Nicotine exposure impairs germ cell development in human fetal ovaries cultured in vitro

Cheng, Shun‐Feng; Qin, Xu‐Jie; Han, Zeli; Sun, Xiao‐Feng; Feng, Yanni; Yang, Fan; Ge, Wei; Li, Lan; Zhao, Yong; Felici, Massimo De; Zou, Shu-Hua; Zhou, Yi; Shen, Wei

doi:10.18632/aging.101492

Cited by 17 publications

(10 citation statements)

References 66 publications

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“…The chosen nicotine concentrations were based on 12µg representing approximately 1% of the nicotine inhaled per cigarette (i.e. about 1.2mg per cigarette [32]) and 200µg representing approximately 1% of the nicotine inhaled by smoking 15-20 cigarettes per day [32]; these concentrations were also consistent with those used in previous studies [31,[33][34][35]. The treatments with CSE and nicotine had no significant effect on cell viability, as determined by flow cytometry (data not shown).…”

Section: Treatment Of Modcs With Cse or Nicotinesupporting

confidence: 62%

“…This provides a molecular basis for the reported inhibition of DC maturation and function by CSE and nicotine [6][7][8][9][10][11][12][13][14][15][16][17][18][19]. The concentrations of CSE (0.5% and 3%) and nicotine (12µg/ml and 200µg/ml) employed in this study were based on those used in previous studies [24,27,28,30,31,[33][34][35]. Although the systemic blood concentrations of nicotine in smokers are much lower (20-60 ng/ml) [36,37], our aim was to produce a reasonable model of the concentrations of cigarette smoke constituents (including nicotine) in the tissues of the respiratory tract directly exposed to these tobacco constituents during smoking.…”

Section: Discussionmentioning

confidence: 99%

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Tobacco smoke and nicotine suppress expression of activating signaling molecules in human dendritic cells

et al. 2018

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Cigarette smoke has significant toxic effects on the immune system, and increases the risk of developing autoimmune diseases; one immunosuppressive effect of cigarette smoke is that it inhibits the T cell-stimulating, immunogenic properties of myeloid dendritic cells (DCs). As the functions of DCs are regulated by intra-cellular signaling pathways, we investigated the effects of cigarette smoke extract (CSE) and nicotine on multiple signaling molecules and other regulatory proteins in human DCs to elucidate the molecular basis of the inhibition of DC maturation and function by CSE and nicotine. Maturation of monocyte-derived DCs was induced with the TLR3-agonist poly I:C or with the TLR4-agonist lipopolysaccharide, in the absence or presence of CSE or nicotine. Reverse-phase protein microarray was used to quantify multiple signaling molecules and other proteins in cell lysates. Particularly in poly I:C-matured DCs, cigarette smoke constituents and nicotine suppressed the expression of signaling molecules associated with DC maturation and T cell stimulation, cell survival and cell migration. In conclusion, constituents of tobacco smoke suppress the immunogenic potential of DCs at the signaling pathway level.

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Section: Treatment Of Modcs With Cse or Nicotinesupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

Tobacco smoke and nicotine suppress expression of activating signaling molecules in human dendritic cells

et al. 2018

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“…[33][34][35][36] Although the underlying relationship between smoking and earlier onset of menopause is not well defined, previous studies have hypothesized the irreversible toxic effect of smoking on ovarian function. 37,38 Nicotine has been found to induce apoptosis of ovarian culture that may reduce ovarian reserve oocytes. 37 Ruan and Mueck (2015) have demonstrated that smoking drastically affects both endogenous E2 and FSH levels and may cause a decrease or inactivation of the FSH hormone.…”

Section: Discussionmentioning

confidence: 99%

“…37,38 Nicotine has been found to induce apoptosis of ovarian culture that may reduce ovarian reserve oocytes. 37 Ruan and Mueck (2015) have demonstrated that smoking drastically affects both endogenous E2 and FSH levels and may cause a decrease or inactivation of the FSH hormone. 39 These observations agree with the E2 and FSH hormone profile among premature/early menopause in our study.…”

Section: Discussionmentioning

confidence: 99%

Age of Natural Menopause Among Jordanian Women and Factors Related to Premature and Early Menopause

