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Neural tube was entirely closed and normal in appearance in regular dose cotinine group. On histopathological transverse plane sections, neural tube was visible on ventral side of superficial ectoderm with an isolated circular appearance which is almost identical to control group. (A): aorta, (N): Notocord with normal tubular structure in ventral side of neural tube, (✱): Neural tube lumen with normal structure (Hematoxylin-Eosin X400).
Source publication
Nicotine is a well-known agent among 4000 chemicals in cigarettes. About 70 to 80% of nicotine is converted to cotinine, a major metabolite. The aim of the present study is to investigate the effect of cotinine on neural tube development in a chick embryo model.
Sixty fertile, specific pathogen free eggs were divided into 6 groups for this study. I...
Context in source publication
Context 1
... distinct basal membrane was detected on the dorsal site of the neural tube and this was termed as a marker of complete separation from superficial ectoderm. The notochord was prominent on the transverse sections of the ventral side of neural tube (Figure 2) whereas much of the embryos in group 2 had an open neural tube. The defects were such that the neural folds showed no signs of contact over the neuroepithelium. ...
Citations
... From these numbers, approximately 15-25% of women continue smoking during pregnancy [1]. Over 4000 chemicals, toxicants, and carcinogens are present in cigarette smoke [4]. Both active and passive smokers are exposed to these chemicals through the mainstream smoke inhaled by the smoker, and through the side stream smoke that burns off the end of cigarettes [5]. ...
... Treated embryos also had a lack of separation between the embryo's surface and the spinal cord roof [16]. Additionally, Dalgic et al. [4], analyzed changes in stage 12 of development to ob-serve the effects of cotinine, a major metabolite of nicotine, on neural tube closure. Stage 12 embryos have a leftward-turned head, a defined telencephalon, a slight S-shape to the heart, and an anterior closure of the neuropore. ...
... However, of the ten embryos treated with high cotinine doses, only six reached stage 12, and four of those six had malformations. The embryos had defective neural tubes in the caudal and cranial sections of the thoracic region and had incomplete neural tube closures as the neural folds were not fused above the neuroepithelium [4]. ...
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.
... Cigarette smoke contains more than 4000 compounds, including aldehydes, carbon monoxide, nicotine and other compounds that cause perinatal damage [1,2]. Smoking during pregnancy can cause serious consequences such as perinatal/neonatal death, miscarriage, premature birth, impaired fetal growth, congenital anomalies and neural tube defects [3,4]. Nicotine is a chiral alkaloid accumulates in the leaves of tobacco and repre-sents~0.6%-3.0% of the dry weight [5]. ...
Perinatal exposure to nicotine imbalances the redox status in newborns. This study investigated the effect of Anethum graveolens (dill) extract on oxidative stress and tissue injury in the liver and kidney of mice newborns exposed to nicotine perinatally. Pregnant mice received nicotine (0.25 mg/kg) on gestational day 12 to day 5 after birth and/or A. graveolens extract on gestational day 1 to day 15 after birth. Newborn mice exposed to nicotine showed multiple histopathological alterations in the kidney and liver, including inflammatory cell infiltration and degenerative changes. Nicotine exposure increased hepatic and renal reactive oxygen species (ROS), lipid peroxidation, tumor necrosis factor (TNF-α), interleukin-6 (IL-6) and inducible nitric oxide synthase (iNOS) (p < 0.001), and decreased antioxidant defenses (p < 0.001). A. graveolens supplementation significantly prevented liver and kidney injury, suppressed ROS generation (p < 0.001), lipid peroxidation (p < 0.001) and inflammatory response (p < 0.001), and enhanced antioxidant defenses. In addition, A. graveolens upregulated hepatic and renal Nrf2 and HO-1 mRNA and increased HO-1 activity in normal and nicotine-exposed mice. In conclusion, A. graveolens protects against perinatal nicotine-induced oxidative stress, inflammation and tissue injury in the liver and kidney of newborn mice. A. graveolens upregulated hepatic and renal Nrf2/HO-1 signaling and enhanced antioxidant defenses in mice.
... model for the investigation of prenatal fetus development, including neural tube closure. Moreover, several earlier reports have employed this model to examine the influence of different compounds, such as cotinine, meloxicam, and phenytoin, on early embryonic neural tube development (5,8,11,13,34,35). ...
