Maternal Nicotine Exposure During Pregnancy and Lactation: I. Effect on Glycolysis in the Lungs of the Offspring (original) (raw)
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Pathophysiology, 2003
The aim of this study was to investigate the effect of maternal nicotine exposure during gestation and lactation on: (1) the development of the gas exchange area of the lungs of the offspring; and (2) to determine whether these effects are reversible. Pregnant rats received daily nicotine (subcutaneously 1 mg kg −1 body weight) during gestation and lactation. Nicotine administration started 1 day after mating and lasted until weaning on postnatal day 21. The offspring were exposed to nicotine via the placenta and mother's milk only. The lung tissue of the neonates was collected on postnatal days 14, 21, 35 and 42 and prepared for morphometry. The results obtained show that maternal nicotine exposure resulted in bigger alveolar volumes and suppressed alveolarisation in the lungs of the offspring. Flattening of the alveoli occurred as the animals aged and as a consequence the internal surface area available for gas exchange decreased; a condition that resembles panlobular emphysema. It is unlikely that these effects of maternal nicotine exposure during gestation and lactation on lung development in the offspring was due to a lower birth weight, or a reduction in the period of gestation, or a poor supply of nutrients to the offspring. The changes in the gas-exchange region of the nicotine-exposed rat pups appear to be irreversible.
Biomedical response of neonatal rat lung to maternal nicotine exposure
Pathophysiology, 1995
The influence of maternal nicotine exposure (1 mg/kg body mass/day, SC) on the biochemical response of neonatal lung was investigated. Maternal nicotine exposure during pregnancy suppressed glycolysis irreversibly and thus energy supply to especially type I epithelial cells. The lactate dehydrogenase (LDH), alkaline phosphatase (ALP) and glucose 6-phosphate dehydrogenase (G6PDH) activity in bronchoalveolar lavage (BAL) increased, thereby indicating damage to type I and II cells. The lower total lung G6PDH activity of the neonatal lungs exposed to nicotine might reduce the capacity of the lung to protect itself against foreign substances to which it is exposed, thereby rendering it more susceptible to damage.
AJP: Lung Cellular and Molecular Physiology, 2006
Boros LW, Lee W-P, Torday JS. In utero nicotine exposure alters fetal rat lung alveolar type II cell proliferation, differentiation, and metabolism. We recently suggested that alveolar interstitial fibroblast-to-myofibroblast transdifferentiation may be a key mechanism underlying in utero nicotine-induced lung injury. However, the effects of in utero nicotine exposure on fetal alveolar type II (ATII) cells have not been fully determined. Placebo, nicotine (1 mg/kg), or nicotine (1 mg/kg) ϩ the peroxisome proliferatoractivated receptor (PPAR)-␥ agonist prostaglandin J2 (PGJ2, 0.3 mg/kg) was administered intraperitoneally once daily to time-mated pregnant Sprague-Dawley rats from embryonic day 6 until their death on embryonic day 20. Fetal ATII cells were isolated, and ATII cell proliferation, differentiation (surfactant synthesis), and metabolism (metabolic profiling with the stable isotope [1,2-13 C2]-D-glucose) were determined after nicotine exposure in utero or in vitro. In utero nicotine exposure significantly stimulated ATII cell proliferation, differentiation, and metabolism. Although the effects on ATII cell proliferation and metabolism were almost completely prevented by concomitant treatment with PGJ 2, the effects on surfactant synthesis were not. On the basis of in utero and in vitro data, we conclude that surfactant synthesis is stimulated by nicotine's direct effect on ATII cells, whereas cell proliferation and metabolism are affected via a paracrine mechanism(s) secondary to its effects on the adepithelial fibroblasts. These data provide evidence for direct and indirect effects of in utero nicotine exposure on fetal ATII cells that could permanently alter the "developmental program" of the developing lung. More importantly, concomitant administration of PPAR-␥ agonists can effectively attenuate many of the effects of in utero exposure to nicotine on ATII cells. chronic lung disease; smoking; surfactant; fibroblast; peroxisome proliferator-activated receptor-␥ THERE IS COMPELLING EVIDENCE to suggest that although maternal smoking during pregnancy causes accelerated alveolar type II (ATII) cell differentiation at birth, there are significant longterm deleterious effects on pulmonary outcome (5-7, 9, 10, 15, 35). However, the mechanism(s) underlying these paradoxical pulmonary effects remain(s) largely unknown (23, 24, 28). ATII cell growth and differentiation and, hence, alveolar integrity are regulated by a number of autocrine, paracrine, and endocrine factors. In particular, mesenchymal-epithelial interactions are critically important for normal lung development and injury/repair (29 -31, 33). We recently implicated the Address for reprint requests and other correspondence:
