Jumping the gun: Smoking constituent BaP causes premature primordial follicle activation and impairs oocyte fusibility through oxidative stress

Sobinoff, Alexander P.; Pye, Victoria; Nixon, Brett; Roman, Shaun D.; McLaughlin, Eileen A.

doi:10.1016/j.taap.2012.01.028

Cited by 82 publications

(44 citation statements)

References 48 publications

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“…Tobacco toxins affect multiple sites in hormonal synthesis and overall physiology to the deleterious effect on fecundity, fetal survival and age at natural menopause 1 7 8 32. Recent studies support the hypothesis that tobacco exposure through active smoking adversely affects fertility 1 4 6 21 32. Our large secondary data analysis of the WHI OS concurs with these established studies both in the primary analysis and in quantified levels of age starting smoking and average number of cigarettes smoked per day throughout life.…”

Section: Discussionsupporting

confidence: 79%

“…Recent studies also support the hypothesis that tobacco exposure through active smoking adversely affects fertility 1 4 6 21 32. Findings from laboratory and epidemiological studies specify mechanisms postulated for delayed conception, including fetal ovarian germ cell loss, increases in zona pellucida thickness, and pathways in steroidogenesis that were negatively affected by tobacco smoke exposure 5 6 23 32–34 41 42.…”

Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 93%

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Associations between lifetime tobacco exposure with infertility and age at natural menopause: the Women's Health Initiative Observational Study

et al. 2015

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 78%

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Associations between lifetime tobacco exposure with infertility and age at natural menopause: the Women's Health Initiative Observational Study

et al. 2015

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“…Wu et al (2010) reported that the high levels of maternal BaP-DNA adducts may contribute to an increased risk of a missed abortion during early pregnancy. Several studies also have confirmed a relationship between infertility and BaP (Archibong et al, 2012;Sobinoff et al, 2012). Even although BaP has been reported to cause serious harm to female reproductive health, the effect of this EDC on early pregnancy is not yet clear.…”

Section: Introductionmentioning

confidence: 99%

Benzo(a)pyrene inhibits migration and invasion of extravillous trophoblast HTR‐8/SVneo cells via activation of the ERK and JNK pathway

Liu

Wang

Shen

et al. 2015

J of Applied Toxicology

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Benzo(a)pyrene (BaP) is a persistent organic pollutant (POP) that is a serious threat to human health. Numerous studies have shown that BaP causes adverse effects in pregnancy, but the mechanism remains unclear. The moderate invasion of trophoblast cells into the endometrium is an important factor during successful embryo implantation. The aim of this study was to investigate the effect and mechanism of BaP on the invasion and migration of trophoblast cells. HTR-8/SVneo cells were treated with different concentrations (1, 5, 10, 25, 50 and 100 μM) of BaP. The invasion and migration of HTR-8/SVneo cells were observed after BaP treatment. The protein levels related to migration and invasion was detected by Western blot. The results confirmed that BaP inhibits the migration and invasion of extravillous trophoblast HTR-8/SVneo cells. Further investigations indicated that the protein levels of MMP-2, MMP-9 and E-cadherin in HTR-8/SVneo cells were changed by BaP treatment. Moreover, the data demonstrated that BaP activated the MAPK signaling pathway. Pretreatment with specific inhibitors of MAPK rescued BaP-induced change in the migration and invasion of HTR-8/SVneo cells. Taken together, our results indicated that BaP inhibits invasion and the migration of HTR-8/SVneo cells, which might cause a failure in early pregnancy. Copyright © 2015 John Wiley & Sons, Ltd.

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“…This is particularly relevant to the female reproductive system, whereby the initial quantity and quality of the ovarian follicular pool are crucial to continued normal fertility [5]. A wide variety of environmental factors experienced during early development have been demonstrated to induce a longstanding impact on fertility; these include perinatal exposure to smoking [6,7], endocrine-disrupting chemicals [8,9], including excess prenatal testosterone exposure [10], and poor nutrition [11]. Recent advances in our understanding of the impact of early-life events on later-life predisposition to pathology have begun to elucidate a critical role for immunological factors.…”

Section: Introductionmentioning

confidence: 99%

Factors in Early-Life Programming of Reproductive Fitness

2015

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Fertility rates have been declining worldwide, with a growing number of young women suffering from infertility. Infectious and inflammatory diseases are important causes of infertility, and recent evidence points to the critical role of the early-life microbial environment in developmental programming of adult reproductive fitness. Our laboratory and others have demonstrated that acute exposure to an immunological challenge early in life has a profound and prolonged impact on male and female reproductive development. This review presents evidence that perinatal exposure to immunological challenge by a bacterial endotoxin, lipopolysaccharide, acts at all levels of the hypothalamic-pituitary-gonadal axis, resulting in long-lasting changes in reproductive function, suggesting that disposition to infertility may begin early in life.

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Jumping the gun: Smoking constituent BaP causes premature primordial follicle activation and impairs oocyte fusibility through oxidative stress

Cited by 82 publications

References 48 publications

Associations between lifetime tobacco exposure with infertility and age at natural menopause: the Women's Health Initiative Observational Study

Associations between lifetime tobacco exposure with infertility and age at natural menopause: the Women's Health Initiative Observational Study

Benzo(a)pyrene inhibits migration and invasion of extravillous trophoblast HTR‐8/SVneo cells via activation of the ERK and JNK pathway

Factors in Early-Life Programming of Reproductive Fitness

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