... It was shown previously, that injection of high doses of cotinine (the principle metabolite of nicotine) in ovo induces malformations at the cranial part of the thoracic neural tube (Dalgic et al., 2009). The goal of this study was to evaluate the effect of nicotine injections onto development of chicken embryos. ...
... Millex® syringe filter units (Sigma-Aldrich, St. Louice, Missouri, USA). Then the outer egg shell was wiped with alcohol, the injection was delivered from the blunt pole of the egg, and the hole was sealed with scotch tape (Dalgic et al., 2009). After injections, eggs were placed in the incubator. ...
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.
... Adverse perinatal outcomes and health complications, including respiratory disorders and childhood cancers, are associated with exposure to smoking in utero [2][3][4]. Additionally, low birth weight, premature birth, neonatal death, neural tube defects, and congenital anomalies have been identified as adverse effects of maternal smoking [5,6]. ...
... Date are M ± SEM. * P < 0 05, * * P < 0 01, and * * * P < 0 001 versus control, and # P < 0 05 versus nicotine. 6 Oxidative Medicine and Cellular Longevity improved the locomotor activity in both control and nicotine-induced female mice. ...
Nicotine exposure during pregnancy induces oxidative stress and leads to behavioral alterations in early childhood and young adulthood. The current study aimed to investigate the possible protective effects of green tea (Camellia sinensis) against perinatal nicotine-induced behavioral alterations and oxidative stress in mice newborns. Pregnant mice received 50 mg/kg C. sinensis on gestational day 1 (PD1) to postnatal day 15 (D15) and were subcutaneously injected with 0.25 mg/kg nicotine from PD12 to D15. Nicotine-exposed newborns showed significant delay in eye opening and hair appearance, and declined body weight at birth and at D21. Nicotine induced neuromotor alterations in both male and female newborns evidenced by the suppressed righting, rotating and cliff avoidance reflexes. Nicotine-exposed newborns exhibited declined memory, learning and equilibrium capabilities, as well as marked anxiety behavior. C. sinensis significantly improved the physical development, neuromotor maturation and behavioral performance in nicotine-exposed male and female newborns. In addition, C. sinensis prevented nicotine-induced tissue injury and lipid peroxidation, and enhanced antioxidant defenses in the cerebellum and medulla oblongata of male and female newborns. In conclusion, this study shows that C. sinensis confers protective effects against perinatal nicotine-induced neurobehavioral alterations, tissue injury and oxidative stress in mice newborns.
... Many studies have been done on chicken embryos to investigate the etiology of NTD. They evaluated the effects of environmental factors and drugs (Cetinkal et al., 2010;Dalgic et al., 2009;Guvenc et al., 2013;Simsek et al., 2012;Temiz et al., 2009;Whitsel et al., 2002). In this study, it was observed that the width of the neural tube was altered with the Riparin III concentrations evaluated. ...
... High fever in the mother during the first month of pregnancy, alcohol use during pregnancy, and use of some antiepileptic drugs can be specified in the etiology of neural tube closure defects (Honein et al., 2001;Tuncbilek et al., 1999). It has been demonstrated in experimental studies looking at early stage chick embryos that ethanol, high dose meloxicam, high dose progesterone, the folic acid antagonist methotrexate, and cotinine in cigarettes, causes neural tube closure defect (Barutcuoglu et al., 2001;Cetinkal et al., 2010;Dalgic et al., 2009;Erdincler et al., 2006;Vatansever et al., 2003). Glatiramer acetate affects spinal cord development through Forkhead box protein P1 (FOXP1) in the chick embryo model at high doses (Taskapilioglu et al., 2015). ...
... Principally, it increases the risk of mouth, oral cavity, pharynx, larynx, esophagus, pancreas, lung, cervix, bladder, and kidney cancers (2)(3)(4)(5). Moreover, maternal smoking is the greatest identified cause of fetal weight deficiency, premature birth, miscarriage, perinatal/ neonatal death, neural tube defects, and congenital anomalies (6)(7)(8)(9)(10)(11). Furthermore, it adversely affects the development of organs and tissues serving several functions in cardiovascular and skeletal systems (12). ...
Background/aim:
The aim of this study was to determine the antioxidative effect of curcumin on nicotine-induced mice testis.