International Archives of Occupational and Environmental Health, 2002
Objective: Histopathological examination of changes in foetal and newborn rats, and histopathological and morphometric assessments of changes in lungs, placenta, liver and kidneys of adult rats exposed to cigarette smoke were performed. Methods: Non-pregnant and pregnant Wistar female rats were exposed to cigarette smoke at a carbon monoxide concentration of 1,500 mg/m 3 for 6 h per day, 5 days per week, for 3 weeks. Levels of urine nicotine and cotinine were used as measures of exposure. Paraffin-embedded, haematoxylin and eosin (HE)-stained sections were used for examination. Morphometry of studied organs was performed using a computer image analyser. Results: Applied smoke dose and exposure time produced dramatic histopathological changes in lungs of exposed rats (emphysema, emphysematous, inflammatory, metaplastic changes) and reduction in height of respiratorybronchiole epithelium, and considerably less-marked morphological changes in hepatic (number of apoptotic hepatocytes) and renal (height of proximal convoluted tubule epithelium) cells as well as in the placenta (for example, size of giant cells in labyrinth, height of epithelium covering yolk sac). Exposure to cigarette smoke did not result in histopathological changes in lungs and liver of surviving foetuses. The duration of pregnancy was not changed but a tendency for a decrease in the mothers' fertility indices as well as some changes in foetal and newborn parameters was observed. Conclusion: Taking into account the morphological changes observed in adult rat tissues and placentae which can result in definite hormonal and trophic effects on the foetus, the possibility of early or late physiological effects in progeny under the influence of cigarette smoke must be taken into consideration.
Effects of Maternal Nicotine Exposure during Pregnancy and Lactation on
2019
Abstract: Background: Recent epidemiological studies have shown that there is an increased risk of hypertension in children born to women who smoked during pregnancy. Objective: The aim of this study was to examine the effect of fetal and neonatal exposure to nicotine, the major addictive component of cigarette smoke, on blood pressure of offspring and blood vessel structure, as well as if this hypertension induced by maternal nicotine exposure can be prevented or attenuated by vitamin C supplementation during the perinatal period or after weaning. Material and Methods: Female Wistar rats were given nicotine (1 mg/kg/day in 1 ml s.c), either saline (1 ml/day, s.c) and nicotine (1mg/kg/day in 1 ml, s.c) + vitamin C (1g/l in the drinking water) during pregnancy and lactation. It was also animals group that received vitamin C (1g/l) in the drinking water from weaning up to 5 months of age. Blood pressure was determined in the female and male offspring from weaning until 20 weeks of age. At the end of the experimental period (20 weeks), the wall structure of the abdominal aorta in was examined. Results: Maternal nicotine exposure during gestation and lactation resulted in an increased blood pressure of male offspring but not of female offspring. The result of this study also indicates that blood pressure in male offspring increased from the age of 12 weeks onwards for the male offspring of nicotine-exposed animals. Maternal vitamin C supplementation in rats exposed to nicotine during pregnancy and lactation did not prevent development of hypertension of the male offspring, whereas the vitamin C given to pups after weaning significantly improved the nicotine induced hypertension of male offspring. The wall structure of the abdominal aorta of the nicotine group was irregular and abnormal alignment of three tunics, whereas this effect was not observed in the abdominal aortic from the offspring of the saline group. Conclusion: Our study demonstrated that maternal nicotine exposure during gestation and lactation increased blood pressure of male offspring but not of female offspring and caused an alteration in the wall structure of the abdominal aorta, thus providing insight into the mechanisms underlying the increased prevalence hypertension in children exposed to cigarette smoke in utero. Also, the supplementation with vitamin C after weaning leads to a reduction of the hypertension. To our knowledge this is the first time that it is shown that hypertension induced by nicotine exposure during pregnancy and lactation, can be attenuated or even reversed. It will also be of interest to determine whether epigenetic changes occurred. Keywords: Maternal nicotine exposure, neonatal nicotine exposure, hypertension of the offspring, Wistar rats, vitamin C attenuated hypertension of the offspring.