Bustami¹,

Matalka²,

Elyyan

et al. 2021

RMHP

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The aim of this study was to assess factors related to the onset of premature/ early natural menopause among Jordanian women. Methods: A cross-sectional study was conducted in early 2016. Subjects were enrolled based on random drop-off technique to the Obstetrics and Gynecology clinics at the Jordan University Hospital. Women 18 years of age and above were initially eligible to enroll, and women who had surgically induced menopause or specific disease were excluded from the analysis. Relevant data were collected using a questionnaire that included 30 questions. The following variables were collected: socio-demographic, body mass index, chronic conditions, diseases, reproductive characteristics, and health status. Hormone indicators of menopause were tested by measuring estrogen (E2) and follicle-stimulating hormone (FSH) levels. Age at natural menopause (ANM) was self-reported retrospectively and considered an independent variable against BMI, smoking, hormone therapy, and concomitant diseases. Association analysis and multinomial logistic regression were used to examine the associated factors of ANM with adjusted odds ratios (ORs), and their 95% confidence intervals (CIs) were reported. Results: A total of 409 women were included in the analysis, aged between 20−75 years. The mean ANM in our sample was 48.5±5.0, with 2.7% of the women experienced premature menopause (ANM <40) and 7.8% early menopause . Within the menopause women (n=242), the percentage of women who had premature menopause was 4.5%, 13.6% with early menopause, and 21.1% with late menopause (ANM >52). Smoking was the major risk factor for premature/early menopausal age among Jordanian women with an OR of 2.46 (95% CI: 1.08-5.59, p<0.05). On the other hand, women with occasional arthritis symptoms and diseases such as hypertension, diabetes, dyslipidemia, and their combination were associated with average (45-52 years) or late menopause (>52 years). Conclusion: Smoking is the main contributor of premature/early menopause in Jordanian women. Increased awareness and public health policy about the adverse effects of smoking on women's reproductive health are needed.

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“…Petrik et al found α2nAChR and α7nAChR expression in ovarian tissues and isolated granulosa cells and suggested that one mechanism by which nicotine may cause the folliculogenesis defects observed in adult female rats was through the induction of apoptosis in granulosa cells and/ or oocytes via activation of these receptors. 80,81 Harmych et al designated that nicotine inhibits MAPK signaling and spheroid invasion in ovarian cancer cells. 16 In this study, the results indicate that nicotine can suppress spheroid invasion and compaction as well as proliferation in ovarian cancer cell lines, and p38 and ERK MAPK signaling pathways are important mediators of these responses.…”

Section: Ovarian and Uterine Cancermentioning

confidence: 99%

Nicotinic Acetylcholine Receptors as Potential Tumor Biomarkers in Genitourinary Cancers: a Review Study

et al. 2021

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The genitourinary tissues express the different subtypes of nicotinic acetylcholine receptors (nAChRs), which are involved in many physiologic and pathologic processes. New studies have indicated the significant role of nAChRs in multiple tumor-related properties in different types of malignancies. Genitourinary cancers (GUCs) represent a heterogeneous population of cancers, in both histology and approach to treatment. nAChRs are functionally expressed by a variety of immune cells, tumor cells, and tumor-associated cells in the microenvironment of GUCs. In the current review study, publications until May 2021 were included in the literature review to summarize the potential effects and clinical and experimental significance of nAChRs in GUCs pathogenesis. The results yielded substantial and some paradoxical evidence regard the role of different subtypes of nAChRs as potential regulators and predictive biomarkers for GUCs. The accumulated evidence demonstrated that nAChRs levels were increased in the GUCs samples, which provides clinically relevant information on utilizing nAChRs as a new biomarker to improve the prognosis of these cancers. Also, activation or blockade of these receptors may lead to different downstream signaling pathways and cause diverse effects. Regarding the significant global burden of GUCs, evaluation of these receptors and delineating their molecular mechanisms could enrich our understanding of the biology of GUCs and may have new opportunities for clinical impacts.

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Nicotine exposure impairs germ cell development in human fetal ovaries cultured in vitro

Cited by 17 publications

References 66 publications

Tobacco smoke and nicotine suppress expression of activating signaling molecules in human dendritic cells

Tobacco smoke and nicotine suppress expression of activating signaling molecules in human dendritic cells

Age of Natural Menopause Among Jordanian Women and Factors Related to Premature and Early Menopause

Nicotinic Acetylcholine Receptors as Potential Tumor Biomarkers in Genitourinary Cancers: a Review Study

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