dissected and examined morphologically and histopathologically. At the end of the study, a significant dose-dependent decrease was observed in crown-rump lengths, somite numbers, and mean the number of silver-dyed nucleolar regulatory regions (AgNOR) and total AgNOR / nuclear area ratios. Statistically significant differences were observed between the experimental groups in terms of neural tube closure (p <0.05). Ondansetron has been shown to affect neuronal development and vertebral growth in chicken embryos depending on increasing doses.

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The effect of diclofenac sodium on neural tube development in the early stage of chick embryos

Abstract: This study showed that development of neurons are affected in chicken embryos after administration of diclofenac sodium. the exact teratogenic mechanism of diclofenac sodium is not clear; therefore it should be investigated.

Cited by 23 publications

References 41 publications

Okadaic Acid Exposure Induced Neural Tube Defects in Chicken (Gallus gallus) Embryos

Okadaic Acid Exposure Induced Neural Tube Defects in Chicken (Gallus gallus) Embryos

Impact of Bisphenol A on neural tube development in 48‐hr chicken embryos

Effect of ondansetron application on neural tube development in 48-hour chick embryos

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