Materials and methods:
Sixty Swiss albino male mice were divided into five groups, each containing 12 mice. The first group was used as a control. To induce toxicity in the second and third group, nicotine (0.4 mg/kg/day) was injected intraperitoneally into mice for 14 and 28 days, respectively. The mice in the fourth and fifth group were injected with nicotine (0.4 mg/kg/day) and orally treated with curcumin (200 mg/kg) for 14 and 28 days, respectively. Testosterone levels were measured from blood samples and testis tissues were examined under light and electron microscopes.
Results:
Light and electron microscopic examinations of the nicotine-induced groups showed evident degenerations in spermatogenic cells, Sertoli cells, and Leydig cells. The groups treated with curcumin had less testicular alterations. The mice that were sacrificed after 28 days in the groups treated with curcumin showed minor degenerations. Furthermore, the median levels of testosterone significantly decreased in the nicotine-induced groups in comparison with those in the control group.
Conclusion:
The results indicated that curcumin might be a potential therapeutic agent for testicular injury caused by nicotine addiction.
... 40 Moreover, nicotine increases calcium and affects embryonic development in a concentration-dependent manner, 38 while cotinine induces embryological malformation. 41 Fetal levels of nicotine and cotinine can be as high as onethird of those in active maternal smoking and contribute to a 20% risk increase of low birth weight. The adverse effects of prenatal smoke exposure extend into the postnatal period of growth and development, and increasethe risk for infant respiratory illness and perinatal mortality (including a twofold to threefold increase in the chance of sudden infant death syndrome [SIDS]). ...
Objectives:
Cigarette smoke contains over 4000 chemicals including well-characterized toxicants and carcinogens, among which is cotinine. Cotinine is the principal metabolite of nicotine that has adverse affects on the microcirculation via vasoconstriction, hypoxia and the wound-healing cascade. Its impact on spinal cord injury (SCI) has not been investigated yet. The aim of the present study is to investigate the cotinine effect on SCI.
Methods:
48 male Wistar rats were divided into six groups as follows: sham-control, sham-trauma, vehicle-control, vehicle-trauma, cotinine-control, and cotinine-trauma. Initially, a defined concentration of cotinine blood level was maintained by daily intraperitoneal injection of cotinine for 14 days in the cotinine groups. The concentration was similar to the cotinine dose in the blood level of heavy smokers. Only ethyl alcohol was injected in the vehicle groups during the same period. Then, SCI was performed by a Tator clip. The cotinine groups were compared with rats subjected to vehicle and sham groups by immunohistochemical biomarkers such as glial fibrillary acidic protein (GFAP) and 2,3-cyclic nucleotide 3-phosphodiesterase (CNP) expressions. Electron microscopic examination was also performed.
Results:
GFAP-positive cells were noted to be localized around degenerated astrocytes. Marked vacuolization with perivascular and perineural edema was seen in the cotinin consumption groups. These findings showed the inhibition of regeneration after SCI. Similarly, vacuolization within myelin layers was noted in the cotinine groups, which was detected through reduced CNP expression.
Conclusion:
Cotinine, a main metabolite of nicotine, has harmful effects on SCI via GFAP and CNP expression. The findings of the present study support the hypothesis that tobacco causes neuronal degeneration via cotinine.
... Embryo malformation (chicken) [58] Reduction cumulus expansion (pig) [59] Nicotine ...
Cigarette smoking (CS) is a crucial modifiable risk of developing several human diseases and cancers. It causes lung, bladder, breast, and esophageal cancers, respiratory disorders, as well as cardiovascular and metabolic diseases. Because of these adverse health effects, continual efforts to decrease the prevalence and toxicity of CS are imperative. Until the past decades, the impacts of natural compounds have been under investigation on the harmful effects of CS. Turmeric ( Curcuma longa ), a rhizomatous herbaceous perennial plant that belongs to the Zingiberaceae family, is the main source of curcumin. This review is an attempt to find out the current knowledge on CS's harmful effects and protective potential of curcumin in the pulmonary, liver, brain, gastrointestinal, and testis organs. According to the present review, simultaneous consumption of curcumin and CS can attenuate CS toxicities including chronic obstructive pulmonary disease, gastrointestinal toxicity, metabolic diseases, testis injury, and neurotoxicity. Moreover, curcumin suppresses carcinogenesis in the skin, liver, lungs, breast, colon, and stomach. Curcumin mediates these protective effects through antioxidant, anti‐inflammatory, anti‐apoptotic, and anti‐carcinogenicity properties.
