Cigarette smoke condensate exposure delays follicular development and function in a stage-dependent manner

Sadeu, Jean Clair; Foster, Warren G.

doi:10.1016/j.fertnstert.2011.03.072

Cited by 52 publications

(32 citation statements)

References 43 publications

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“…The higher odds of failing between cycle initiation and oocyte retrieval could imply that cigarette smoke disrupts the response to controlled ovarian hyper stimulation protocols or disrupts the ovary itself. This mechanism could be related to findings in animal models, in which cigarette smoke has been found to alter the serum levels of sex hormones and gametogenesis [23, 24]. Although this mechanism accounts only for contemporaneous exposures there seems to be a relation between lower fecundity and cumulative smoking exposure in epidemiological studies [25].…”

Section: Discussionmentioning

confidence: 90%

Discrete survival model analysis of a couple’s smoking pattern and outcomes of assisted reproduction

Vanegas

Chavarro

Williams

et al. 2017

Fertil Res and Pract

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Background: Cigarette smoking has been associated with worse infertility treatment outcomes, yet some studies have found null or inconsistent results. Methods: We followed 225 couples who underwent 354 fresh non-donor assisted reproductive technology (ART) cycles between 2006 and 2014. Smoking history was self-reported at study entry. We evaluated the associations between smoking patterns and ART success using multivariable discrete time Cox proportional hazards models with six time periods: cycle initiation to egg retrieval, retrieval to fertilization, fertilization to embryo transfer (ET), ET to implantation, implantation to clinical pregnancy, and clinical pregnancy to live birth to estimate hazard ratios (HR) and 95% CIs. Time-dependent interactions between smoking intensity and ART time period were used to identify vulnerable periods.

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Section: Discussionmentioning

confidence: 90%

Discrete survival model analysis of a couple’s smoking pattern and outcomes of assisted reproduction

Vanegas

Chavarro

Williams

et al. 2017

Fertil Res and Pract

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“…The doses of CSC (15 ug/ml, 30 ug/ml) were chosen based on doses used in previous studies [22], [23], [24]. Intracellular doxorubicin levels were determined by using flow cytometry to measure the drug's fluorescence in individual cells.…”

Section: Resultsmentioning

confidence: 99%

Cigarette Smoke Promotes Drug Resistance and Expansion of Cancer Stem Cell-Like Side Population

An¹,

Kiang²,

López³

et al. 2012

PLoS ONE

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It is well known that many patients continue to smoke cigarettes after being diagnosed with cancer. Although smoking cessation has typically been presumed to possess little therapeutic value for cancer, a growing body of evidence suggests that continued smoking is associated with reduced efficacy of treatment and a higher incidence of recurrence. We therefore investigated the effect of cigarette smoke condensate (CSC) on drug resistance in the lung cancer and head and neck cancer cell lines A549 and UMSCC-10B, respectively. Our results showed that CSC significantly increased the cellular efflux of doxorubicin and mitoxantrone. This was accompanied by membrane localization and increased expression of the multi-drug transporter ABCG2. The induced efflux of doxorubicin was reversed upon addition of the specific ABCG2 inhibitor Fumitremorgin C, confirming the role of ABCG2. Treatment with CSC increased the concentration of phosphorylated Akt, while addition of the PI3K inhibitor LY294002 blocked doxorubicin extrusion, suggesting that Akt activation is required for CSC-induced drug efflux. In addition, CSC was found to promote resistance to doxorubicin as determined by MTS assays. This CSC-induced doxurbicin-resistance was mitigated by mecamylamine, a nicotinic acetylcholine receptor inhibitor, suggesting that nicotine is at least partially responsible for the effect of CSC. Lastly, CSC increased the size of the side population (SP), which has been linked to a cancer stem cell-like phenotype. In summary, CSC promotes chemoresistance via Akt-mediated regulation of ABCG2 activity, and may also increase the proportion of cancer stem-like cells, contributing to tumor resilience. These findings underscore the importance of smoking cessation following a diagnosis of cancer, and elucidate the mechanisms of continued smoking that may be detrimental to treatment.

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“…However, the mechanisms underlying the association between impairment of follicular development and smoking are not well known. Studies in mice have shown that damage to follicles occurs in early stages of development [7,8] and may be caused by low levels of anti-müllerian hormone and changes in the pro-oxidant/antioxidant balance [8,9]. Also, evidence suggests additional impairment in preovulatory follicles and oocyte maturation that alters ovulation rate [10,11].…”

Section: Introductionmentioning

confidence: 99%

Cigarette smoke impairs granulosa cell proliferation and oocyte growth after exposure cessation in young Swiss mice: an experimental study

et al. 2012

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BackgroundCigarette smoke is associated with decreased female fertility, causing damage to ovarian function and disturbing follicle development. However, the effects of cigarette toxicants on ovarian function depend on duration and intensity of exposure. The aim of this study was to assess the effects of brief, intense exposure to tobacco smoke on granulosa cell number, oocyte growth, and follicle size during puberty in female Swiss mice.MethodsTen female Swiss mice aged 35 days were exposed to tobacco smoke from 3R4F reference research cigarettes. They were exposed to an automatic smoking machine 8 h/day, 7 days/week for 15 days. Ten age-matched controls were kept in a different room and exposed to ambient air. At the end of 15 days, five mice in each group were euthanized and the ovaries were analyzed for follicular morphometry and granulosa cell count. The remaining animals were kept for an additional 30 days for further analysis as an ex-smoker group and control group. Comparison between the two groups was evaluated by the Student’s t-test or a two-way ANOVA followed by Bonferroni post-test was applied for multiple comparisons.ResultsWe found that cigarette smoke impaired antral follicular growth even after exposure cessation (p < 0.001). Both smoking and ex-smoking groups exhibited similar follicle diameter. However, at the same follicular stage, the number of granulosa cells was smaller in the ex-smoking group compared to smoking animals (p < 0.001). This was associated with increased oocyte diameter in ex-smoking animals compared to smoking animals (p < 0.01).ConclusionsThe negative effects of cigarette smoking seem to last even after exposure has been interrupted. Moreover, brief exposure during puberty may induce silent oocyte disruption, which could in turn lead to decreased fecundity rates.

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Cigarette smoke condensate exposure delays follicular development and function in a stage-dependent manner

Cited by 52 publications

References 43 publications

Discrete survival model analysis of a couple’s smoking pattern and outcomes of assisted reproduction

Discrete survival model analysis of a couple’s smoking pattern and outcomes of assisted reproduction

Cigarette Smoke Promotes Drug Resistance and Expansion of Cancer Stem Cell-Like Side Population

Cigarette smoke impairs granulosa cell proliferation and oocyte growth after exposure cessation in young Swiss mice: an experimental study

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