Cigarette smoke inhalation affects the reproductive system of female hamsters

Magers, T.; Talbot, Prudence; DiCarlantonio, G.; Knöll, Martin; Demers, David; Tsai, I-Ming; Hoodbhoy, Tanya

doi:10.1016/0890-6238(95)02002-0

Cited by 69 publications

(48 citation statements)

References 40 publications

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“…OCC pick-up requires adhesion between the tips of the cilia and the cumulus matrix, and factors that increase or decrease adhesion inhibit the rate of pick-up (Lam et al, 2000;Mahi-Brown & Yanagimachi, 1983;Norwood & Anderson, 1980). Inhalation of either MS or SS smoke prior to and during pregnancy increased the number of blebs on the oviductal epithelium of hamsters indicating smoke targets these cells (Magers et al, 1995). Both MS and SS smoke solutions inhibited ciliary beat frequency and oocyte pick-up rate in experiments using hamsters oviductal explants (Knoll & Talbot, 1998).…”

Section: Ovulation Through Fertilizationmentioning

confidence: 99%

“…Indeed, evidence from animal experiments indicates that the number of ovulating follicles decreases when exposed to smoke or smoke constituents. For example, hamsters that inhaled MS smoke for 30 days prior to and for the fi rst 7 days during pregnancy showed a dose dependent decrease in the number of corpora lutea, indicating that ovulation was inhibited (Magers et al, 1995). Moreover, benzo(a)pyrene, a chemical in cigarette smoke, decreased the number of corpora lutea in pregnant mice (Swartz & Mattison, 1985).…”

Section: Ovulation Through Fertilizationmentioning

confidence: 99%

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The effect of cigarette smoke on fertilization and pre-implantation development: assessment using animal models, clinical data, and stem cells

Talbot

Lin

2011

Biol. Res.

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Numerous studies have repeatedly shown that women who smoke experience problems establishing and maintaining pregnancies, and recent work has further demonstrated that the in utero effects of smoke may not be manifested until months or even years after birth. The purpose of this review is to examine the recent literature dealing with the effects of cigarette smoke on the earliest stages of human prenatal development. Studies in this area have included the use of animal models, patients undergoing in vitro fertilization, and embryonic stem cell models. Events leading to fertilization, such as cumulus expansion, hyperactivation of sperm motility, and oocyte pick-up by the oviduct are all impaired by smoke exposure in animal models. Steps crucial to fertilization such as the acrosome reaction and sperm binding to the zona pellucida are likewise inhibited by cigarette smoke. Preimplantation embryos and stem cells that model embryos show a number of adverse responses to smoke exposure, including poor adhesion to extracellular matrices, diminished survival and proliferation, and increased apoptosis. The current literature demonstrates that the earliest stages of prenatal development are sensitive to smoke exposure and indicates that pregnant women should be advised not to smoke during this time.

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Section: Ovulation Through Fertilizationmentioning

confidence: 99%

Section: Ovulation Through Fertilizationmentioning

confidence: 99%

The effect of cigarette smoke on fertilization and pre-implantation development: assessment using animal models, clinical data, and stem cells

Talbot

Lin

2011

Biol. Res.

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“…Cigarette smoke may interfere with the ciliary beat frequency, oocyte pick -up, and smooth muscle contractions of the infundibulum and cause mistiming (too early or too late) of the oocyte into the uterus [53,56] . A dose -dependent decrease in oocyte cumulus complex pick -up rate and ciliary beat frequency was found in a hamster oviduct model when exposing them to mainstream or sidestream smoke [57] , with similar serum cotinine levels as in human smokers [58] . Nicotine led to decreased tubal motility in rhesus monkeys [59] and diminished oviduct blood fl ow in rats [60] .…”

Section: Gamete and Embryo Transport And Uterine Receptivenessmentioning

confidence: 92%

Smoking and Reproduction

Prelog

2011

Cigarette Smoke Toxicity

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“…Sham controls received no treatment. On day 6 between 1 a.m. and 12 p.m., CAMs were fixed in place for 2 h by depositing 3% glutaraldehyde in 0.1 M cacodylate buffer (pH 7.4) both on top of and underneath the CAM, and then processed for light as described previously (Magers et al 1995;Melkonian et al 2000). CAMs were cut out of the eggs, washed in cacodylate buffer, and post-fixed in 1% osmium tetroxide for 30-60 min.…”

Section: Cam Assaymentioning

confidence: 99%

“…As inhalation of cigarette smoke inhibits fetal growth (Martin and Bracken 1986;Stillman et al 1986) and angiogenesis both in corpora lutea (Magers et al 1995) and in wounds (Ma et al 1999), we have used CAMs as a model to study how smoke influences growth and vascular development in vivo. In day 7-11 CAMs, both mainstream (smoke inhaled by an active smoker) and sidestream (smoke burning off the end of a cigarette) smoke solutions caused development of blood vessels that were attenuated and had few branches (Melkonian et al 2000).…”

Section: Introductionmentioning

confidence: 99%

CD44 and tenascin play critical roles in growth and vascular development of the chick chorioallantoic membrane and are targets of cigarette smoke

Melkonian

Wang

Chung

et al. 2004

Anatomy and Embryology

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Chorioallantoic membranes (CAMs) were used to determine which extracellular matrix molecules play essential roles in growth and vascular development in vivo and whether expression of critical molecules is affected by cigarette smoke exposure. Treatment of CAMs on day 5 of development with antibodies to CD44 or tenascin, but not to other matrix molecules, inhibited CAM growth and affected various aspects of blood vessel development including normal growth and branching of vessels, migration of vessels, and formation and differentiation of the capillary plexus. DNA synthesis was inhibited by antibodies to both C44 and tenascin which probably accounted for many of the phenotypic changes observed in treated CAMs. CD44 was located on all cells in day 5 CAMs, and tenascin, while present throughout the CAM, was especially abundant around large, non-migratory mesodermal blood vessels and endodermal cells that were positioned away from the direction of blood vessel migration. These data suggest that while tenascin is required for normal blood vessel migration, high levels of tenascin inhibit migration. The different distributions of CD44 and tenascin in CAMs and the observation that antibodies to either CD44 or tenascin produced similar phenotypes indicate that CD44 and tenascin were not functionally redundant. Mainstream smoke solutions, which produce a phenotype similar to that seen with anti-tenascin and anti-CD44, inhibited expression of CD44 mRNA and increased tenascin mRNA expression. 3-Ethylpyridine, a chemical in cigarette smoke that produced changes in CAM development similar to anti-CD44 and anti-tenascin treatment, also increased tenascin mRNA expression, but did not affect CD44. Together these data show that tenascin and CD44 play critical roles in early growth and vascular development of the CAM and support the idea that 3-ethylpyridine in mainstream smoke impairs CAM growth and vascular development by targeting expression of tenascin. 3-Ethylpyridine is generally regarded as safe and is used in many consumer products including food and tobacco.

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Cigarette smoke inhalation affects the reproductive system of female hamsters

Cited by 69 publications

References 40 publications

The effect of cigarette smoke on fertilization and pre-implantation development: assessment using animal models, clinical data, and stem cells

The effect of cigarette smoke on fertilization and pre-implantation development: assessment using animal models, clinical data, and stem cells

Smoking and Reproduction

CD44 and tenascin play critical roles in growth and vascular development of the chick chorioallantoic membrane and are targets of cigarette smoke

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