Testing of cigarette smoke inhalation for teratogenicity in rats

Reckzeh, G.; Dontenwill, W; Leuschner, F

doi:10.1016/0300-483x(75)90051-7

Cited by 18 publications

(12 citation statements)

References 5 publications

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“…Brain weights were not taken due to the need for rapid dissection of brain tissue required to generate viable slices. Previous studies showed doses of cigarette smoke tolerated by the pregnant rats were similar to those used here did not induce differences in fetal weight, length, or other teratological measures (Reczeh et al, 1975). However, recent studies in the mouse have shown that tobacco smoke produces a dose-related retardation in embryonic growth (Seller and Bnait, 1995).…”

Section: Resultssupporting

confidence: 60%

Smoking during pregnancy: Postnatal effects on arousal and attentional brain systems

et al. 2007

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Prenatal exposure to cigarette smoke is known to produce lasting arousal, attentional and cognitive deficits in humans. The pedunculopontine nucleus (PPN), as the cholinergic arm of the reticular activating system (RAS), is known to modulate arousal, waking and REM sleep. Rapid eye movement (REM) sleep decreases between 10 and 30 days postnatally in the rat, with the greatest decrease occurring at 12-21 days. Pregnant dams were exposed to 150 ml of cigarette smoke for 15 min, 3 times per day, from day E14 until parturition, and the pups allowed to mature. We analyzed a) intrinsic membrane properties of PPN neurons in slices from pups aged 12-21 days, and b) the sleep state-dependent P13 auditory evoked potential, which is generated by PPN outputs, in animals allowed to age to adolescence. We found significant changes in the intrinsic membrane properties of PPN cells in prenatally exposed animals compared to intact ones, rendering these cells more excitable. In addition, we found disturbances in the habituation to repetitive stimulation in adolescent, freely moving animals, suggestive of a deficit in the process of sensory gating. These findings could explain some of the differences seen in individuals whose parents smoked during pregnancy, especially in terms of their hypervigilance and increased propensity for attentional deficits and cognitive/behavioral disorders.

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Section: Resultssupporting

confidence: 60%

Smoking during pregnancy: Postnatal effects on arousal and attentional brain systems

et al. 2007

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“…Speculation fare (25), indicated that Lo definitive conclusions could be drawn at that time. Rickzeh et al (17) found that exposure of female rats to high doses of cigarette smoke during gestation did not result in significant differences in regard to litter weight, litter size, number of implantation sites, the incidence of resorptions, or in the appearance of skeletal abnormalities when compared to untreated controls, thereby supporting the previously mentioned report. Interestingly, in a study of sera obtained at delivery from a large number of pregnant women, Nymand (15) found a significantly lower incidence of lymphocytotoxic antibodies in women who smoked compared to a matched control group of nonsmokers.…”

supporting

confidence: 62%

Effect of Cigarette Smoke Exposure on Maturation of the Antibody Response in Spleens of Newborn Mice

