E-Cigarette Liquid Provokes Significant Embryotoxicity and Inhibits Angiogenesis

Ashour, Anas A; Alhussain, Hashim; Rashid, Umar; Abughazzah, Labiba; Gupta, Ishita; Malki, Ahmed; Vranić, Semir; Moustafa, Ala-Eddin Al

doi:10.3390/toxics8020038

Cited by 8 publications

(4 citation statements)

References 39 publications

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“…Alternatively, extracts from electronic cigarettes have been tested for their effect on angiogenesis and embryo development in the chorioallantoic membrane. Research has established that the extracts killed 70% of the embryos after a 5 day exposure period and, in addition, inhibited angiogenesis [ 50 ].…”

Section: Discussionmentioning

confidence: 99%

Nicotine Exerts Cytotoxic Effects in a Panel of Healthy Cell Lines and Strong Irritating Potential on Blood Vessels

Chioran

Sitaru

Macaşoi

et al. 2022

IJERPH

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The use of tobacco products is a major global public health issue, as it is the leading cause of preventable death worldwide. In addition, nicotine (NIC) is a key component of electronic and conventional cigarettes. Although nicotine’s addictive potential is well known, its health effects are not entirely understood. Thus, the main objective of the present study was to evaluate its toxicological profile both in vitro, at the level of three healthy cell lines, and in ovo, at the level of the chorioallantoic membrane. Five different concentrations of nicotine were used in keratinocytes, cardiomyocytes, and hepatocytes for the purpose of evaluating cell viability, cell morphology, and its impact on nuclei. Additionally, the hen’s egg test on the chorioallantoic membrane (HET-CAM) method was used to assess the biocompatibility and irritant potential of the chorioallantoic membrane. Across all cell lines studied, nicotine was proven to be significantly damaging to cell viability, with the highest concentration tested resulting in less than 2% viable cells. Moreover, the morphology of cells changed dramatically, with alterations in their shape and confluence. Nicotine-induced cell death appears to be apoptotic, based on its impact on the nucleus. In addition, nicotine was also found to have a very strong irritating effect on the chorioallantoic membrane. In conclusion, nicotine has an extremely strong toxicological profile, as demonstrated by the drastic reduction of cell viability and the induction of morphological changes and nuclear alterations associated with cellular apoptosis. Additionally, the HET-CAM method led to the observation of a strong irritating effect associated with nicotine.

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Section: Discussionmentioning

confidence: 99%

Nicotine Exerts Cytotoxic Effects in a Panel of Healthy Cell Lines and Strong Irritating Potential on Blood Vessels

Chioran

Sitaru

Macaşoi

et al. 2022

IJERPH

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“…Moreover, patients with HPV-negative OPSCC are known for high nicotine consumption throughout their lifetime. Ashour and colleagues showed that nicotine upregulates INHBA in chicken embryos ( 27 ). Hence, INHBA overexpression could be attributed to nicotine consumption.…”

Section: Discussionmentioning

confidence: 99%

INHBA is Enriched in HPV-negative Oropharyngeal Squamous Cell Carcinoma and Promotes Cancer Progression

Abou Kors,

Hofmann,

Betzler

et al. 2024

Cancer Research Communications

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Patients with oropharyngeal squamous cell carcinoma (OPSCC) caused by human papilloma virus (HPV) exhibit a better prognosis than those with HPV-negative OPSCC. This study investigated the distinct molecular pathways that delineate HPV-negative from -positive OPSCC to identify biologically relevant therapeutic targets. Bulk mRNA from 23 HPV-negative and 39 -positive OPSCC tumors (n = 62) was sequenced to uncover the transcriptomic profiles. Differential expression followed by gene set enrichment analysis was performed to outline the top enriched biological process in the HPV-negative compared to -positive entity. INHBA, the highest overexpressed gene in the HPV-negative tumor, was knocked down. Functional assays (migration, proliferation, cell death, stemness) were conducted to confirm the target’s oncogenic role. Correlation analyses to reveal its impact on the tumor microenvironment were performed. We revealed that epithelial-to-mesenchymal transition (EMT) is the most enriched process in HPV-negative compared to -positive OPSCC, with INHBA (inhibin beta A subunit) being the top upregulated gene. INHBA knockdown downregulated the expression of EMT transcription factors and attenuated migration, proliferation, stemness, and cell death resistance of OPSCC cells. We uncovered that INHBA associates with a pro-tumor microenvironment by negatively correlating with anti-tumor CD8+ T and B cells while positively correlating with pro-tumor M1 macrophages. We identified three miRNAs that are putatively involved in repressing INHBA expression. Our results indicate that the upregulation of INHBA is tumor-promoting. We propose INHBA as an attractive therapeutic target for the treatment of INHBA-enriched tumors in HPV-negative OPSCC patients to ameliorate prognosis.

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“…The effects of nicotine are dose-dependent, and it was found that while high doses inhibit cell division, low doses could stimulate angiogenesis therefore other dominant chemicals present in cigarette smoke could be responsible for decreased cell division and vessel growth [32]. A recent study has observed that E-cigarette liquid inhibits angiogenesis of the CAM for 5 days due to the upregulation of ATF-3, FOXA2, INHBA, MAPRE-2, and RIPK-1 and downregulation of SERPINA-4 AND VEGF-C genes necessary for embryogenesis as well as angiogenesis [35]. Investigation of pulmonary arteries during chick embryo development in the presence of cigarette smoke extract impaired endothelium-dependent vasodilation proving the effect of cigarette smoke on fetal vascular endothelial vasorelaxant pathways causing the development of pulmonary hypertension in the newborn [36].…”

Section: Abnormal Angiogenesismentioning

confidence: 99%

Effects of Nicotine on Chicken Embryo Development: A Review

Federico,

Hidoyatov,

Nimmagadda

et al. 2024

AJZ

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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.

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E-Cigarette Liquid Provokes Significant Embryotoxicity and Inhibits Angiogenesis

Cited by 8 publications

References 39 publications

Nicotine Exerts Cytotoxic Effects in a Panel of Healthy Cell Lines and Strong Irritating Potential on Blood Vessels

Nicotine Exerts Cytotoxic Effects in a Panel of Healthy Cell Lines and Strong Irritating Potential on Blood Vessels

INHBA is Enriched in HPV-negative Oropharyngeal Squamous Cell Carcinoma and Promotes Cancer Progression

Effects of Nicotine on Chicken Embryo Development: A Review

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