Comparative Biochemistry and Physiology Part C: Pharmacology, Toxicology and Endocrinology, 1997
There have been a few studies that examined the oxidative stress effects of nicotine during pregnancy and lactation. We aimed to determine the adverse effects of maternal nicotine exposure during pregnancy and lactation on oxidant-antioxidant system, and to determine a protective effect of ascorbic acid (Asc). Gravid rats were assigned into four groups. In Group 1, pregnant rats received 6-mg/kg/day nicotine subcutaneously during pregnancy from 1 to 21 days of gestation and lactation (until postnatal day 21). Group 2 received nicotine and Asc for the same period. In Group 3, the rats received nicotine during lactation. Control pregnant rats (Group 4) received only saline subcutaneously. Serum malondialdehyde (MDA), myeloperoxidase (MPO), and superoxide dismutase (SOD) levels were determined at 21 days of age. Nicotine exposure decreased birth weight and pregnancy weight gain. MDA values of the rat pups exposed to nicotine in both Groups 1 and 2 were higher than those of control and Group 3. SOD and MPO values of the groups were similar. Mean birth weight and serum MDA levels of Groups 1 and 2 were similar. Nicotine exposure via placental transfer increases oxidative stress as manifested by an increase in MDA level. Asc supplementation does not prevent the adverse effects of maternal nicotine exposure.
Background: Nicotine is one of the most toxic and addictive agents in cigarette smoke. Maternal cigarette smoking may affect lung development and maturation of the fetus. Recently, it has been reported that blood vessels promote alveolar growth during development and contribute toward the maintenance of alveolar structures throughout postnatal life. Aim of the work: The aims of this study were to determine the effects of perinatal nicotine exposure on the histological structures of the developing alveoli of offspring with special reference to the role of vascular endothelial growth factors (VEGF). Materials and methods: Ten healthy pregnant rats were divided equally into control (I) and treated (II) groups. Rats of group II were subjected to a daily subcutaneous injection of 1 mg/kg of nicotine from the seventh day of gestation until the end of the experiment. Their offspring were subdivided into two subgroups at 2 and 21 postnatal days. At the time of sacrifice, all rats were anesthetized with ether and lung samples were processed for light and electron microscopic examination. Also, an immunohistochemical study was carried out for VEGF. The alveolar diameter, thickening of interalveolar septa, number of vacuolated interstitial cells, and the surface area of VEGF immunoexpression were determined and analyzed statistically. Results: In the nicotine-exposed groups, widening in alveoli and thinning of interalveolar septa in the offspring were observed. Also, the same offspring showed a reduction in VEGF immunoexpression. All these results were confirmed statistically especially at 3 weeks of age or at the time of weaning. Also, swelling in pneumocyte type I and deformed blood air barriers with a subsequent statistical increase in the number of vacuolated interstitial cells (pneumocyte type II) were observed. Conclusion: In the current work, it was found that perinatal exposure to nicotine altered lung development, an effect that may be mediated by decreased VEGF. Thus, avoidance of maternal smoking during pregnancy and lactation is highly recommended.
The maternal and fetal physiologic effects of nicotine
Seminars in Perinatology, 1996
The effects of nicotine are seen in every trimester of pregnancy, from increased spontaneous abortions in the first trimester, to increased premature delivery rates and decreased birth weights in the final trimester. The birth weight of a baby is dependent on two factors: the gestational age of the fetus at the time of delivery and the rate of fetal growth. Nicotine has been shown to affect both of these factors. Carbon monoxide, also found in tobacco, forms carboxyhemoglobin, which inhibits the release of oxygen into fetal tissues. Nicotine readily gains access to the fetal compartment via the placenta, with fetal concentrations generally 15% higher than maternal levels. The primary metabolite of nicotine, cotinine, has a half-life of 15 to 20 hours and serum concentrations that are 10-fold higher than nicotine; thus, cotinlne provides a better index of nicotine exposure because of its longer half-life. Nicotine concentrates in fetal blood, amniotic fluid, and breastmilk. The fetus and neonate may also have environmental tobacco exposure that may be significant. In animal models and humans, nicotine increases maternal blood pressure and heart rate, with a concomitant reduction in uterine blood flow. An increase in fetal heart rate is also seen, which is thought to be caused by catecholamine release. The impact of nicotine on the respiratory and central nervous system is also reviewed. In conclusion, the physiological effect of tobacco on fetal growth seems to be a culmination of both the vasoconstricfive effects of nicotine on the uterine and potentially the umbilical artery and the effects on oxygenation by carboxyhemoglobin.