Herscowitz

1979

Pediatr Res

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postpartum. However, beginning at day 10 and for each subsequent time period assayed thereafter, there was a statistically significant reduction in the number of splenic PFC observed in the smokeexposed animals. On day 10, the PFC response of smoke-exposed mice was reduced by 3375, on day 14, there was a 60% reduction, whereas animals exposed to smoke from 4-10 wk showed a 90?& reduction of the splenic PFC response. Speculation fare (25), indicated that Lo definitive conclusions could be drawn at that time. Rickzeh et al. (17) found that exposure of female rats to high doses of cigarette smoke during gestation did not result in significant differences in regard to litter weight, litter size, number of implantation sites, the incidence of resorptions, or in the appearance of skeletal abnormalities when compared to untreated controls, thereby supporting the previously mentioned report. Interestingly, in a study of sera obtained at delivery from a large number of pregnant women, Nymand (15) found a significantly lower incidence of lymphocytotoxic antibodies in women who smoked compared to a matched control group of nonsmokers. In addition, the smokers had a higher incidence of urinary tract infections as well as febrile and nonfebrile virus diseases during pregnancy than did nonsmokers. Unfortunately, no mention was made of the physiologic or immunologic status of the offspring in the above study nor is any information available regarding the effect of cigarette smoke on the maturation of the immune response. The finding that exposure of newborn mice to cigarette smokeThe purpose of the present study was to determine effect, resulted in a marked inhibition of the maturation of the splenic if any, smoke exposure of neonatal animals would have on the antibody response to SRBC is consistent with previous reports of maturation of immune responsiveness as measured by the appearthe immunosuppressive effects of cigarette smoke exposure in ex~erimental animals and humans. I t is wssible that this inhibitorv ance of splenic PFC's. effect is manifest at the level of the macrophage or the thymusderived lymphocyte, both of which have been suggested to be functionally immature in the newborn mouse.The immune response to many, if not most, immunogens appears to involve a complex series of interactions among three heterogeneous functional cell types: bone marrow-derived lymphocytes (B cells), thymus-derived lymphocytes (T cells), and macrophages. It is now well accepted that the ability to respond immunologically to challenge with foreign materials undergoes a process of maturation that begins during embryonic development (21). Whereas it has been suggested that most cases of immunologic immaturity in neonatal animals or immunologic deficiency in adults can be attributed to the absence or a functional abnormality in immunocompetent B and/or T lymphocytes, there is also evidence to suggest that immaturity or defects in macrophage function can account for a lack of immune responsiveness (1, 7).Exposure of experimental animals and h...

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“…The results of these studies are highly controversial and suggest that some animal species such as rat and mouse are not suitable to serve as models for the effect of smoking on the human fetus. Thus, although in most studies the smoke expo sure far exceeded that of very heavy human smokers, there were no detrimental effects on fetal growth and development (22,26). Fur thermore, Younoszai et al (28) could not relate the reduction in fetal growth to either nicotine or carbon monoxide content, and attributed it to 'factors as yet unrecognized' in tobacco smoke.…”

Section: Discussionmentioning

confidence: 99%

“…In attempts to study the effect of exposure to cigarette smoke or of nicotine administration on fetal development, pregnant animals were exposed to heavy doses of smoke (22,26,28) or nicotine (3 -5 , 12, 24, 25). Chronic exposure (3 -5 , 12, 22, 28) was shown to affect litter size and weight, duration of pregnancy, incidence of abortion and newborn mortality.…”

Section: Introductionmentioning

confidence: 99%

Effect of Nicotine on the Development of Fetal and Suckling Rats

Hamosh¹,

Simon²,

Hamosh³

1979

Neonatology

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Nicotine, administered at a dose of 100 μg/kg/day from day 14 of gestation, did not affect maternal food intake, weight gain, length of gestation, litter size or fetal development; however, a daily dose of 1 mg/kg led to smaller litter size and higher incidence of stillbirth. Continued maternal administration of nicotine (100 μg/kg/day) until 12 days postpartum did not affect newborn growth (body weight and length and size of heart and lung) during the first week after birth; during the second week, however, the nicotine-treated group lagged behind the controls. The stomachs of pups of nicotine-treated rats contained less food than those of controls; this difference increased with age, becoming more than 40% at 12 days. We suggest that lower milk production of nicotine-treated rats interferes with the normal development of the offspring during periods of rapid growth.

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Testing of cigarette smoke inhalation for teratogenicity in rats

Cited by 18 publications

References 5 publications

Smoking during pregnancy: Postnatal effects on arousal and attentional brain systems

Smoking during pregnancy: Postnatal effects on arousal and attentional brain systems

Effect of Cigarette Smoke Exposure on Maturation of the Antibody Response in Spleens of Newborn Mice

Effect of Nicotine on the Development of Fetal and Suckling Rats

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